scholarly journals Inhibition of protein kinase Cε prevents hepatic insulin resistance in nonalcoholic fatty liver disease

2007 ◽  
Vol 117 (3) ◽  
pp. 739-745 ◽  
Author(s):  
Varman T. Samuel ◽  
Zhen-Xiang Liu ◽  
Amy Wang ◽  
Sara A. Beddow ◽  
John G. Geisler ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Liver Disease ◽  
Protein Kinase ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Hepatic Insulin Resistance ◽  
Nonalcoholic Fatty Liver

scholarly journals Inflammation as a potential link between nonalcoholic fatty liver disease and insulin resistance

2013 ◽  
Vol 218 (3) ◽  
pp. R25-R36 ◽  
Author(s):  
Mohamed Asrih ◽  
François R Jornayvaz
Keyword(s):  
Insulin Resistance ◽  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Metabolic Energy ◽  
Hepatic Insulin Resistance ◽  
Major Health Problem ◽  
Nonalcoholic Fatty Liver

Nonalcoholic fatty liver disease (NAFLD) has become a major health problem in developed countries. It has affected more than 30% of the general population and is commonly associated with insulin resistance, which is a major risk factor for the development of type 2 diabetes and a central feature of the metabolic syndrome. Furthermore, accumulating evidences reveal that NAFLD as well as insulin resistance is strongly related to inflammation. Cytokines and adipokines play a pivotal role in inflammatory processes. In addition, these inflammatory mediators regulate various functions including metabolic energy balance, inflammation, and immune response. However, their role in modulating ectopic lipids involved in the development of insulin resistance, such as diacylglycerols and ceramides, remains unknown. The aim of this review is first to describe the pathophysiology of insulin resistance in NAFLD. In particular, we discuss the role of ectopic lipid accumulation in the liver. Secondly, we also summarize recent findings emphasizing the role of main inflammatory markers in both NAFLD and insulin resistance and their potential role in modulating hepatic fat content in NAFLD and associated hepatic insulin resistance.

Considering the Links Between Nonalcoholic Fatty Liver Disease and Insulin Resistance: Revisiting the Role of Protein Kinase C ε

Hepatology ◽  
2019 ◽  
Vol 70 (6) ◽  
pp. 2217-2220 ◽  
Author(s):  
Varman T. Samuel ◽  
Max C. Petersen ◽  
Brandon M. Gassaway ◽  
Daniel F. Vatner ◽  
Jesse Rinehart ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Protein Kinase C ◽  
Liver Disease ◽  
Protein Kinase ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Nonalcoholic Fatty Liver ◽  
Kinase C

scholarly journals Effect of a ketogenic diet on hepatic steatosis and hepatic mitochondrial metabolism in nonalcoholic fatty liver disease

2020 ◽  
Vol 117 (13) ◽  
pp. 7347-7354 ◽  
Author(s):  
Panu K. Luukkonen ◽  
Sylvie Dufour ◽  
Kun Lyu ◽  
Xian-Man Zhang ◽  
Antti Hakkarainen ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Fatty Acids ◽  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Ketogenic Diet ◽  
Fatty Liver Disease ◽  
Redox State ◽  
Hepatic Insulin Resistance ◽  
Nonalcoholic Fatty Liver

Weight loss by ketogenic diet (KD) has gained popularity in management of nonalcoholic fatty liver disease (NAFLD). KD rapidly reverses NAFLD and insulin resistance despite increasing circulating nonesterified fatty acids (NEFA), the main substrate for synthesis of intrahepatic triglycerides (IHTG). To explore the underlying mechanism, we quantified hepatic mitochondrial fluxes and their regulators in humans by using positional isotopomer NMR tracer analysis. Ten overweight/obese subjects received stable isotope infusions of: [D7]glucose, [13C4]β-hydroxybutyrate and [3-13C]lactate before and after a 6-d KD. IHTG was determined by proton magnetic resonance spectroscopy (1H-MRS). The KD diet decreased IHTG by 31% in the face of a 3% decrease in body weight and decreased hepatic insulin resistance (−58%) despite an increase in NEFA concentrations (+35%). These changes were attributed to increased net hydrolysis of IHTG and partitioning of the resulting fatty acids toward ketogenesis (+232%) due to reductions in serum insulin concentrations (−53%) and hepatic citrate synthase flux (−38%), respectively. The former was attributed to decreased hepatic insulin resistance and the latter to increased hepatic mitochondrial redox state (+167%) and decreased plasma leptin (−45%) and triiodothyronine (−21%) concentrations. These data demonstrate heretofore undescribed adaptations underlying the reversal of NAFLD by KD: That is, markedly altered hepatic mitochondrial fluxes and redox state to promote ketogenesis rather than synthesis of IHTG.

scholarly journals Hepatic Insulin Resistance Is Not Pathway Selective in Humans With Nonalcoholic Fatty Liver Disease

Diabetes Care ◽  
2020 ◽  
pp. dc201644
Author(s):  
Kasper W. ter Horst ◽  
Daniel F. Vatner ◽  
Dongyan Zhang ◽  
Gary W. Cline ◽  
Mariette T. Ackermans ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Hepatic Insulin Resistance ◽  
Nonalcoholic Fatty Liver
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