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![GIP gene consists of 6 exons and located on human chromosome 17. PreproGIP undergoes proteolytic processing for the generation of GIP. GIP comprises of 42 amino acids [31].](profile/Hayder-Al-Aubaidy/publication/298331758/figure/fig1/AS:398397170307072@1471996695977/GIP-gene-consists-of-6-exons-and-located-on-human-chromosome-17-PreproGIP-undergoes.png)
GIP gene consists of 6 exons and located on human chromosome 17. PreproGIP undergoes proteolytic processing for the generation of GIP. GIP comprises of 42 amino acids [31].
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![Fig. 2. Signifying role of GIP in peripheral tissues [31].](profile/Hayder-Al-Aubaidy/publication/298331758/figure/fig2/AS:718015612071936@1548199670482/Signifying-role-of-GIP-in-peripheral-tissues-31_Q320.jpg)
This review paper highlights the major advances investigating the roles of glucose dependent insulinotropic polypeptide and its receptors in glucose metabolism and their potential use in management of type 2 diabetes mellitus. It also focusses on the role of dipeptidyl peptidase-4 inhibitors in the treatment of this disease. This study discussed th...
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... why it was termed as the ''Gastric Inhibitory Polypeptide'' [20]. Later studies confirmed that GIP was capable of stimulating secretion of insulin in animals and humans. Since the inhibitory effect was revealed at pharmacological doses and incretin effect at physiological level so GIP was renamed as glucose dependent insulinotropic peptide [21] (Fig. ...
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... Glucagon-like peptide-1 (GLP1) and glucose-dependent insulinotropic peptide (GIP) are two major incretin hormones that mediate glycemic control via satiety promotion, glucagon secretion suppression and gastric emptying rate reduction [3][4][5][6]. They are responsible for about 50% to 65% insulin secreted during ingestion but this effect does not last due to their extremely short half-lives following secretion [7,8]. This metabolic characteristic is as a result of rapid degradation by dipeptidyl peptidase IV (DPP-IV), resulting in loss From the peaks, 41 phytocompounds ranging from 2-furanmethanediol, dipropionate (5.702) to 17-octadecynoic acid (20.721) were identified for NLE based on their mass spectra and retention time ( Table 1). ...
... This domain has been reported to be larger in DPP-IV compared to other DPP isoforms, thereby having the ability to accommodate the large hydrophobic phytyl side chain of vitamin E suggesting class 3 binding [50]. Since these hit compounds exhibited lower binding energies and bound tightly to DPP-IV, they may play a role in preventing the rapid degradation of GLP1 and GIP, concomitantly having a remarkable impact on glycemic homeostasis and ultimately diabetes [8]. The binding classification of these lead compounds has not been previously reported to the best of our knowledge. ...
Dipeptidyl peptidase IV (DPP-IV) is a pharmacotherapeutic target in type 2 diabetes. Inhibitors of this enzyme constitute a new class of drugs used in the treatment and management of type 2 diabetes. In this study, phytocompounds in Nauclea latifolia (NL) leaf extracts, identified using gas chromatography–mass spectroscopy (GC-MS), were tested for potential antagonists of DPP-IV via in silico techniques. Phytocompounds present in N. latifolia aqueous (NLA) and ethanol (NLE) leaf extracts were identified using GC–MS. DPP-IV model optimization and molecular docking of the identified compounds/standard inhibitors in the binding pocket was simulated. Drug-likeness, pharmacokinetic and pharmacodynamic properties of promising docked leads were also predicted. Results showed the presence of 50 phytocompounds in NL extracts of which only 2-O-p-methylphenyl-1-thio-β-d-glucoside, 3-tosylsedoheptulose, 4-benzyloxy-6-hydroxymethyl-tetrahydropyran-2,3,5-triol and vitamin E exhibited comparable or better binding iGEMDOCK and AutoDock Vina scores than the clinically prescribed standards. These four compounds exhibited promising drug-likeness as well as absorption, distribution, metabolism, excretion and toxicity (ADMET) properties suggesting their candidature as novel leads for developing DPP-IV inhibitors.
