Homeostatic model assessment of insulin resistance closely related to lobular inflammation in nonalcoholic fatty liver disease

2020 ◽  
Vol 32 (1) ◽  
pp. 80-86
Author(s):  
Fang-Zhou Ye ◽  
Wen-Yue Liu ◽  
Kenneth I. Zheng ◽  
Xiao-Yan Pan ◽  
Hong-Lei Ma ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Model Assessment ◽  
Nonalcoholic Fatty Liver ◽  
Homeostatic Model Assessment ◽  
Homeostatic Model ◽  
Lobular Inflammation

scholarly journals Insulin Resistance in Nonalcoholic Fatty Liver Disease: Experience from Bangladesh

2016 ◽  
Vol 4 (2) ◽  
pp. 86-91 ◽  
Author(s):  
Golam Azam ◽  
Shahinul Alam ◽  
SKM Nazmul Hasan ◽  
Sheikh Mohammad Noor E Alam ◽  
Jahangir Kabir ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Model Assessment ◽  
Nonalcoholic Fatty Liver ◽  
Homeostatic Model Assessment ◽  
Low Hdl ◽  
Study Population

Background: Insulin resistance (IR) has largely been hypothesized as central in multifactorial pathogenesis of nonalcoholic fatty liver disease (NAFLD). This study was aimed to explore the association of IR with NAFLD and nonalcoholic steatohepatitis (NASH).Methods: We enrolled 219 patients of NAFLD with sonographic evidence of fatty changes in liver excluding patients with alcohol intake and other causes of fatty change during June 2012 to July 2014.Liver biopsy was done for 110 patients with elevated ALT of >30 U/L for male and >18 U/L for female. We have measured IR by homeostatic model assessment of insulin resistance (HOMA-IR).Results: Age of the study population was 40.6 ± 10.0 years, male and female was 83 (37.9%) and 136 (62.1%), ALT was 42.0 (16-861) U/L, AST was 32 (16-608) U/L and GGT was 39 (10-243) U/L. According to Asian criteria 54 (25.9%) were non-obese, 139 (64.1%) had metabolic syndrome, 163 (74.8%) were hypertriglyceridemic, 200 (91.3%) had low HDL and 170 (77.4%) had high waist. Hypertensive and diabetic were 58 (26.7%) and 57 (26.1%) respectively. IR was 1.9±1.3 with the range of 0.4 to 9.3 and only 87 (39.7%) were above normal. Of the 110 biopsied, 65 (59.1%) had NASH. Normal and raised IR was associated with 32 (50.8%) and 33 (70.2%) NASH respectively (p < 0.05). Correlation between IR and steatosis, ballooning and fibrosis was not significant except lobular inflammation. IR was similar in NASH (2.2 ±1.6) and non NASH (1.9±1.6).Conclusion: Large proportion of NAFLD patients had normal IR. IR had inconsistent association with histological activity.Bangladesh Crit Care J September 2016; 4 (2): 86-91

Nonalcoholic Fatty Liver Disease and Estimated Insulin Resistance in Obese Youth: A Mendelian Randomization Analysis

2020 ◽  
Vol 105 (11) ◽  
Author(s):  
Anita Morandi ◽  
Anna Di Sessa ◽  
Chiara Zusi ◽  
Giuseppina Rosaria Umano ◽  
Dania El Mazloum ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Mendelian Randomization ◽  
Genetic Risk Score ◽  
Model Assessment ◽  
Causal Association ◽  
Nonalcoholic Fatty Liver

