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A REVIEW ON DIABETES MELLITUS: TYPE1 & TYPE2

Authors:
  • Dev Bhoomi Institute of Pharmacy and Research

Abstract

Diabetes mellitus (DM) also known as simply diabetes, is a group of metabolic diseases in which there are high blood sugar levels over a prolonged period This high blood sugar produces the symptoms of frequent urination, increased thirst, and increased hunger. Untreated, diabetes can cause many complications. Acute complications include diabetic ketoacidosis and nonketotic hyperosmolar coma. There are three main types of diabetes mellitus: Type 1 DM results from the body's failure to produce enough insulin. This form was previously referred to as "insulin-dependent diabetes mellitus" (IDDM) or "juvenile diabetes". The cause is unknown Type 2 DM begins with insulin resistance, a condition in which cells fail to respond to insulin properly. As the disease progresses a lack of insulin may also develop. This form was previously referred to as "non insulin-dependent diabetes mellitus" (NIDDM) or "adult-onset diabetes". The primary cause is excessive body weight and not enough exercise. Gestational diabetes, is the third main form and occurs when pregnant women without a previous history of diabetes develop a high blood glucose level. Prevention and treatment involves a healthy diet, physical exercise, not using tobacco, and being a normal body weight. Blood pressure control and proper foot care are also important for people with the disease. Type 1 diabetes must be managed with insulin WORLD JOURNAL OF PHARMACY AND PHARMACEUTICAL SCIENCES SJIF Impact Factor 7.632
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Saha et al. World Journal of Pharmacy and Pharmaceutical Sciences
A REVIEW ON DIABETES MELLITUS: TYPE1 & TYPE2
1Roshan Kumar, *2Purabi Saha, 4Yogendra Kumar, 3Soumitra Sahana,
Anubhav Dubey5 and Om Prakash5
1Department of Pharmacy, SBS College of Pharmacy, Patti, Punjab [India]
2Department of Pharmacy, Uttranchal University, Dehradun, [India]
3B. Pharma, Birbhum Pharmacy School, Birbhum, West Bengal [India].
4Department of Pharmacy, Shri Ramnathsingh Institute of Pharmaceutical Science and
Technology Shitoli Gwalior M.P India.
5Department of Pharmacology Advance Institute of Biotech and Paramedical Sciences
Kanpur India.
ABSTRACT
Diabetes mellitus (DM) also known as simply diabetes, is a group of
metabolic diseases in which there are high blood sugar levels over a
prolonged period This high blood sugar produces the symptoms of
frequent urination, increased thirst, and increased hunger. Untreated,
diabetes can cause many complications. Acute complications include
diabetic ketoacidosis and nonketotic hyperosmolar coma. There are
three main types of diabetes mellitus: Type 1 DM results from the
body's failure to produce enough insulin. This form was previously
referred to as "insulin-dependent diabetes mellitus" (IDDM) or
"juvenile diabetes". The cause is unknown Type 2 DM begins with insulin resistance, a
condition in which cells fail to respond to insulin properly. As the disease progresses a lack
of insulin may also develop. This form was previously referred to as "non insulin-dependent
diabetes mellitus" (NIDDM) or "adult-onset diabetes". The primary cause is excessive body
weight and not enough exercise. Gestational diabetes, is the third main form and occurs
when pregnant women without a previous history of diabetes develop a high blood glucose
level. Prevention and treatment involves a healthy diet, physical exercise, not using tobacco,
and being a normal body weight. Blood pressure control and proper foot care are also
important for people with the disease. Type 1 diabetes must be managed with insulin
WORLD JOURNAL OF PHARMACY AND PHARMACEUTICAL SCIENCES
SJIF Impact Factor 7.632
Volume 9, Issue 10, 838-850 Review Article ISSN 2278 4357
*Corresponding Author
Purabi Saha
Department of Pharmacy,
Uttranchal University,
Dehradun, [India]
Article Received on
02 August 2020,
Revised on 23 August 2020,
Accepted on 12 Sept. 2020
DOI: 10.20959/wjpps202010-17336
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Saha et al. World Journal of Pharmacy and Pharmaceutical Sciences
injections. Type 2 diabetes may be treated with medications with or without insulin. Insulin
and some oral medications can cause low blood sugar.
KEYWORDS: Diabetes mellitus, diagnosis, cause and treatment.
INTRODUCTION
Diabetes mellitus, disorder of macromolecule metabolism characterised by impaired ability
of the body to supply or answer endocrine and thereby maintain correct levels of sugar
(glucose) within the blood.[1] malady} may be a chronic disease that happens once the duct
gland is not any longer able to build endocrine, or once the body cannot observe use of the
endocrine it produces. endocrine may be a endocrine created by the duct gland that acts sort
of a key to let aldohexose from the food we have a tendency to eat pass from the blood
stream into the cells within the body to supply energy. All macromolecule foods square
measure countermined into aldohexose within the blood. endocrine helps aldohexose get into
the cells.[2] The endocrine endocrine moves sugar from the blood into your cells to be keep or
used for energy. With polygenic disease, your body either willn‘t build enough endocrine or
will effectively use the endocrine it does build Untreated high blood glucose from polygenic
disease can injury your nerves, eyes, kidneys, and alternative organs.[3] it's one amongst the
foremost common metabolic syndromes, since there square measure two hundred million
diabetic people within the world; this creates a desire to know the etiology of the illness and
also the factors influencing its onset. Many infective processes square measure concerned
within the development of diabetes; these vary from response destruction of the β-cells of the
duct gland with subsequent endocrine deficiency to abnormalities that end in resistance to
endocrine action. Deficient action of endocrine not off course tissues and symptom square
measure the idea of the abnormalities in macromolecule, fat, and super molecule metabolism,
inflicting diabetes‘ characteristic clinical options, small and-macro tube complications and
exaggerated risk of upset.[4] Inadequate production of endocrine (which is created by the duct
gland and lowers blood glucose), or Inadequate sensitivity of cells to the action of
endocrine.[5] The duct gland makes endocrine, however the endocrine created doesn't work
because it ought to. This condition is named endocrine resistance. to higher perceive
polygenic disease, it helps to understand additional regarding however the body uses food for
energy (a method known as metabolism). Your body is created from countless cells. to create
energy, the cells want food during a} very straightforward type. once you eat or drink, a lot of
of your food is countermined into an easy sugar known as aldohexose. aldohexose provides
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the energy your body desires for daily activities.[6] If you turn out very little or no endocrine,
or square measure endocrine resistant, an excessive amount of sugar remains in your blood.
