Repeated stress-induced IL-1β may contribute to the development of visceral obesity through impairments in non-visceral WAT function.
Repeated exposure to acute stress may induce a maladaptive shift in the inflammatory milieu of subcutaneous adipose tissue marked by a repeated, regionally specific rise in IL-1β. In turn, this may lead to subcutaneous dysfunction or impairments in the depots’ ability to 1) uptake lipids, 2) resynthesize and/or retain lipids, and 3) expand via hyperplasia in the face of positive energy balance. These IL-1β-induced WAT dysfunctions may occur through the following mechanisms: 1) reduced lipoprotein lipase (LPL) activity - a decrease in LPL activity reduces lipid uptake which reduces triglyceride re-synthesis and storage and increases circulating lipid concentrations; 2) reduced Lipin-1 expression - decreased Lipin-1 expression negatively affects triglyceride re-synthesis and storage which further increases net circulating lipid concentrations; 3) reduced adipogeneic potential. IL-1β signaling activates the transcription factor NF-kβ which then reduces PPARγ activity. A reduction in PPARγ impairs adiopgenesis, or the differentiation of preadipocytes into mature, lipid storing, adipocytes. Collectively these effects may contribute toward the development of visceral obesity by a) reducing the size of non-visceral adipose depots relative to visceral adipose due to an imbalance in lipolytic flux (lipolysis
lipogenesis) and/or b) by shunting circulating lipids to non-visceral WAT for deposition due to the increased concentration of circulating lipids and reduced lipogenic/adipogenic potential of non-visceral WAT. Abbreviations: TG - triglyceride; FFA - free fatty acid; LPL - lipoprotein lipase; ACS - AcylCoA synthase; GK- glycerol kinase; NFkβ- nuclear factor kappa beta; PPARγ - peroxisome proliferator-activated receptor gamma.
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