Exercise regulates lipid droplet dynamics in normal and fatty liver

Fuente, Francisco Pino-de la; Quezada, Laura; Sepúlveda, Carlos Augusto González; Monsalves-Alvarez, Matías; Rodríguez, Juan Manuel; Sacristán, Camila; Chiong, Mario; Llanos, Miguel; Espinosa, Alejandra; Troncoso, Rodrigo

doi:10.1016/j.bbalip.2019.158519

Cited by 33 publications

(39 citation statements)

References 41 publications

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“…The net effect of the accumulation of triacylglycerides, as well as other lipid intermediaries such as diacylglycerol, is to inhibit insulin signaling in its target tissues [29]. The pro-inflammatory scenario also affects essential tissues associated with metabolic homeostasis; skeletal muscle, which is the primary regulator of postprandial glycemia, can be altered by lipid intermediaries, pro-inflammatory cytokines and ROS, promoting an IR status [21,30]. Several nutritional strategies are being proposed to achieve the prevention of metabolic abnormalities, including diet supplementation of foods with a high content of bioactive phytochemicals.…”

Section: Discussionmentioning

confidence: 99%

“…Several nutritional strategies are being proposed to achieve the prevention of metabolic abnormalities, including diet supplementation of foods with a high content of bioactive phytochemicals. Polyphenols are present in a wide variety of fruits such as apples, grapes, and raspberry, producing benefits through decreasing fat accumulation in mice fed with a HFD [29][30][31]. This study assessed the effect of PP pulp administration on tissue-specific alteration induced by obesity, focusing on the inflammatory and redox disequilibrium in both skeletal muscle and liver.…”

Section: Discussionmentioning

confidence: 99%

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Physalis peruviana L. Pulp Prevents Liver Inflammation and Insulin Resistance in Skeletal Muscles of Diet-Induced Obese Mice

et al. 2020

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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.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Physalis peruviana L. Pulp Prevents Liver Inflammation and Insulin Resistance in Skeletal Muscles of Diet-Induced Obese Mice

et al. 2020

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“…1c), implying that the lower body weight in the HFd+GS group resulted from a lower calorie intake. The diameter of fat cells may indirectly reflect lipid metabolism (36). Histological analysis demonstrated that the GS group significantly reduced the size of the white adipose tissue compared with the HFd group (P<0.01), implying that GS reduces adipocyte mass in HFd-fed mice ( Fig.…”

Section: Resultsmentioning

confidence: 90%

Ginsenosides reduce body weight and ameliorate hepatic steatosis in high fat diet‑induced obese mice via endoplasmic reticulum stress and p‑STAT3/STAT3 signaling

Yao

2020

Mol Med Report

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obesity has been increasing globally for over three decades. according to previous studies, dietary obesity is usually associated with endoplasmic reticulum stress (erS) and STaT3 signaling, which result in interference with the homeostatic control of energy and lipid metabolism. Ginsenosides (GS) administered to mice will modulate adiposity and food intake; however, the mechanism of food inhibition is unknown. The aim of the present study was to investigate whether GS may inhibit erS and regulate STaT3 phosphorylation in GT1-7 cells (a mouse hypothalamus gonadotropin-releasing hormone neuron cell line) and the hypothalamus in order to reduce the body weight and ameliorate hepatic steatosis in high fat diet (HFd)-induced obese mice. in the present study, GS inhibited the appetite, reduced the body weight, visceral fat, body fat content and blood glucose, and ameliorated the glucose tolerance of the obese mice compared with HFd mice. in addition, the levels of aspartate aminotransferase and alanine aminotransferase, triglyceride (TG), leptin and insulin in the serum were reduced compared with HFd mice. There was less TG in the liver, but more in the feces compared with HFd mice. using hematoxylin and eosin staining of HepG2 cells and liver tissues, GS were demonstrated to improve the non-alcoholic fatty liver of the HFd-induced obese mice and reduce the diameter of the fat cells compared with HFd mice. GS also increased oxygen consumption and carbon dioxide emissions in the metabolic cage data compared with HFd mice. in the GT1-7 cells, GS alleviated the erS induced by tunicamycin and enhanced the activation of the STaT3 phosphorylation pathway. Furthermore the erS of the liver was relieved to achieve the aforementioned pharmacological effects. GS were used in the homeostatic control of the energy and lipid metabolism of a diet-induced obesity model. in conclusion, present studies suggest that GS exert these effects by increasing STaT3 phosphorylation expression and reducing the erS. Thus, GS reduce body weight and ameliorate hepatic steatosis in HFd-induced obese mice.

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“…Studies have revealed that pharmacological inhibition of MTP can be used to treat hyperlipidaemia in rats with monosodium L-glutamate-induced obesity, while increases in MPT gene or protein expression can be used to treat NAFLD [33][34][35]. Studies have also indicated that upregulating PPAR-α, carnitine palmitoyltransferase-1a (CPT-1a) and fatty TG lipase (ATGL) to enhance FA oxidation and lipolysis can improve NAFLD in micee [36,37].…”

Section: Pathogenesis Of Nafld and Glycolipid Metabolismmentioning

confidence: 99%

Mutual interaction between endoplasmic reticulum and mitochondria in nonalcoholic fatty liver disease

Wang¹,

He²,

Tsai

et al. 2020

Lipids Health Dis

104

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Nonalcoholic fatty liver disease (NAFLD) is a common metabolic syndrome. Imbalances between liver lipid output and input are the direct causes of NAFLD, and hepatic steatosis is the pathological premise and basis for NAFLD progression. Mutual interaction between endoplasmic reticulum stress (ERS) and oxidative stress play important roles in NAFLD pathogenesis. Notably, mitochondria-associated membranes (MAMs) act as a structural bridges for functional clustering of molecules, particularly for Ca 2+ , lipids, and reactive oxygen species (ROS) exchange. Previous studies have examined the crucial roles of ERS and ROS in NAFLD and have shown that MAM structural and functional integrity determines normal ER-mitochondria communication. Upon disruption of MAM integrity, miscommunication directly or indirectly causes imbalances in Ca2+ homeostasis and increases ERS and oxidative stress. Here, we emphasize the involvement of MAMs in glucose and lipid metabolism, chronic inflammation and insulin resistance in NAFLD and summarize MAM-targeting drugs and compounds, most of which achieve their therapeutic or ameliorative effects on NAFLD by improving MAM integrity. Therefore, targeting MAMs may be a viable strategy for NAFLD treatment. This review provides new ideas and key points for basic NAFLD research and drug development centred on mitochondria and the endoplasmic reticulum.

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Exercise regulates lipid droplet dynamics in normal and fatty liver

Cited by 33 publications

References 41 publications

Physalis peruviana L. Pulp Prevents Liver Inflammation and Insulin Resistance in Skeletal Muscles of Diet-Induced Obese Mice

Physalis peruviana L. Pulp Prevents Liver Inflammation and Insulin Resistance in Skeletal Muscles of Diet-Induced Obese Mice

Ginsenosides reduce body weight and ameliorate hepatic steatosis in high fat diet‑induced obese mice via endoplasmic reticulum stress and p‑STAT3/STAT3 signaling

Mutual interaction between endoplasmic reticulum and mitochondria in nonalcoholic fatty liver disease

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