glucose levels square measure more than traditional for people with polygenic disease.[7]
WHO graded Islamic Republic of Pakistan at seventh on polygenic disease prevalence list.[8]
Recent read on the prevalence has shown that regarding quite four.7 million individuals
tormented by polygenic disease.[9] polygenic disease symptoms square measure excessive
thirst, frequent voiding, sweating, blurred vision, fulminant weight loss, fatigue and slow
healing sores. largely patient with polygenic disease suffer from thirst, polyphagia and
nephropathy.[10] physiological condition polygenic disease solely occur throughout
physiological state. secretion changes influence endocrine that cause ineffective endocrine
production, leading to raised {blood aldohexose blood sugar glucose} level which high
glucose level effects embryo.[11] found fast dysglycemia in thirty eight.95% of a Venezuelan
sample, with a prevalence of fourteen.25% for DM and forty.7% for prediabetes. it had been
additionally found that high blood pressure, hypercholesteremia, dysglycemia and DM were
additional current in females.[12] In distinction, the WHO report shows Associate in Nursing
calculable prevalence of eight.8% for DM in South American nation. The International
polygenic disease Federation (IDF) estimates, in its 2016 report, a prevalence of
eleven.1%.[13] the chance of considerable will increase in prevalence of diabetes-related
complications partially thanks to the increase in rates of fleshiness.The possibility that the
rise within the variety of persons with DM and also the complexness of their care may
overwhelm existing health care systems .The need to require advantage of recent discoveries
on the individual and social edges of improved polygenic disease management and
interference by delivery life-saving discoveries into wider observe.[14]
Risks of polygenic disorder throughout physiological condition
Diabetes throughout physiological condition will increase fatal and maternal morbidity and
mortality. Neonates are in danger of metabolism distress, symptom, symptom, pathology,
polycythaemia, and hyper viscousness.[15]
Poor management of pre-existing (presentational) or physiological state polygenic disorder
throughout organogenesis (up to regarding ten week‘s gestation) will increase risk of the
following.
1) Major innate malformations
2) Spontaneous abortion
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Poor management of polygenic disorder later in physiological condition will increase risk of
the following.
•Fatal macrosomia (usually outlined as fatal weight > 4000 grams or > 4500 grams at birth)
Preeclampsia
Shoulder dystocia
Cesare AN delivery
Stillbirth
However, physiological state polygenic disorder may result in fatal macrosomia albeit
glucose is unbroken nearly traditional.[16]
Classification of diabetes
The first principally accepted classification of diabetes was revealed by UN agency within
the year 1980[17] and, it's changed within the year 1985.[18] the foremost common and
necessary sort of Primary or upset diabetes, that is focus of our discussion. It should vary
from secondary diabetes which incorporates kinds of symptom related to recognizable causes
within which destruction of exocrine gland islets is induced by inflammatory exocrine gland
diseases, surgery, tumors, certain medication, iron full (Hemochromatosis) and sure acquired
or genetic endocrinopathies.[19] The classification encompasses each clinical stages and
aetiological sorts of diabetes and different classes of hyperglycemia.[20] Assigning a sort of
polygenic disorder to a personal usually depends on the circumstances gift at the time of
identification, and man diabetic people don't simply match into one category[21] Primary
diabetes most likely represents a heterogeneous group of disorders that have symptom as a
typical feature[19] The new classification of diabetes contains stages which mirror the assorted
degrees of symptom in individual subjects with any of the malady processes that may cause
diabetes[22, 23] The recent and new terms of insulin-dependent(IDDM) or noninsulin-
dependent (NIDDM) that were planned by UN agency in1980 and 1985 have disappeared
and also the terms of latest classification system identifies four sorts of polygenic disorder
mellitus: type 1(IDDM), sort 2(NIDDM),―other specific types‖ and gestational polygenic
disorder (WHO professional Committee 1999). These were mirrored within the sequent
International terminology of Diseases (IND) in1991and the tenth revision of the International
Classification of Diseases (ICD-10) in 1992.[20]
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1. Hormone Dependent diabetes (Type1 IDDM)
This type of diabetes is additionally known as reaction diabetes and antecedently referred to
as juvenile-onset or ketosisprone polygenic disease. The individual may additionally ask for
with different autoimmune disorders like Graves‘ malady, Hashimoto‘s thyroiditis, and
Addison‘s malady.[24] kind I diabetes is also referred to as insulin- dependent diabetes
(IDDM), this occurs chiefly in youngsters and young adults; the onset is usually abrupt and
may be life threatenin.[4] kind one is sometimes characterized by the presence of anti
glutamic aciddecarboxylase, island cell or hormone antibodies that determine the reaction
processes that ends up in beta-cell destruction.[34] kind one polygenic disease (due to the
destruction of b-cell that is usually resulting in absolute hormone deficiency) (American
Diabetes Association, 2014). the speed of destruction of betacell is kind of variable; it are
often occur speedily in some individuals and slow in others.[18] there's a severe deficiency or
absence of hormone secretion because of destruction of ß-islets cells of the duct gland.