... Prediabetes mellitus is a pathological state that represents an elevation of plasma glucose above the normal range but below that of clinical diabetes (1)(2)(3)(4)(5). Prediabetes mellitus is characterized by impaired fasting glucose (IFG) and/or impaired glucose tolerance (IGT) (4,5). ...
... IFG and IGT are risk factors for type 2 diabetes, and the risk is even greater when IFG and IGT occur together (1,2). The annual risk of prediabetes developing into diabetes is 5-10%, with a similar proportion converting back to normoglycaemia (2,3). ...
... Prediabetes mellitus is a pathological state between normoglycemia and diabetes mellitus, which is characterized by IGT and mild hyperglycemia (1)(2)(3). In the present study, a prediabetic rat model was established based on the method of Rato et al (22), and was used to examine blood glucose levels and glucose intolerance. ...
Previous studies by our group have indicated that exercise intervention can ameliorate endothelial dysfunction, which is an early pathophysiological change of prediabetes mellitus. The present study aimed to test the hypothesis that nitric oxide synthases (NOSs), which are expressed in blood vessel endothelium, contribute to the mitigation of vascular endothelium-dependent dysfunction by aerobic exercise in prediabetes mellitus. A prediabetic rat model was established by feeding the rats an additional high-energy diet, and was confirmed by testing blood glucose levels, the area-under-the-curve for the blood glucose tests (P<0.05) and the changes to the histological morphology of the thoracic aorta. Further examination identified that NOS expression changed significantly between the control and prediabetes groups, indicating endothelial dysfunction in the prediabetic rats. Following aerobic exercise, a significant increase in NOS, endothelial (eNOS) mRNA and protein expression (P<0.05), and a significant decrease in NOS, inducible (iNOS) mRNA and protein expression (P<0.05) was identified in the prediabetic rats compared with the control group. No significant change in nitric oxide synthase, brain expression was observed in the prediabetic rat group compared with the control group. Notably, there was also a significant increase and decrease in eNOS and iNOS activity, respectively, in the prediabetes group compared with the control group (P<0.05). Furthermore, nitric oxide (NO) concentration in the vascular endothelium was detected, which revealed a significant increase in NO concentration in the prediabetic rats following aerobic exercise compared with the control (P<0.05). The present study provided results that demonstrated that aerobic exercise ameliorated the vascular endothelium-dependent dysfunction through the NOS/NO signaling pathway, which is primarily regulated by NOS expression and activity, in prediabetes mellitus. The current study provided the theoretical basis for the use of exercise intervention to prevent diabetes mellitus during the early stage.
... In 2010, the global prevalence of IGT is about 343 million and the International Diabetes Federation predicts that prediabetic patients will reach 471 million by 2035 (IDF, 2015). Furthermore, the annual probability of prediabetes converted to diabetes is about 5-10%, with similar proportion converting back to normoglycaemia (Gupta et al., 2016). ...
Prediabetes is considered to be an at a risk state, with an annualized 5-10% conversion rate of diabetes and the similiar proportion converting back to normoglycaemia. The global incidence of prediabetes is increasing and will reach to 471 million patients in 2030. The elevation of blood sugar is a continuum and hence prediabetes cannot be considered an entirely benign status and present insulin resistance (IR) and β-cell dysfunction, so that the development of prediabetic complications and vascular endothelial dysfunction. Therefore, it is crucial to early recognition and treatment of prediabetic individuals. For prediabetic individuals, lifestyle modification is the cornerstone of diabetes prevention with evidence of a 40-70% relative risk reduction. In the review, we include the possible mechanism of IR-induced vascular endothelial dysfunction, and exercise intervention improving the vascular endothelial dysfunction. These results showed clearly positive effects of physical exercise intervention and provided a direct clinical evidence of the effectiveness of this approach for preventing early diabetes.
