Abstract
Obesity is reaching epidemic worldwide and is risk factor for cardiovascular disease and type 2 diabetes. Although plasma high density lipoprotein (HDL) and apolipoprotein A-I (apoA-I) are inversely correlated to obesity, whether HDLs have anti-obesity effect remains unclear until a recent study reporting the direct anti-obesity effect of apoA-I and its mimetic peptide. However, the mechanism is not fully understood. Increasing adipose energy expenditure through attainment of brown adipocyte phenotype in white adipose tissue is considered a potential strategy to combat obesity. Specific inhibition of autophagy in adipose tissue is associated with reduced adiposity which is attributed to the attainment of brown adipocyte phenotype in white adipose tissue and the increased energy expenditure. HDL and apoA-I could activate PI3K-Akt-mTORC1 signaling which negatively regulates autophagy. The links between HDL/apoA-I and autophagy brings a new understanding on the anti-obesity effect of HDL and apoA-I.
Highlights
Obesity is the most common nutritional disorder and is associated with important comorbidities such as dyslipidemia, atherosclerosis, type 2 diabetes and insulin resistance [1]
Proneness to obesity and metabolic disease correlates with decreased brown adipose tissue (BAT) activity, whereas resistance to obesity correlates with increased BAT function or the induction of brown adipocyte-like gene expression in white adipose tissue [21,22,23,24,25,26,27]
Excess lipid storage in hypertrophied adipocyte leads to increased endocytoplasmic reticulum (ER) activity, which overwhelms the capacity of ER to properly fold nascent protein, causing ER stress and subsequent oxidative stress in the mitochondria, free fatty acids (FFAs) release and proinflammatory state of adipoctye, which all impinge on mTOR and induce autophagy [43]
Summary
Obesity is the most common nutritional disorder and is associated with important comorbidities such as dyslipidemia, atherosclerosis, type 2 diabetes and insulin resistance [1]. Proneness to obesity and metabolic disease correlates with decreased BAT activity, whereas resistance to obesity correlates with increased BAT function or the induction of brown adipocyte-like gene expression in white adipose tissue [21,22,23,24,25,26,27]. Excess lipid storage in hypertrophied adipocyte leads to increased endocytoplasmic reticulum (ER) activity, which overwhelms the capacity of ER to properly fold nascent protein, causing ER stress and subsequent oxidative stress in the mitochondria, FFA release and proinflammatory state of adipoctye, which all impinge on mTOR and induce autophagy [43] In this sense, activated autophagy may serve as a protective mechanism necessary for cell survival in the challenging environment that develops in adipose tissue. HDL may activate PI3K-Akt signaling through SR-BI and S1P receptor (Figure 2)
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