Treatment with injections of hormone is required.[4] Markers of immune destruction, together
with island cell auto-antibodies, and/or motorcar antibodies to hormone, and auto antibodies
to amino acid enzyme (GAD) area unit gift in 85-90 you look after people with kind one
diabetes once fasting diabetic hyperglycaemia is at first detected.[19] The exact reason behind
diabetes is stay unknown, although, in the majority, there's proof of AN reaction mechanism
involving auto-antibodies that destroy the betaislet cells.[4]
1Non-Insulin Dependent polygenic disorder Mellitus(Type2 Niddm)
Type a pair of diabetes is additionally called ketosis-resistant diabetes mellitus. The
progressive hypoglycemic agent secretary defect on the background ofinsulin resistance
(American polygenic disorder Association, 2014).[20] People with this sort of polygenic
disorder oftentimes ar proof against the action of hypoglycemic agent.[21] The semi
permanent complications in blood vessels, kidneys, eyes and nerves occur in each varieties
and are the major causes of morbidity and death from polygenic disorder.[1] The causes ar
multifunctional and predisposing issue includes: Obesity, inactive way, increasing age
(affecting middle aged and older people), Genetic issue (Ross and Wilson 2010), such
patients are at exaggerated risk of developing macrovascular and small tube
complications.[22,23]
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Gestational diabetes
The aldohexose intolerance occurring for the primary time ordiagnosed throughout gestation
is brought up as physiological state diabetes mellitus (GDM).[2] ladies World Health
Organization develop Type1 diabetes mellitus throughout gestation and girls with
undiagnosed symptomless kind a pair of diabetes that's discovered throughout gestation ar
classified with physiological state Diabetes Mellitus (GDM).[16] physiological state diabetes
(GDM) (diabetes diagnosed throughout gestation that's not clearly over diabetes).[17] The
hysiological state diabetes may develops throughout gestation could and should and will}
disappear once delivery; within the long run, youngsters born to mothers with GDM are at
larger risk of fat and kind a pair of polygenic disorder in later life, a development attributed to
the consequences of intra uterine exposure to hyper glycemia.
4. Alternative Specific sort (Monogenic Types)
The most common variety of heritable kinds of polygenic disease is developed with
mutations on body twelve in a very internal organ transcription issue brought up as
hepatocyte nuclear issue (HNF)-1a.They additionally brought up as genetic defects of beta
cells. These varieties of polygenic disease are of times characterised by onset of symptom at
associate early age (generally before age of twenty five years). they're additionally brought
up as maturity onset polygenic disease of the young (MODY)[18] or ketoacidosis-resistant
diabetes mellitus in youth or with defects of internal secretion action; persons with diseases
of the exocrine duct gland, like rubor or cystic fibrosis; persons with pathology related to
alternative endocrinopathies (e.g. acromegaly); and persons with pancreatic pathology caused
by medicine, chemicals or infections.[23] Some medicine additionally utilized in the mix with
the treatment of HIV/ AIDS or once organ transplantation. Genetic abnormalities that lead to
the lack to convert proinsulin to internal secretion are known in a very few families, and such
traits ar genetic in associate chromosome dominant pattern. They comprise but 100 percent of
DM cases.[17]
Some Common Sign and Symptoms
In DM, cells fails to metabolized aldohexose within the normal manner, effectively become
starved.[25] The long run effect of DM which incorporates progressive development of the
particular complications of retinopathy with potential visual defect, renal disorder which will
result in failure,and pathology with risk of foot ulceration, neurologist joint and features of
involuntary pathology and sexual dysfunction[26] People with polygenic disease area unit at
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will increase risk of diseases. Other, varied symptoms area unit determined due toi.
Gluconeogenesis from amino acids and body macromolecule, causing muscle wasting, tissue
breakdown and moreincreases the blood sugar level. ii. destructive metabolism of body fat,
cathartic a number of its energy andexcess production of organic compound bodies.[25]
Etiology of DM
The word etiology springs from Greek word ―aetiologia‖.Hence, etiology is outlined because
the science of finding causes andorigins during which a unwellness is arise, It includes
1. it's presently believed that the juvenile-onset (insulindependent) type has associate degree
automobile immune etiology.
2. Viruses may additionally play a task within the etiology of polygenic disease like cox
sackieB.
3. epidemic parotitis and German measles viruses all are shown toproduce morphologic
changes within the islet-cell structure.
4. The genetic role within the etiology of polygenic disease iscontroversial. probably a
genetic attribute makes associate degree = individual‘s exocrine gland additional liable to one
amongst the on top of viruses.[45] Causes of polygenic disease Milliteus Disturbances or
abnormality in gluco-receptor of ß cell in order that they reply to higher aldohexose
concentration or relative ß cell deficiency. In either manner, hypoglycaemic agent secretion is
impaired; might progress to ß cell failure.[25] the idea of principal in small vascular
unwellness resulting in neural drive, and therefore the direct effects of hyperglycemia on
vegetative cell metabolism.[26]
1. Reduced sensitivity of peripheral tissues to insulin: reduction in range of hypoglycaemic
agent receptors, ‗down regulation‘ of hypoglycaemic agent receptors. several supersensitized
and Hyper insulin aemic, however traditional glycaemic; and have associated
dyslipideaemic, hyperuriaemiac, abdominal obesity. so there's relative hypoglycaemic agent
resistance, particularly at the extent of liver, muscle and fat. Hyperinsulinaemic has been
involved in inflicting angiopathy.[24]
2. way over hyperglycemia internal secretion (glucagon) etc.obesity; causes relative
hypoglycaemic agent deficiency the ß cells lagbehind. 2 theories have in contestible
abnormalities innitric oxide metabolism, leading to altered perineural blood flow and nerve
injury.[25]
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3. different rare types of DM area unit those thanks to specific genetic defects (type 3) like
―maturity onse tdiabetes of young‖ (MODY) different endocrine disorders, pancreatectomy
and physiological state DM (GDM).[24]
4. thanks to imbalance of specific receptor will cause polygenic disease mellitus. Some
specific receptors area unit Glucagon-like peptide-1(GLP-1) receptor, peroxisomes
proliferator activated (γ) receptor (PPARγ), beta3 (ß3) ardent-receptor some enzymes like α
glycosidase, dipeptidyl protease IV enzyme etc.[24]
5. Current analysis on diabetic pathology is targeted on oxidative stress, advanced glycation-
end merchandise, protein kinase C and therefore the polyol pathway.[27]
Diagnosis of DM
The designation of polygenic disease in associate degree symptomless subject ought to never
be created on the idea of one abnormal blood sugar value. If a designation of polygenic
disease is formed, the practitioner should feel assured that the designation is totally
established since the consequences for the individual area unit extensive and long.[28] The
designation of polygenic disease mllitus embrace, excretory product sugar, blood sugar,
aldohexose tolerance check, urinary organ threshold of aldohexose, diminished aldohexose
tolerance, exaggerated aldohexose tolerance, renal symptom, extended aldohexose tolerance
curve, cortisone stressed aldohexose tolerance check, endo venous aldohexose tolerance test,
oral aldohexose tolerance check.