Abstract Context Nonalcoholic fatty liver disease (NAFLD) is associated with insulin resistance (IR) and predicts type 2 diabetes. Currently, it is uncertain whether NAFLD may directly cause IR or vice versa. Objective To test the hypothesis that NAFLD is causally related to IR. Design and Methods We performed a Mendelian randomization (MR) in 904 obese children/adolescents using an NAFLD-related genetic risk score (GRS) as an instrumental variable. We assessed NAFLD by ultrasonography and IR by homeostasis model assessment (HOMA-IR). We also interrogated the MAGIC Consortium dataset of 46 186 adults to assess the association between PNPLA3 rs738409 (ie, the most robust NAFLD-related polymorphism) and HOMA-IR, and we performed a 2-sample MR with 2 large datasets to test reverse causation (HOMA-IR increasing the risk of NAFLD). Results Nonalcoholic fatty liver disease prevalence increased by 20% for every increase in the GRS (β-coefficient = 0.20, P &lt; 0.001), and NAFLD was associated with ln-HOMA-IR (β-coefficient = 0.28, P &lt; 0.001). Thus, the expected increase in ln-HOMA-IR for every increase in the GRS (expected β-coefficient) was 0.056 (0.28*0.20) in the case of complete NAFLD-HOMA-IR causal association, and 0.042 in the case of 75% causality. In our cohort, the GRS did not predict ln-HOMA-IR (β-coefficient = 0.007, P = 0.75). In the MAGIC cohort, the PNPLA3 rs738409 did not associate with ln-HOMA-IR. The 2-sample MR failed to show a causal association between ln-HOMA-IR and NAFLD. Conclusions Our study shows that genetically-influenced NAFLD does not increase HOMA-IR, and genetically-influenced HOMA-IR does not increase the risk of NAFLD. Shared pathogenic pathways or NAFLD subtypes not “captured” by our MR design might underpin the association between NAFLD and HOMA-IR.

scholarly journals The Association between SOCS1−1656G>A Polymorphism, Insulin Resistance and Obesity in Nonalcoholic Fatty Liver Disease (NAFLD) Patients

2019 ◽  
Vol 8 (11) ◽  
pp. 1912 ◽  
Author(s):  
Agnieszka Kempinska-Podhorodecka ◽  
Ewa Wunsch ◽  
Piotr Milkiewicz ◽  
Ewa Stachowska ◽  
Malgorzata Milkiewicz
Keyword(s):  
Insulin Resistance ◽  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Taqman Assay ◽  
Cytokine Signaling ◽  
Model Assessment ◽  
Nonalcoholic Fatty Liver ◽  
Risk Variants

Suppressor of cytokine signaling (SOCS) proteins prevent uncontrolled cytokine signaling and appear to play a role in the pathological processes behind obesity and insulin resistance. The polymorphism of the SOCS1 gene (rs243330, −1656G>A) is associated with obesity and glucose sensitivity. To estimate the effect of this SOCS1 gene polymorphism on nonalcoholic fatty liver disease (NAFLD) susceptibility, we performed a study on 138 patients with ultrasound-confirmed NAFLD and 1000 healthy blood donors. The relationship between the SOCS1−1656G>A polymorphism and serum biochemical parameters in NAFLD was additionally investigated. The SOCS1 variant was genotyped using a dedicated TaqMan assay. The frequency of rs243330 polymorphism did not differ between patients and controls. However, in a cohort of obese individuals (BMI ≥ 30 kg/m2) the occurrence of the G allele of the SOCS1−1656G>A polymorphism was strongly associated with NAFLD (odds ratio (OR) 1.6; 95% CI,1.1–2.5; p = 0.009), and carriers of the AA genotype have lower risk of developing NAFLD (OR 0.4; 95% CI, 0.2–0.7; p = 0.004). Overweight NAFLD patients who were carriers of GG genotypes had significantly lower levels of homeostasis model assessment of insulin resistance (HOMA-IR) values (p = 0.03 vs. AA), and the obese GG homozygotes had lower serum concertation of triglyceride (GG vs. AA; p = 0.02). Serum liver enzyme activities were not modified by the presence of SOCS1 risk variants. In conclusion, the observed phenotype of overweight NAFLD patients with non-elevated levels of TG and HOMA-IR, which is associated with genetic variants of SOCS1, provides a rationale for further research on the pathophysiology of fatty liver disease.

scholarly journals Nonalcoholic Fatty Liver Disease Relationship with Metabolic Syndrome in Class III Obesity Individuals

