700 Plasma adiponectin in non alcoholic fatty liver disease is related to hepatic insulin resistance and hepatic fat content

2005 ◽  
Vol 42 ◽  
pp. 255-256
Medicina ◽  
2019 ◽  
Vol 55 (10) ◽  
pp. 629
Author(s):  
Yajie Zhang ◽  
Dajiang Lu ◽  
Renwei Wang ◽  
Weijie Fu ◽  
Shengnian Zhang

Background and Objectives: Recent studies have shown that low skeletal muscle mass can contribute to non-alcoholic fatty liver disease through insulin resistance. However, the association between muscle mass/strength and hepatic fat content remains unclear in postmenopausal women. Methods: In this study, we assessed the associations between muscle mass/strength and various severities of non-alcoholic fatty liver disease. Using single-voxel proton magnetic resonance spectroscopy, 96 postmenopausal women between the ages of 50 and 65 were divided into four groups (G0–G3) by hepatic fat content: G0 (hepatic fat content <5%, n = 20), G1 (5% ≤ hepatic fat content < 10%, n = 27), G2 (10% ≤ hepatic fat content < 25%, n = 31), and G3 (hepatic fat content ≥25%, n = 18). Muscle mass indexes were estimated as skeletal muscle index (SMI)% (total lean mass/weight × 100) and appendicular skeletal muscular mass index (ASM)% (appendicular lean mass/weight × 100) by dual energy X-ray absorptiometry. Maximal isometric voluntary contraction of the handgrip, elbow flexors, and knee extensors was measured using an adjustable dynamometer chair. Fasting plasma glucose, insulin, and follicle-stimulating hormones were assessed in venous blood samples. Results: The results showed negative correlations between hepatic fat content and SMI% (r = −0.42, p < 0.001), ASM% (r = −0.29, p = 0.005), maximal voluntary force of grip (r = −0.22, p = 0.037), and knee extensors (r = −0.22, p = 0.032). Conclusions: These significant correlations almost remained unchanged even after controlling for insulin resistance. In conclusion, negative correlations exist between muscle mass/strength and the progressed severity of non-alcoholic fatty liver disease among post-menopausal women, and the correlations are independent of insulin resistance.


2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Sachiko Hattori ◽  
Kazuomi Nomoto ◽  
Tomohiko Suzuki ◽  
Seishu Hayashi

Abstract Background Dipeptidyl peptidase 4 (DPP4) is a serine exopeptidase able to inactivate various oligopeptides, and also a hepatokine. Hepatocyte-specific overexpression of DPP4 is associated with hepatic insulin resistance and liver steatosis. Method We examined whether weekly DPP4 inhibitor omarigliptin (OMG) can improve liver function as well as levels of inflammation and insulin resistance in type 2 diabetic patients with non-alcoholic fatty liver disease (NAFLD). Further, we investigated the effects of OMG in a diabetic patient with biopsy-confirmed nonalcoholic steatohepatitis (NASH). Results In NAFLD patients, OMG significantly decreased levels of aminotransferase, aspartate aminotransferase, gamma-glutamyl transpeptidase, homeostatic model assessment of insulin resistance (HOMA-IR), and high-sensitivity C-reactive protein (hsCRP), while no significant change was seen in hemoglobin A1c or body mass index. In the NASH patient, liver function improved markedly, and levels of the hepatic fibrosis marker FIB-4 decreased in parallel with HOMA-IR and hsCRP. Slight but clear improvements in intrahepatic fat deposition and fibrosis appeared to be seen on diagnostic ultrasonography. Conclusion Weekly administration of the DPP4 inhibitor OMG in ameliorating hepatic insulin resistance may cause beneficial effects in liver with NAFLD/NASH.


2019 ◽  
Vol 1 (1) ◽  
pp. 81-91
Author(s):  
Baibaswata Nayak ◽  
Suraj Kumar Nongthombam ◽  
Neelanjana Roy ◽  
Neeti Nadda ◽  
Krishnendu Mondol ◽  
...  

Background: Non-alcoholic fatty liver disease (NAFLD) is now predominant globally due to increased sedentary lifestyle and obesity. Recently, high prevalence of NAFLD also has been documented in non-obese individuals with increased risk of cirrhosis and hepatocellular carcinoma. The systemic and hepatic manifestations of NAFLD severity in obese and non-obese Indian patients are not clear.Methods: The clinically diagnosed NAFLD patients (n=54, non-obese and obese) were assessed for liver injury and hepatic fat content by histopathology, Fibroscan and MRS. Liver biopsy and hepatic venous sampling were performed by trans-jugular approach and mRNA expression was assessed by real-time PCR.Result: High liver fat content (LFC, 20. 4 ± 10. 4%, 16 ± 11. 5% and 9. 34 ± 15. 4%) and increased abdominal obesity (WHR, 1. 03 ± 0. 06, 0. 97 ± 0. 05 and 0. 93 ± 0. 06) was observed in both obese and non-obese NAFLD patients as compare to disease control. Histopathological examination of liver indicated increased fibrosis (grade ≥ 1) in both obese (76%) and non-obese (64%) group. Significant increased levels of LBP, MDA and adipokines levels (p < 0. 001) were observed in hepatic and systemic circulation of obese and non-obese groups than healthy and diseased controls. A positive correlation of biomarkers for liver injury was found between hepatic and systemic circulation. Hepatic gene expression of adipokines and cytokines also corroborated this trend among groups.Conclusion: The extent of liver injury is quite high in both non-obese and obese NAFLD patients. The drivers of injury in these patients are due to hepatic fat and SIBO induced endotoxin mediated up-regulation of proinflammatory adipocytokines and oxidant stress in liver.


2017 ◽  
Vol 72 (5) ◽  
pp. 425.e9-425.e14 ◽  
Author(s):  
N.Y. Yu ◽  
T. Wolfson ◽  
M.S. Middleton ◽  
G. Hamilton ◽  
A. Gamst ◽  
...  

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