Treatment of DM
The treatment is to beat the causative cause and to give high doses of normal hypoglycaemic
agent. The hypoglycaemic agent demand comes back to traditional once the condition has
been controlled[29] the aims of management of DM will be achieved by:
1. to revive the disturbed metabolism of the diabetic as nearly to traditional as is according to
comfort and safety.
2. to forestall or delay progression of the short and long run hazards of the unwellness.
3. to supply the patient with data, motivation and means to undertake this own enlightened
care.
A. styles of medical aid concerned In DM
1 vegetative cell medical aid Researchers have shown that monocytes/ macrophages is also
main players that contribute to those chronic inflammations and hypoglycaemic agent
resistance in T2DM patients.[30] vegetative cell professional medical aid, a completely unique
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technology, is intended to regulate or reverse immune dysfunctions.[31] The procedure
includes: assortment of patients‘ blood current through a control system, purification of
lymphocytes from the entire blood, co-culture of them with adherent twine blood-derived
multi-potent stem cells (CB-SCs) in vitro and administration of the educated lymphocytes
(but not the CB-SCs) to the patient‘s circulation.[31]
A. varieties of medical aid concerned In DM
1. Somatic cell medical aid
Researchers have shown that monocytes/ macrophages could also be main players that
contribute to those chronic inflammations and hypoglycaemic agent resistance in T2DM
patients.[30] somatic cell professional person medical aid, a unique technology, is intended to
regulate or reverse immune dysfunctions.[31] The procedure includes: assortment of patients‘
blood current through a control system, purification of lymphocytes from the total blood, co-
culture of them with adherent wire blood-derived multi-potent stem cells (CB-SCs) in vitro
and administration of the educated lymphocytes (but not the CB-SCs) to the patient‘s
circulation
2. inhibitor medical care
A variety of antioxidants, like vitamins, supplements, plant-derived active substances and
medicines with inhibitor effects, are used for aerophilous stress treatment in T2DM patients.
Vitamin C, tocopherol tocopherol carotene square measure ideal supplements against
aerophilous stress and its complications.[32] Antioxidant that play a crucial role in lowering
the chance of developing polygenic disease and its complications.
3. anti-inflammatory drug treatment
The changes indicate that inflammation plays a polar role inthe pathological process of
T2DM and its complications.[32, 33] In T2DM, particularly in animal tissue, exocrine gland
islets, the liver, the vasculature and current leukocytes,[34] that embrace altered levels of
specific cytokines and chemokines, the number and activation state of various white blood
corpuscle populations, increased programmed cell death and tissue pathology.[34, 35]
Immunomodulatory drugs square measure provided.
B. Dietary Management
Adequate caloric worth Dietary management ought to be taken properly by the each diabetic
and non-diabetic patient such as.
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1. Balanced in reference to super molecule, sugar and fats, in all cases it's necessary to limit
sugar intake.
2. ought to change as closely as attainable to traditional
3. Food intake ought to be divided into often spaced meals of similar size
4. cut back total calorie intake by decreasing each fat and carbohydrate
5. Patient should be suggested to be constant in his dietary habits from day to day.
C. Newer endocrine Delivery Devices
A number of innovations are created to enhance ease and accuracy of endocrine
administration further on attain tight glycaemia management. These square measure
endocrine syringes, pen devices, inhaled endocrine, endocrine pumps, implantable pumps,
other routes of endocrine delivery.
D. Oral hypoglycemic or medicament Agents
Clinically helpful biguanide phenformin was made parallel to sulfonylurea‘s in 1957. Newer
approaches have perpetually been explored and have of late yielded thiazolidinediones,
meglitinide analogues, α-glucosidase inhibitors, and also the latest are dipeptidyl peptidase-
4(DPP-4) inhibitors.[17]
Important options of Oral hypo glycemic Agents
Diabetes mellitus may be thought of a illness of the fashionable world with a good impact of
morbidity, morality and also the quality of kind of the affected individual. diabetes may be a
frequent complication of neurologist syndrome that is caused by chronic exposure to
Glucocorticoids by many clinical symptoms like central fat, proximal muscles weakness,
hirsuteness and neuroscience disturbance, macro-vascular complication involuntary
pathology, digestive problems, dental issues etc.[17]
CONCULSION
Diabetes is very critical and serious complication in todays life. The lifestyle and day today
circumstances are play major role in occurring this type of serious complications. In this
review we get some idea regarding diabetes mellitus.
Author contribution
All author participated Equally.
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Conflict of interest
None
Funding
None
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36. WHO. Study Group Diabetes Mellitus, Technical report.
... If it develops clinically, diabetes is characterized by fasting and postprandial hyperglycemia, atherosclerosis, and microangiopathic vascular disease [1]. Type 2 diabetes is a disorder of the body's metabolic system that is characterized by high blood sugar levels due to decreased insulin secretion by pancreatic beta cells also known as insulin action [2]. ...
... Diabetes causes many complications such as heart disease, stroke, neuropathy, and kidney failure, and can even lead to amputation if there is gangrene anywhere on the body. [2]. Diabetes can cause various losses, including the impact on the social environment and the impact on the sufferer's finances. ...
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Diabetes Mellitus (DM) Type-2 is a chronic disease that occurs due to uncontrolled blood glucose levels in the body. Uncontrolled glucose levels in people with Type-2 Diabetes Mellitus can cause various kinds of complications, therefore this research aims to create an Android application that can help people with Type-2 Diabetes Mellitus in controlling blood glucose levels. This application creation method includes the stages of preparation and application creation by conducting previous literature studies, which produce a theoretical model. The result of this research is a lifestyle management application for type 2 diabetes mellitus patients called Selfcare Glucose Management (SCGM), which has 4 kinds of features, including a feature that can calculate daily calorie needs by displaying various types of food with a predetermined weight and number of calories, an alarm feature that functions to remind patients to take medication and inject insulin, a physical activity training feature and a feature that contains educational material about Diabetes Mellitus. This application has been tested using application measurement methods in the form of repeated manual calculations or calibration and obtained results that match the expected values. It is hoped that this application can be developed to be more interactive and communicative in its use.
