Abstract
A chronic high-fat diet (HFD) produces obesity, leading to pathological consequences in the liver and skeletal muscle. The fat in the liver leads to accumulation of a large number of intrahepatic lipid droplets (LD), which are susceptible to oxidation. Obesity also affects skeletal muscle, increasing LD and producing insulin signaling impairment. Physalis peruviana L. (PP) (Solanaceae) is rich in peruvioses and has high antioxidant activity. We assessed the ability of PP to enhance insulin-dependent glucose uptake in skeletal muscle and the capacity to prevent both inflammation and lipoperoxidation in the liver of diet-induced obese mice. Male C57BL/6J mice were divided into groups and fed for eight weeks: control diet (C; 10% fat, 20% protein, 70% carbohydrates); C + PP (300 mg/kg/day); HFD (60% fat, 20% protein, 20% carbohydrates); and HFD + PP. Results suggest that PP reduces the intracellular lipoperoxidation level and the size of LD in both isolated hepatocytes and skeletal muscle fibers. PP also promotes insulin-dependent skeletal muscle glucose uptake. In conclusion, daily consumption of 300 mg/kg of fresh pulp of PP could be a novel strategy to prevent the hepatic lipoperoxidation and insulin resistance induced by obesity.
Highlights
Obesity is the result of the imbalance between calorie intake and expenditure, resulting in the accumulation of adipose tissue, which is potentiated by physical inactivity [1,2]
Considering that high-fat diet (HFD) induces lipid accumulation in the liver, we focused on evaluating whether Physalis peruviana L. (PP) is protective when faced with the fat increase in isolated hepatocytes and whole liver tissue
Obesity is a of Non-Alcoholic Fatty Liver Disease (NAFLD) driving an aberrant accumulation of lipids in the liver, which produces inflammatory leading cause of NAFLD driving an aberrant accumulation of lipids in the liver, which produces signals that recruit immune cells [8,23]
Summary
Obesity is the result of the imbalance between calorie intake and expenditure, resulting in the accumulation of adipose tissue, which is potentiated by physical inactivity [1,2]. Integrated metabolism is promoted by the coordinated action of insulin in the liver, adipose tissue, and skeletal muscle. The interplay between the functions of these organs contributes to systemic glucose regulation. Insulin secreted by the pancreas regulates physiological glucose concentration, acting on skeletal muscle and adipose tissue to favor glucose uptake in an insulin-dependent way [3,4]. With over-feeding, metabolic alterations in different tissues disturb glucose homeostasis, triggering a systemic insulin resistance (IR) condition [5]. Liver-specific metabolic abnormalities are present in IR-associated obesity, such as Non-Alcoholic Fatty Liver Disease (NAFLD) and steatohepatitis [6]
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