Abstract
BackgroundFatty acids (FA) derived from adipose tissue and liver serve as the main fuel in thermogenesis of brown adipose tissue (BAT). Catalase, a peroxisomal enzyme, plays an important role in maintaining intracellular redox homeostasis by decomposing hydrogen peroxide to either water or oxygen that oxidize and provide fuel for cellular metabolism. Although the antioxidant enzymatic activity of catalase is well known, its role in the metabolism and maintenance of energy homeostasis has not yet been revealed. The present study investigated the role of catalase in lipid metabolism and thermogenesis during nutrient deprivation in catalase-knockout (KO) mice.ResultsWe found that hepatic triglyceride accumulation in KO mice decreased during sustained fasting due to lipolysis through reactive oxygen species (ROS) generation in adipocytes. Furthermore, the free FA released from lipolysis were shuttled to BAT through the activation of CD36 and catabolized by lipoprotein lipase in KO mice during sustained fasting. Although the exact mechanism for the activation of the FA receptor enzyme, CD36 in BAT is still unclear, we found that ROS generation in adipocytes mediated the shuttling of FA to BAT.ConclusionsTaken together, our findings uncover the novel role of catalase in lipid metabolism and thermogenesis in BAT, which may be useful in understanding metabolic dysfunction.Graphical
Highlights
Fatty acids (FA) derived from adipose tissue and liver serve as the main fuel in thermogenesis of brown adipose tissue (BAT)
BAT differs from white adipose tissue (WAT) as it contains small and multilocular lipid droplets (LDs) and abundant mitochondria containing uncoupling protein 1 (UCP1), which is used for dissipation of energy in the form of heat [1]
The main fuel for BAT thermogenesis is the oxidation of fatty acids (FA) derived from WAT through lipolysis or through VLDL and acyl carnitines produced in the liver [2]
Summary
Fatty acids (FA) derived from adipose tissue and liver serve as the main fuel in thermogenesis of brown adipose tissue (BAT). The main fuel for BAT thermogenesis is the oxidation of fatty acids (FA) derived from WAT through lipolysis or through VLDL and acyl carnitines produced in the liver [2]. During stress or nutrient-deprivation, TG are the major form of lipids in the adipose tissue, where lipolysis takes place and induces the release free fatty acids (FFA) and glycerol into the circulation and mobilized into the liver, where it induces excessive β-oxidation for energy homeostasis [3,4,5]. ANGPTLs, are a family of proteins structurally similar to angiopoietins, that play an important role in lipid metabolism, inflammation and cancer [7]; Among ANGPTLs, ANGPTL3, ANGPTL4, and ANGPTL8 play major roles in the trafficking and metabolism of lipid by suppressing LPL activity [3, 8]. To fuel BAT thermogenesis, the FA transporter enzyme and LPL must be activated
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