... Diabetes is a metabolic condition characterized by elevated blood glucose levels (1)(2)(3)(4)(5)(6). Diabetes Mellitus has several categories: Type 1, type 2, maturity-onset response to insulin, known as insulin resistance (1). ...
... Diabetes is a metabolic condition characterized by elevated blood glucose levels (1)(2)(3)(4)(5)(6). Diabetes Mellitus has several categories: Type 1, type 2, maturity-onset response to insulin, known as insulin resistance (1). Type 2 diabetes mellitus is one of the most significant challenges of modern and developing societies. ...
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Background: Patients with chronic illnesses like type 2 diabetes mellitus (T2DM) are at a higher risk of depression and psychiatric disorders, potentially leading to adverse outcomes. Eating disorders appear to be one of the factors contributing to T2DM and resulting in poor glycemic control and complications. Objectives: This study aimed to compare the prevalence of eating disorders and suicidal ideation between morbid and non-morbid T2DM patients. Methods: A cross-sectional questionnaire was conducted at the Yazd Diabetes Research Center from August 2021 to March 2022. A total of 232 T2DM patients aged between 30 and 65 were included in the study. Through convenience sampling, data were collected using structured questionnaires to assess eating disorders, suicidal ideation, and demographic information. Statistical analyses were performed to evaluate the associations between variables. Results: The study revealed that there was no statistically significant difference in the prevalence of eating disorders between the two groups of T2DM patients (P = 0.083). However, upon considering age as a contributing factor, it was observed that younger patients afflicted with morbid T2DM exhibited a markedly higher incidence of eating disorders when compared to their non-morbid counterparts (P = 0.019). In contrast, a significant distinction emerged in terms of suicidal ideation between the two groups (P = 0.015), with patients suffering from morbid T2DM reporting elevated rates of contemplating suicide. Subgroup analyses further underscored a heightened prevalence of suicidal ideation among female patients and those aged 30 - 59 who were afflicted with morbid T2DM. Conclusions: This study highlights the importance of mental health assessment in T2DM patients, particularly those with morbid disease, younger age, higher Body Mass Index (BMI), and poor glycemic control. Early detection and intervention for eating disorders and suicidal ideation could significantly improve the overall well-being and outcomes of T2DM patients.
... Diabetes mellitus is a metabolic disorder characterized by the body's inability to produce or respond to insulin properly, so it cannot regulate blood sugar levels at normal levels [1]. Based on data from the International Diabetes Federation (IDF), the prevalence of type 2 diabetes mellitus (T2DM) jumped from 7.3 million in 2009 to 10.3 million in 2017 [2]. ...
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This study used a combination of leaves extracts from Ruellia tuberosa L. and Tithonia diversifolia plants encapsulated using gum Arabic. The selection of leaves in medicinal plants because they are rich in bioactive compounds that provide health benefits. The encapsulation technique was microencapsulation through freeze-drying, since the nanoencapsulation for the plant extracts is unlikely to be conducted due to their large particle sizes. The resulting microcapsules were then tested their biological activities in vitro. Several conditions affect microcapsules’ production, including pH, gum Arabic concentration, and stirring time were assessed. The optimum conditions were chosen based on the highest encapsulation efficiency. The results showed that the optimum microcapsules preparation was achived at pH 5, gum Arabic concentration of 4% (w/v), and stirring time of 60 min with an encapsulation efficiency of 84.29%. The in vitro assays include inhibition of alpha-amylase and antioxidant activities, resulted in the respective IC50 values of 54.74 μg/mL and 152.74 μg/mL. Releases of bioactive compounds from the microcapsules were investigated under pH 2.2 and pH 7.4 from 30 to 120 min. Results indicated a release of 43.10% at pH 2.2 and 42.26% at pH 7.4 during 120 min, demonstrating the controlled release behavior of the encapsulated bioactive compounds; nonetheless, their release behavior was not pH-dependent. This study confirms that microencapsulation has an important role in the development of plant extracts with maintained biological functions as well as maintaining their stability.
... Insulin or pharmaceuticals combined with it is effective in treating type 2 diabetes.. Low blood sugar is a side www.cmhrj.com effect of some oral medications and insulin [5]. According to the clinical study that concluded, there was a significant positive correlation between lipid profiles and HBA1c level. ...
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This study was aimed to evaluate the connection between lipid profile and glycated hemoglobin (Hba1c) parameters (LDL, HDL VLDL, cholesterol and triglyceride) in the patients of type 2 diabetes mellitus compare with healthy person, also determine the significant differences between these parameters among healthy and diabetic patients, after assumed whole blood and serum specimens from laboratory of Diabetes and Endocrinology Center in Marjan hospital and private in the Babylon City between the period from October 2022 to February 2023. The results revealed significant differences (P ˂ 0.05) between study groups in the levels of Hba1c, also it was revealed significant increase (P ˂ 0.05) in all lipid profile include: cholesterol, LDL, HDL, VLDL levels in diabetic group of study compare with control, the results showed significant positive correlation between VLDL and Hba1c in diabetic group, also it was revealed positive correlation between cholesterol and Hba1c in control and diabetic groups, and the results showed negative correlation between triglycerides and Hba1c in both control and diabetic groups, and the results revealed significant positive correlation between body mass index and glycated glucose (Hba1c) in diabetic group. The research was concluded that the lipid profile level in diabetic patients is correlated with the HbA1c value and the significant positive correlation was conducted between HDL and Hba1c in diabetic group, also the study was concluded significant differences (P ˂ 0.05) between diabetic and healthy group in the levels of Hba1c and other lipid profile parameters.
... Furthermore, it has been extensively documented that diallyl trisulfide exhibits a high level of contact/fumigant toxicity against S. oryzae (LD50 = 6.2 μg/mg; LC50 = 8.4 mg/L), S. zeamais (LD50 = 5.54 μg/mg; LC50 = 6.32 mg/L), and T. castaneum (LD50 = 1.02 μg/mg; LC50 = 0.83 mg/L) [35]. Similar to the previous example, it has been demonstrated that diallyl trisulfide, which has a mortality rate of 100% when exposed to 0.125 μL/L for a period of 48 hours, is more hazardous to R. speratus than diallyl disulfide, which has a mortality rate of 33% when exposed to 0.125 μL/L for 48 hours [36]. The contact toxicity of diallyl trisulfide against Bursaphelenchus xylophilus was found to be significantly higher (LC50 of 2.79 μL/L) compared to diallyl disulfide (LC50 of 37.06 μL/L) throughout the study [37]. ...
