Figure 3
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Nonalcoholic fatty liver disease (NAFLD) is a clinical condition that encompasses various forms of liver damage not caused by chronic alcohol consumption. In the absence of other etiologies, it ranges from steatosis to nonalcoholic steatohepatitis and cirrhosis. The prevalence of NAFLD has considerably increased over the last years owing to the cur...
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Introduction : Perforation is defined as an abnormal opening in any organ or viscous. Perforation of hollow viscous is one of the common surgical emergency in India ..Chronic alcoholism, Smoking, chronic use of Non steroid anti-inflammatory drugs (NSAIDS) are major risk factors for perforations Materials and methods : This study was hospital based...
Citations
... However, the independent contribution of NAFLD to cardiovascular disease in DM1 has yet to be established. IR leads to an increased risk of developing both NAFLD and cardiovascular disease thus improving IS, which is the basics of NAFLD management [17] could also result in decreased cardiovascular risk for people with DM1. ...
... Patients with NAFLD were older (43 [38][39][40][41][42][43][44][45][46][47][48][49][50][51][52] vs. 38 [28][29][30][31][32][33][34][35][36][37][38][39][40][41][42][43][44] years, P<0.001), with longer history of diabetes (20 [17][18][19][20][21] vs. 18 [11][12][13][14][15][16][17][18][19][20] ...
... Patients with NAFLD were older (43 [38][39][40][41][42][43][44][45][46][47][48][49][50][51][52] vs. 38 [28][29][30][31][32][33][34][35][36][37][38][39][40][41][42][43][44] years, P<0.001), with longer history of diabetes (20 [17][18][19][20][21] vs. 18 [11][12][13][14][15][16][17][18][19][20] ...
Introduction:
Insulin resistance (IR) in type 1 diabetes (DM1) is associated with increased insulin dose requirements, poor glycemic control and increased risk of chronic complications. IR increases lipid synthesis and hepatic lipid content. Disruption in hepatic lipid accumulation and export leads to liver steatosis resulting in non-alcoholic liver disease (NAFLD).
Objectives:
The aim of the study was to explore the relationship between indirect IR markers and NAFLD in DM1.
Patients and methods:
Analyzed were 151 patients with DM1 (59 men), aged [median (LQ, UQ)] 40 (33-47) years with diabetes duration 19 (13-21) years. HbA1c was 7.5 (6.8-8.2) % [58 (51-66) mmol/mol]. The following indirect IR markers were evaluated: estimated glucose distribution rate (eGDR), visceral adiposity index (VAI) and triglyceride to HDL cholesterol ratio (TG/HDL-C). Fatty infiltration of the liver was quantified using transient elastography. NAFLD was defined by controlled attenuation parameter ≥ 238 dB/m.
Results:
NAFLD was observed in 65 (43%) patients. Patients with NAFLD were less insulin sensitive: eGDR (8.93 [6.39-9.97] vs. 9.94 [8.09-11.13] mg/kg/min, P=0.001), VAI (1.52 [1.2-2.64] vs. 1.34 [0.92-1.74], P=0.014), TG/HDL-C (1.35 [0.95-2.11] vs. 1.11 [0.77-1.6], P=0.02) and were characterized by higher HbA1c 7.75 (7.2-8.4) vs. 7.3 (6.5-8.1) % [61 (55-68) vs. 56 (48-65) mmol/mol], P=0.02. In multivariable regression, indirect IR markers were independently associated with NAFLD: eGDR (OR 0.86 [95% CI: 0.77-0.97], P=0.01), VAI (OR 1.61 [1.05-2.49], p=0.03) and TG/HDL-C ratio (OR 1.88 [1.11-3.18], P=0.02), adjusted for sex, diabetes duration and HbA1c.
Conclusions:
In DM1, NAFLD is more likely to be present in less insulin sensitive individuals.
... No data supports its use for NAFLD despite initial enthusiasm related to its mechanism of action, because of a lack of efficacy in reducing fibrosis. 53 However, metformin appears to be effective as a chemopreventive agent for HCC and other tumors. 54 A previous study has reported partial inhibition of glutaminase activity (about 20%), both in chemical and cell assays compared with controls. ...
