Molecular mediators of hepatic steatosis and liver injury

Abstract

Obesity and its associated comorbidities are among the most prevalent and challenging conditions confronting the medical profession in the 21st century. A major metabolic consequence of obesity is insulin resistance, which is strongly associated with the deposition of triglycerides in the liver. Hepatic steatosis can either be a benign, noninflammatory condition that appears to have no adverse sequelae or can be associated with steatohepatitis: a condition that can result in end-stage liver disease, accounting for up to 14% of liver transplants in the US. Here we highlight recent advances in our understanding of the molecular events contributing to hepatic steatosis and nonalcoholic steatohepatitis.

The differential effects of high-fat and high fructose diets on the liver of male albino rat and the proposed underlying mechanisms

“…All these features are named collectively NAFLD [3]. Observed only in the HFD and HFHF groups, ballooned hepatocytes are delimited to the most severe form of hepatic injury and indicate cell necrosis [7].…”

Insulin resistance: the conflict between biological settings of energy metabolism and human lifestyle (a glance at the problem from evolutionary viewpoint)

“…Инсулин стимулирует поглощение клетками глюкозы, активируя экспрессию и выставление на плазматическую мембрану дополни-тельного количества глюкозных транспортеров ГЛЮТ4. Одновременно этот гормон индуцирует экспрессию ферментов липогенеза: ацетил-КоА-карбоксилазу, синтазу ЖК и пальмитоил-КоА-элонгазу [4] и стеарил-КоА-десатуразу [5]. Последние два фермента удлиняют пальмитиновую насыщенную ЖК (НЖК) на молекулу ацетил-КоА (на 2 атома углерода) с образованием С18:0 стеариновой ЖК [6].…”

The Role of Fatty Acid Metabolism and Apolipoproteins in Ths-Induced Hepatic Steatosis in Mice

“…The ability of the liver to process fatty acids and transport lipids to other tissues is affected by toxins, diet and drugs [26][27][28][29][30][31][32][33][34]. Previously, we have shown that exposure to THS toxins results in lipid accumulation in hepatocytes of exposed mice.…”