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There is a possibility that diallyl disulfide and diallyl trisulfide can alleviate neuropathic pain in rats that have been subjected to CCI. The mechanisms by which these compounds alleviate pain entail an increase in the levels of H2S, BDNF, and Nrf2 in the sciatic nerve and the dorsal root ganglion (DRG). The use of garlic as a functional food and as a great source of pharmacologically active compounds is widely recognised and generally accepted. One of the most important bioactive components of garlic is called diallyl disulfide (DADS), and it possesses a number of beneficial biological effects. These capabilities include anti-inflammatory, antioxidant, antibacterial, cardiovascular protective, neuroprotective, and anticancer actions. In this review, the biological roles of DADS were reviewed in a systematic manner, and the molecular mechanisms that underlie these functions were explored. We have high hopes that this review will not only offer direction and insight into the existing body of literature, but will also make it possible for future study and the development of DADS for the intervention and treatment of other disorders.
... Diabetes mellitus (DM) is considered the oldest chronic disease that is characterized by high glucose levels in the blood. It mainly occurs due to the scarcity of insulin production and can be classified into two types: type 1 (T1DM) and type 2 (T2DM) DM (1,2). The condition arises from the destruction of pancreatic beta-cells which consequently cannot produce insulin. ...
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Introduction Diabetes mellitus (DM) is recognized as one of the oldest chronic diseases and has become a significant public health issue, necessitating innovative therapeutic strategies to enhance patient outcomes. Traditional treatments have provided limited success, highlighting the need for novel approaches in managing this complex disease. Methods In our study, we employed graph signature-based methodologies in conjunction with molecular simulation and free energy calculations. The objective was to engineer the CA33 monoclonal antibody for effective targeting of the aP2 antigen, aiming to elicit a potent immune response. This approach involved screening a mutational landscape comprising 57 mutants to identify modifications that yield significant enhancements in binding efficacy and stability. Results Analysis of the mutational landscape revealed that only five substitutions resulted in noteworthy improvements. Among these, mutations T94M, A96E, A96Q, and T94W were identified through molecular docking experiments to exhibit higher docking scores compared to the wild-type. Further validation was provided by calculating the dissociation constant (KD), which showed a similar trend in favor of these mutations. Molecular simulation analyses highlighted T94M as the most stable complex, with reduced internal fluctuations upon binding. Principal components analysis (PCA) indicated that both the wild-type and T94M mutant displayed similar patterns of constrained and restricted motion across principal components. The free energy landscape analysis underscored a single metastable state for all complexes, indicating limited structural variability and potential for high therapeutic efficacy against aP2. Total binding free energy (TBE) calculations further supported the superior performance of the T94M mutation, with TBE values demonstrating the enhanced binding affinity of selected mutants over the wild-type. Discussion Our findings suggest that the T94M substitution, along with other identified mutations, significantly enhances the therapeutic potential of the CA33 antibody against DM by improving its binding affinity and stability. These results not only contribute to a deeper understanding of antibody-antigen interactions in the context of DM but also provide a valuable framework for the rational design of antibodies aimed at targeting this disease more effectively.
... Furthermore, it has been extensively documented that diallyl trisulfide exhibits a high level of contact/fumigant toxicity against S. oryzae (LD50 = 6.2 μg/mg; LC50 = 8.4 mg/L), S. zeamais (LD50 = 5.54 μg/mg; LC50 = 6.32 mg/L), and T. castaneum (LD50 = 1.02 μg/mg; LC50 = 0.83 mg/L) [35]. Similar to the previous example, it has been demonstrated that diallyl trisulfide, which has a mortality rate of 100% when exposed to 0.125 μL/L for a period of 48 hours, is more hazardous to R. speratus than diallyl disulfide, which has a mortality rate of 33% when exposed to 0.125 μL/L for 48 hours [36]. The contact toxicity of diallyl trisulfide against Bursaphelenchus xylophilus was found to be significantly higher (LC50 of 2.79 μL/L) compared to diallyl disulfide (LC50 of 37.06 μL/L) throughout the study [37]. ...
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A big problem in healthcare around the world is neurological illnesses. There is a huge healthcare and financial burden on society worldwide due to the dramatically increased risk of chronic sickness and diseases linked with posed lifestyle changes. Fine treatment for sick illnesses with few known adverse effects is the goal of research. A number of functional food studies have been launched in the last few decades in an effort to identify meals with enhanced therapeutic activity and reduced adverse effects. As a result, research into nutraceutical therapy for illness prevention and various extraction procedures for disorders has been underway. Progressive memory loss characterises Alzheimer's disease (AD), a neurodegenerative disorder. The pharmaceutical options available today are expensive, come with unwanted side effects, and are in short supply. Scientists and researchers have noticed that nutraceuticals have a big impact. The anti-Alzheimer's efficacy of nutraceuticals was examined in a number of clinical and preclinical investigations. The study of new therapeutic targets, such as the pathophysiological mechanisms and unique cascades, has resulted from the growing understanding of the AD pathogenesis. Therefore, the most effective and well-known nutraceuticals will be showcased in the present development, together with brief mechanisms involving antioxidants, autophagy control, anti-inflammatory, mitochondrial homeostasis, and more. Nutraceuticals have real-world impacts, and getting your hands on phytochemicals and other vital bioactive ingredients from therapeutically active foods is a top priority. Because of this, the term "functional foods" has been muddied and replaced with similar ones such as "pharmafoods," "medifoods," "vita foods," or "medicinal foods." Nutraceuticals are in high demand to counteract neurological interventions, and there is an urgent need to stick to healthy options. Nutraceuticals may play a preventative role in neurological therapies due to the demonstrated correlation between dietary patterns and lifestyle factors and neurodegeneration. Examining high-quality clinical trials is the focus of the present study, which touches on several important neurological topics. In light of nutraceuticals' promise as multi-targeted therapy for Alzheimer's disease, it is critical to assess them as promising lead molecules for the development of new drugs. Prospective studies should, according to the authors' understanding, take into account blood-brain barrier permeability alteration, bioavailability, and features of randomised clinical trials.
