مقاله انگلیسی رایگان در مورد تاثیر رژیم غذایی با چربی بالا و تمرینات شدید بر متابولیسم لیپید -2018 Wageningen Academic

Abstract

Lipogenic and lipolytic pathways are tightly regulated by nuclear receptors and binding proteins, such as farnesoid x receptor (FXR) and sterol regulatory element binding protein 1c (SREBP-1c). We designed this research to study the effects of high-intensity interval training (HIIT) and high-fat diet (HFD) on hepatic and adipose FXR and SREBP-1c gene expression beside the plasma levels of lipid profile and insulin. 24 male Wistar rats were randomly divided into normal (~12% fat) and HFD (~56% fat) groups with or without participating in the 8 weeks HIIT protocol. Results from two-way ANOVA and Pearson tests (P<0.05) showed that the HFD rats experienced a larger weight gain correlated with dyslipidemia and hyperinsulinemia, higher hepatic and adipose SREBP-1c expression and lower hepatic FXR expression compared with normal diet fed rats. Although HIIT rats showed higher hepatic FXR and lower hepatic and adipose SREBP-1c expression and lower weight gain compared with untrained rats, plasma lipid profile levels had not any significant difference between trained and untrained rats. Interestingly, hepatic FXR expression was negatively correlated with weight gain and SREBP1c expression in both tissues while only the hepatic SREBP-1c was positively correlated to insulin levels. In conclusion, HFD-induced dyslipidemia could occur via the activation of the hepatic SREBP-1c pathway under the insulin effect. Although HIIT rats showed lower SREBP-1c correlated to hepatic FXR activation it seems diet is more effective on lipid profile than HIIT. Also, in presence of HFD, HIIT only affects adipose lipolysis.

Introduction

Postprandial high fat diet (HFD)-induced dyslipidemia has been shown to be an independent risk factor for metabolic and cardiovascular diseases (Tan et al., 2014). Lifestyle interventions are mostly used for lipid lowering effects. It has been shown in human studies, that even one session of aerobic (Kolifa et al., 2004) or resistant (Petitt et al., 2003) exercise can reduce postprandial triglyceride (TG) content in a sex-independent manner that apparently is related to increased lipoprotein lipase activity and decreased endogenous hepatic very low-density lipoprotein (VLDL) secretion (Tan et al., 2014). Increased hepatic lipolytic pathways after exercise appear to decrease liver free fatty acid stores, resulting in decreased endogenous hepatic synthesis and secretion of TG-rich VLDLs (Magkos, 2009).