2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
A. Cordeiro ◽  
S. E. Pereira ◽  
C. J. Saboya ◽  
A. Ramalho
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Blood Pressure Measurement ◽  
Model Assessment ◽  
Class Iii ◽  
Nonalcoholic Fatty Liver

Introduction. Obesity is represented mainly by abdominal obesity and insulin resistance (IR), both present in most individuals diagnosed with metabolic syndrome (MS). IR is the key risk factor in the pathogenesis of nonalcoholic fatty liver disease (NAFLD).Objective. To relate NAFLD to MS in class III obese individuals.Methodology. A descriptive cross-sectional study with class III obese individuals, aged ≥ 20–60 years. Blood pressure measurement, weight, height, body mass index (BMI), waist circumference (WC) and blood glucose, insulin, high-density lipoprotein cholesterol (HDL-c), and triglycerides data were obtained. HOMA-IR (homeostatic model assessment insulin resistance) calculation was carried out with a cutoff value of 2.71 for IR evaluation. The diagnosis of NAFLD was performed by liver biopsy and the diagnosis of MS was performed in accordance with the National Cholesterol Education Program/Adult Treatment Panel III (NCEPATP III).Results. Of the 50 individuals evaluated, 86% were women and BMI means were 45.4 ± 3.6 Kg/m2. The overall individuals had NAFLD, 70% steatosis, and 30% steatohepatitis. The diagnosis of MS occurred in 56% but showed no significant association with NAFLD (P=0.254). Triglycerides (178 ± 65.5 mg/dL) and insulin (28.2 ± 22.6 mcU/mL) mean values were significantly higher in steatohepatitis (P=0.002andP=0.042, resp.) compared to individuals with steatosis. IR was confirmed in 76% and showed a relationship with NAFLD severity.Conclusion. NAFLD was not related to MS; however, MS components, evaluated in isolation, as well as IR, were related to the presence and severity of NAFLD.

scholarly journals Shear wave elastography reveals a high prevalence of liver fibrosis in overweight or obese Hispanic youth

2020 ◽  
Vol 20 (82) ◽  
pp. 162-168
Author(s):  
Sanjeet Sandhu ◽  
◽  
Carisse Orsi ◽  
Gary L. Francis ◽  
Zhu Wang ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Liver Disease ◽  
High Risk ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Hispanic Youth ◽  
Nonalcoholic Fatty Liver ◽  
High Prevalence ◽  
Homeostatic Model

Background: Obesity, prediabetes, and type 2 diabetes are risk factors for nonalcoholic fatty liver disease. Inflammation and hepatocellular damage associated with nonalcoholic fatty liver disease lead to progressive non-alcoholic steatohepatitis, fibrosis and cirrhosis. Current tests to identify fibrosis (liver biopsy) are invasive and not conducive to serial examination. For that reason, we used the newer technique of shear wave elastogrophy (SWE) to detect fibrosis in overweight or obese Hispanic youth and sought to determine if carbohydrate tolerance or insulin resistance were associated with fibrosis in this high risk population. Methods: A total of 67 Hispanic youth (8–18 years of age) with overweight or obesity who were referred for multidisciplinary evaluation were included. SWE was used to identify those with suspected fibrosis. Results of SWE were then compared with glycohemoglobin (A1c), insulin resistance (homeostatic model of insulin resistance), and biochemical parameters. Results: The prevalence of suspected fibrosis (SWE >5.10 kPa) in overweight or obese Hispanic youth was 62.7% (42/67). Patients with suspected fibrosis (SWE ≥5.10 kPa) had significantly higher levels of serum aspartate aminotransferase, alanine aminotransferase and the aminotransferase to platelet ratio index when compared to patients without significant fibrosis (SWE <5.01 kPa). However, there were no significant differences between the groups in body mass index, A1c, or homeostatic model of insulin resistance. Conclusions: SWE detected a high prevalence (62.7%) of suspected hepatic fibrosis in a group of high risk, overweight or obese Hispanic youth suggesting that SWE is a useful tool for surveillance and longitudinal studies.

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