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The prevalence of cardiovascular diseases (CVDs) is constantly rising, making them a major health burden. In terms of global mortality and morbidity, they are still at the top. An alternate method of treating many illnesses, including CVDs, is the use of medicinal herbs. There is a current, unprecedented push to include herbal remedies into contemporary healthcare systems. The widespread conviction in their safety and the fact that they offer more effective treatment at a lower cost than conventional modern medicines are two of the main factors propelling this movement. However, there has not been enough testing of the purported safety of herbal remedies. As a result, people need to know that medical herbs can be toxic, have possibly fatal side effects, and can interact negatively with other drugs. Experimental evidence suggests that medicinal herbs may be useful in the treatment of cardiovascular diseases (CVDs) due to their ability to inhibit multiple risk factors for these conditions. So, in order to successfully use herbs in CVD therapy, there have been numerous initiatives to transition medicinal herb research from the lab to the clinic. Presented below are cardiovascular diseases (CVDs) and the variables that put people at risk for developing them. Next, we provide a synopsis of herbal medicine's role in the treatment of disease, with a focus on cardiovascular diseases. In addition, information is compiled and examined about the ethnopharmacological therapeutic possibilities and medicinal qualities against cardiovascular diseases of four commonly used plants: ginseng, gingko biloba, ganoderma lucidum, and gymnostemma pentaphyllum. The use of these four plants in the treatment of cardiovascular diseases (CVDs) including myocardial infarction, hypertension, peripheral vascular disorders, coronary heart disease, cardiomyopathies, and dyslipidemias has been well examined. We are also making an effort to describe the current in vitro and in vivo investigations that have attempted to examine the cellular and molecular underpinnings of the four plants' cardio-protective effects. Lastly, we highlighted the effectiveness, safety, and toxicity of these four medicinal herbs by reviewing and reporting the results of current clinical trials. GRAPHICAL ABSTRACT 84 This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)
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The relative roles of obesity, insulin resistance, insulin secretory dysfunction, and excess hepatic glucose production in the development of non-insulin-dependent diabetes mellitus (NIDDM) are controversial. We conducted a prospective study to determine which of these factors predicted the development of the disease in a group of Pima Indians. A body-composition assessment, oral and intravenous glucose-tolerance tests, and a hyperinsulinemic--euglycemic clamp study were performed in 200 non-diabetic Pima Indians (87 women and 113 men; mean [+/- SD] age, 26 +/- 6 years). The subjects were followed yearly thereafter for an average of 5.3 years. Diabetes developed in 38 subjects during follow-up. Obesity, insulin resistance (independent of obesity), and low acute plasma insulin response to intravenous glucose (with the degree of obesity and insulin resistance taken into account) were predictors of NIDDM: The six-year cumulative incidence of NIDDM was 39 percent in persons with values below the median for both insulin action and acute insulin response, 27 percent in those with values below the median for insulin action but above that for acute insulin response, 13 percent in those with values above the median for insulin action and below that for acute insulin response, and 0 in those with values originally above the median for both characteristics. Insulin resistance is a major risk factor for the development of NIDDM: A low acute insulin response to glucose is an additional but weaker risk factor.
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To study the prevalence and determinants of glucose intolerance in a general Caucasian population. A random sample of 50- to 74-year old Caucasians (n = 2,484) underwent oral glucose tolerance tests. Multiple regression analyses were performed to study the association of 2-h postload plasma glucose values with potential determinants. Prevalence of known and newly detected diabetes and impaired glucose tolerance was 3.6, 4.8, and 10.3%, respectively. In women, but not in men, the association of body mass index with 2-h glucose was fully accounted for by the waist-to-hip ratio. Maternal history of diabetes was twice as prevalent as paternal history, but paternal history only was associated with 2-h glucose. In addition, paternal history was a stronger determinant in men than in women. An independent positive association with 2-h plasma glucose was found for alcohol use of > 30 g/day in women and for intake of total protein, animal protein, and polyunsaturated fatty acids in men. An independent inverse association with 2-h plasma glucose was demonstrated for height (both sexes), alcohol use of < or = 30 g/day (both sexes), energy intake (in men), and, unexpectedly, current smoking (in men). The prevalence of diabetes in elderly Caucasians was 8.3%. In men, dietary habits may unfavorably influence glucose tolerance independent of obesity.
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Islet cell antibodies (ICAs) are predictive of type I diabetes in first-degree relatives, but this immunohistochemical assay has proven difficult to standardize. As an alternative, we assessed the use of radioassays for antibodies against three molecularly characterized islet autoantigens, including ICA512bdc (amino acid residues 256-979 of the IA-2 molecule, incorporating the intracellular domain). We measured insulin autoantibodies (IAAs), GAD autoantibodies (GAAs), and ICA512bdc autoantibodies (ICA512bdcAAs) by radioassay, in addition to ICAs, in 882 first-degree relatives of patients with type I diabetes, 50 of whom later developed diabetes with a median follow-up of 2.0 years (maximum 11.3 years). The cutoff for each radioassay was determined by testing >200 control subjects. When autoantibody frequencies among the relatives were analyzed according to relationship to the proband, the offspring of diabetic fathers had a higher frequency of ICA5I2bdcAAs (P = 0.008), IAAs (P = 0.0001) and GAAs (P = 0.0001) than the offspring of diabetic mothers. ICA512bdcAAs and IAAs both showed a significant association with HLA-DR4-DQ8 (P = 0.0005). Among relatives developing diabetes, 98% had one or more of IAAs, GAAs, or ICA512bdcAAs, and 80% had two or more of these autoantibodies, compared with none of the control subjects. Using survival analysis to allow for different lengths of follow-up, there was a significant increase in the risk of diabetes with the number of these autoantibodies present, comparing zero, one, two, and three autoantibodies (P < 0.0001, log-rank test), and by Cox regression analysis, this was independent of ICAs and age. For relatives with two or more of these autoantibodies, the risk of diabetes within 3 years was 39% (95% CI, 27-52) and the risk within 5 years was 68% (95% CI, 52-84). Relatives with all three autoantibodies had a risk within 5 years estimated to be 100%. The presence of low first-phase insulin release further increased the risk for relatives with one or two autoantibodies. We conclude that the presence of two or more autoantibodies (out of IAAs, GAAs, and ICA512bdcAAs) is highly predictive of the development of type I diabetes among relatives.
