No effect of resveratrol on VLDL-TG kinetics and insulin sensitivity in obese men with nonalcoholic fatty liver disease

2018 ◽  
Vol 20 (10) ◽  
pp. 2504-2509 ◽  
Author(s):  
Marianne K. Poulsen ◽  
Birgitte Nellemann ◽  
Bo Martin Bibby ◽  
Hans Stødkilde-Jørgensen ◽  
Steen B. Pedersen ◽  
...  
Keyword(s):  
Liver Disease ◽  
Insulin Sensitivity ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Nonalcoholic Fatty Liver

scholarly journals Short-term exercise reduces markers of hepatocyte apoptosis in nonalcoholic fatty liver disease

2012 ◽  
Vol 113 (1) ◽  
pp. 1-6 ◽  
Author(s):  
Ciaran E. Fealy ◽  
Jacob M. Haus ◽  
Thomas P. J. Solomon ◽  
Mangesh Pagadala ◽  
Chris A. Flask ◽  
...  
Keyword(s):  
Liver Disease ◽  
Insulin Sensitivity ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Fat Oxidation ◽  
Whole Body ◽  
Hepatocyte Apoptosis ◽  
Short Term ◽  
Nonalcoholic Fatty Liver

Increased hepatocyte apoptosis is a hallmark of nonalcoholic fatty liver disease (NAFLD) and contributes to the profibrogenic state responsible for the progression to nonalcoholic steatohepatitis (NASH). Strategies aimed at reducing apoptosis may result in better outcomes for individuals with NAFLD. We therefore examined the effect of a short-term exercise program on markers of apoptosis—plasma cytokeratin 18 (CK18) fragments, alanine aminotransferase (ALT), aspartate aminotransferase (AST), soluble Fas (sFas), and sFas ligand (sFasL)—in 13 obese individuals with NAFLD [body mass index 35.2 ± 1.2 kg/m2, >5% intrahepatic lipid (IHL) assessed by 1H-MR spectroscopy]. Exercise consisted of treadmill walking for 60 min/day on 7 consecutive days at ∼85% of maximal heart rate. Additionally, subjects underwent an oral glucose tolerance test and a maximal oxygen consumption (V̇o2max) test before and after the exercise intervention. The Matsuda index was used to assess insulin sensitivity. We observed significant decreases in CK18 fragments (558.4 ± 106.8 vs. 323.4 ± 72.5 U/l, P < 0.01) and ALT (30.2 ± 5.1 vs. 24.3 ± 4.8 U/l, P < 0.05), and an increase in whole body fat oxidation (49.3 ± 6.1 vs. 69.4 ± 7.1 mg/min, P < 0.05), while decreases in circulating sFasL approached statistical significance (66.5 ± 6.0 vs. 63.0 ± 5.7 pg/ml, P = 0.06), as did the relationship between percent change in circulating CK18 fragments and ALT (r = 0.55, P = 0.05). We also observed a significant correlation between changes in fat oxidation and circulating sFasL (rho = −0.65, P < 0.05). There was no change in IHL following the intervention (18.2 ± 2.5 vs. 17.5 ± 2.1%, NS). We conclude that short-term exercise reduces a circulatory marker of hepatocyte apoptosis in obese individuals with NAFLD and propose that changes in the proapoptotic environment may be mediated through improved insulin sensitivity and increased oxidative capacity.

scholarly journals Hepatic iron concentration correlates with insulin sensitivity in nonalcoholic fatty liver disease

2018 ◽  
Vol 2 (6) ◽  
pp. 644-653 ◽  
Author(s):  
Laurence Britton ◽  
Kim Bridle ◽  
Janske Reiling ◽  
Nishreen Santrampurwala ◽  
Leesa Wockner ◽  
...  
Keyword(s):  
Liver Disease ◽  
Insulin Sensitivity ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Iron Concentration ◽  
Hepatic Iron ◽  
Nonalcoholic Fatty Liver ◽  
Hepatic Iron Concentration

scholarly journals Glucokinase links Krüppel-like factor 6 to the regulation of hepatic insulin sensitivity in nonalcoholic fatty liver disease