The prevalence of non-alcoholic fatty liver disease (NAFLD) is increasing worldwide, reflecting the current epidemics of obesity, insulin resistance, type 2 diabetes mellitus, and metabolic syndrome. NAFLD is characterized by the accumulation of fat in the liver, and is known to be a cause of cirrhosis. Although many pathways have been proposed, the cause of NAFLD-linked fibrosis progression is still unclear, which posed challenges for the development of new therapies to prevent NASH-related cirrhosis and hepatocellular carcinoma. Cirrhosis is associated with activation of hepatic stellate cells (HSC) and accumulation of excess extracellular matrix proteins, and inhibiting the activation of HSCs would be expected to slow the progression of NAFLD-cirrhosis. Multiple molecular signals and pathways such as oxidative stress and glutaminolysis have been reported to promote HSC activation. Both mechanisms are plausible antifibrotic targets in NASH, as the activation of HSCs the proliferation of myofibroblasts depend on those processes. This review summarizes the role of the glutaminolysis-ammonia-urea cycle axis in the context of NAFLD progression, and shows how the axis could be a novel therapeutic target.
... As established in the pathophysiology, RAS is essential in NAFLD pathophysiology. Therefore, angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptors blockers (ARB) influence cytokine production [76]. The RAS hepatic effect is mediated by angiotensin II receptor type I, which mediates the actions of angiotensin-II in hepatocytes, bile duct cells, hepatic stellate cells and vascular endothelial cells [77]. ...
Non-alcoholic fatty liver disease is a highly prevalent disease worldwide with a renowned relation to cardiovascular disease and chronic kidney disease. These diseases share a common pathophysiology including insulin resistance, oxidative stress, chronic inflammation, dysbiosis and genetic susceptibilities. Non-alcoholic fatty liver disease is especially prevalent and more severe in type 2 diabetes. Patients with non-alcoholic fatty liver disease should have liver fibrosis assessment in order to identify those at the highest risk of adverse outcomes so that appropriate management strategies can be implemented. Early diagnosis and treatment of non-alcoholic fatty liver disease could ameliorate the burden of cardiovascular disease and chronic kidney disease.
Resumen
La enfermedad por hígado graso no alcohólica supone un problema de salud creciente como consecuencia del aumento de la obesidad y la diabetes en la población. Una causa poco común de la misma, pero que cada vez se diagnostica con más frecuencia, es la secundaria a una duodenopancreatectomía cefálica. En estos casos los mecanismos fisiopatológicos son diferentes, aunque pueden acabar desarrollando de igual manera una enfermedad progresiva. Por tanto, se debe hacer un seguimiento estrecho de estos pacientes y establecer estrategias terapéuticas adecuadas.
Background & aims:
The pandemic of coronavirus disease 2019 (COVID-19) has witnessed more than 4.5 million deaths as of the time of writing. Whether nonalcoholic fatty liver disease (NAFLD) increase the risk for severe COVID-19 remains unclear. We sought to address this question using two-sample Mendelian randomization (TSMR) analysis approaches in large cohorts.
Methods:
We performed large-scale TSMR analyses to examine whether there is a causal relationship between NAFLD, serum alanine aminotransferase (ALT), grade of steatosis, NAFLD Activity Score (NAS), or fibrosis stage and severe COVID-19. To maximize the power of this analysis, we performed a genome-wide meta-analysis (GWMA) to identify single-nucleotide polymorphisms (SNPs) associated with NAFLD. We also examined the impact of 20 major co-morbid factors of NAFLD on severe COVID-19.
Results:
Univariate analysis of the UK Biobank (UKB) data demonstrated a significant association between NAFLD and severe COVID-19 (OR=3.06, p=1.07×10-6). However, this association disappeared after demographic and co-morbid factors adjusted (OR=1.61, p=0.08). TSMR study indicated that NAFLD (OR=0.97, p=0.61), ALT level (OR=1.03, p=0.47), grade of steatosis (OR=1.08, p=0.41), NAS (OR=1.02, p=0.39), and fibrosis stage (OR=1.01, p=0.87) were not associated with severe COVID-19. Among all NAFLD-related co-morbid factors, BMI (OR=1.73, p=7.65×10-9), waist circumference (WC, OR=1.76, p=2.58×10-5), and hip circumference (HC, OR=1.33, p=7.26×10-3) were the only ones demonstrated a causal impact on severe COVID-19.
Conclusions:
There is no evidence supporting that NAFLD is a causal risk factor for severe COVID-19. Previous observational associations between NAFLD and COVID-19 are likely attributed to the correlation between NAFLD and obesity.