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A survey conducted in 1988-1989, in the city of Madras, South India, showed that the prevalence of diabetes mellitus in adults was 8.2% and prevalence of impaired glucose tolerance (IGT) was 8.7%. The present survey was another cross-sectional study conducted 5 years later in the same urban area to study the temporal changes in the prevalence of diabetes and IGT. The two sample populations surveyed were similar in age structure and socioeconomic factors. In the second survey in 1994-1995, a total of 2,183 subjects, 1,081 men and 1,102 women, with a mean age of 40 +/- 12 years were tested by an oral glucose tolerance test; fasting and 2-h post-glucose plasma glucose were measured. Anthropometric measurements, details of physical activity and clinical history of diabetes were recorded. Age-standardised prevalence of diabetes had increased to 11.6% from 8.2% in 1989 and IGT was 9.1%, similar to 8.7% in 1989. Multiple regression analysis showed age, waist:hip ratio, body mass index (BMI) and female sex were correlated to diabetes. Family history of diabetes showed interaction with age and BMI. Prevalence of IGT correlated to age, BMI and waist:hip ratio. This study highlights the rising trend in the prevalence of non-insulin-dependent diabetes (NIDDM) in urban Indians. The persistent high prevalence of IGT may also be a predictor of a further increase in NIDDM in the future. No significant differences in the anthropometric data were noted in this compared to the previous study.
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To determine if impaired fasting glucose (IFG; fasting plasma glucose level 6.1-6.9 mmol/l) can predict future type 2 diabetes as accurately as does impaired glucose tolerance (IGT; 2-h plasma glucose level 7.8-11.0 mmol/l). A longitudinal population-based study was performed with surveys in 1987 and 1992 on the island of Mauritius, assessing diabetes status by the oral glucose tolerance test. A total of 3,717 subjects took part in both surveys. Of these subjects, 3,229 were not diabetic in 1987 and formed the basis of this study. At baseline, there were 607 subjects with IGT and 266 subjects with IFG. There were 297 subjects who developed diabetes by 1992. For predicting progression to type 2 diabetes, the sensitivity, specificity, and positive predictive values were 26, 94, and 29% for IFG and 50, 84, and 24% for IGT, respectively. Only 26% of subjects that progressed to type 2 diabetes were predicted by their IFG values, but a further 35% could be identified by also considering IGT. The sensitivities were 24% for IFG and 37% for IGT in men and 26% for IFG and 66% for IGT in women, respectively. These data demonstrate the higher sensitivity of IGT over IFG for predicting progression to type 2 diabetes. Screening by the criteria for IFG alone would identify fewer people who subsequently progress to type 2 diabetes than would the oral glucose tolerance test.
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The goal of this study was to estimate the prevalence of diabetes and the number of people of all ages with diabetes for years 2000 and 2030. Data on diabetes prevalence by age and sex from a limited number of countries were extrapolated to all 191 World Health Organization member states and applied to United Nations' population estimates for 2000 and 2030. Urban and rural populations were considered separately for developing countries. The prevalence of diabetes for all age-groups worldwide was estimated to be 2.8% in 2000 and 4.4% in 2030. The total number of people with diabetes is projected to rise from 171 million in 2000 to 366 million in 2030. The prevalence of diabetes is higher in men than women, but there are more women with diabetes than men. The urban population in developing countries is projected to double between 2000 and 2030. The most important demographic change to diabetes prevalence across the world appears to be the increase in the proportion of people >65 years of age. These findings indicate that the "diabetes epidemic" will continue even if levels of obesity remain constant. Given the increasing prevalence of obesity, it is likely that these figures provide an underestimate of future diabetes prevalence.
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As our knowledge of type 1 (insulin-dependent) diabetes increases, so does our appreciation for the pathogenic complexity of this disease and the challenges associated with its treatment. Many new concepts about the pathogenesis of this disorder have arisen. The role of genetics versus environment in disease formation has been questioned, and the basis on which type 1 diabetes is characterised and diagnosed is the subject of much debate. Additionally, the care and treatment of patients with type 1 diabetes has seen a rapid evolution; with genetically engineered insulins, glucose monitoring devices, and algorithms all contributing to a decrease in disease-related complications. We focus this seminar on these changing views, and offer a new perspective on our understanding of the pathogenesis of type 1 diabetes and on principles for therapeutic management of patients with this disorder.
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Type 1 diabetes (T1D) results from the destruction of pancreatic beta cells. Genetic factors are believed to be a major component for the development of T1D, but the concordance rate for the development of diabetes in identical twins is only about 40%, suggesting that nongenetic factors play an important role in the expression of the disease. Viruses are one environmental factor that is implicated in the pathogenesis of T1D. To date, 14 different viruses have been reported to be associated with the development of T1D in humans and animal models. Viruses may be involved in the pathogenesis of T1D in at least two distinct ways: by inducing beta cell-specific autoimmunity, with or without infection of the beta cells, [e.g. Kilham rat virus (KRV)] and by cytolytic infection and destruction of the beta cells (e.g. encephalomyocarditis virus in mice). With respect to virus-mediated autoimmunity, retrovirus, reovirus, KRV, bovine viral diarrhoea-mucosal disease virus, mumps virus, rubella virus, cytomegalovirus and Epstein-Barr virus (EBV) are discussed. With respect to the destruction of beta cells by cytolytic infection, encephalomyocarditis virus, mengovirus and Coxsackie B viruses are discussed. In addition, a review of transgenic animal models for virus-induced autoimmune diabetes is included, particularly with regard to lymphocytic choriomeningitis virus, influenza viral proteins and the Epstein-Barr viral receptor. Finally, the prevention of autoimmune diabetes by infection of viruses such as lymphocytic choriomeningitis virus is discussed.