Hepatology ◽  
2012 ◽  
Vol 55 (4) ◽  
pp. 1083-1093 ◽  
Author(s):  
Lars P. Bechmann ◽  
Amalia Gastaldelli ◽  
Diana Vetter ◽  
Gillian L. Patman ◽  
Laura Pascoe ◽  
...  
Keyword(s):  
Liver Disease ◽  
Insulin Sensitivity ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Nonalcoholic Fatty Liver ◽  
Hepatic Insulin Sensitivity

scholarly journals Maternal Hyperleptinemia Improves Offspring Insulin Sensitivity in Mice

Endocrinology ◽  
2016 ◽  
Vol 157 (7) ◽  
pp. 2636-2648 ◽  
Author(s):  
Omonseigho O. Talton ◽  
Kathleen A. Pennington ◽  
Kelly E. Pollock ◽  
Keenan Bates ◽  
Lixin Ma ◽  
...  
Keyword(s):  
Liver Disease ◽  
Insulin Sensitivity ◽  
Glucose Tolerance ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Leptin Receptor ◽  
Wild Type ◽  
Nonalcoholic Fatty Liver ◽  
Liver Triglycerides

Maternal obesity and gestational diabetes are prevalent worldwide. Offspring of mothers with these conditions weigh more and are predisposed to metabolic syndrome. A hallmark of both conditions is maternal hyperleptinemia, but the role of elevated leptin levels during pregnancy on developmental programming is largely unknown. We previously found that offspring of hyperleptinemic mothers weighed less and had increased activity. The goal of this study was to determine whether maternal leptin affects offspring insulin sensitivity by investigating offspring glucose metabolism and lipid accumulation. Offspring from two maternal hyperleptinemic models were compared. The first model of hyperleptinemia is the Leprdb/+ mouse, which has a mutation in one copy of the gene that encodes the leptin receptor, resulting in a truncated long form of the receptor, and hyperleptinemia. Wild-type females served as the control for the Leprdb/+ females. For the second hyperleptinemic model, wild-type females were implanted with miniosmotic pumps, which released leptin (350 ng/h) or saline (as the control) just prior to mating and throughout gestation. In the offspring of these dams, we measured glucose tolerance; serum leptin, insulin, and triglyceride levels; liver triglycerides; pancreatic α- and β-cell numbers; body composition; incidence of nonalcoholic fatty liver disease; and the expression of key metabolic genes in the liver and adipose tissue. We found that the offspring of hyperleptinemic dams exhibited improved glucose tolerance, reduced insulin and leptin concentrations, reduced liver triglycerides, and a lower incidence of nonalcoholic fatty liver disease. Overall, maternal hyperleptinemia was beneficial for offspring glucose and lipid metabolism.

scholarly journals Update on Ppar and Nonalcoholic Fatty Liver Disease

PPAR Research ◽  
2012 ◽  
Vol 2012 ◽  
pp. 1-5 ◽  
Author(s):  
Gene P. Ables
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Liver Disease ◽  
Insulin Sensitivity ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Current Knowledge ◽  
Nonalcoholic Fatty Liver

Nonalcoholic fatty liver disease (NAFLD) is the most common initial presentation of obesity and insulin resistance. Uninterrupted progression of hepatic lipid accumulation often leads to fatty liver disease and eventually cirrhosis. Insulin resistance is one of the characteristics of type 2 diabetes. Several types of treatment have been employed against type 2 diabetes some of which ameliorate NAFLD. The frequent line of treatment to improve insulin sensitivity is the use of thiazolidinediones (TZD) which activate the nuclear receptor, peroxisome proliferator activated receptor gamma (Pparγ). Although TZDs are proven to be very effective in promoting insulin sensitivity, its actions onPparγhave been complicated, specifically on NAFLD. According to studies in different models,Pparγmanifests both beneficial and undesirable effects on NAFLD. This paper will focus on the current knowledge ofPparγand its effect on NAFLD.

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