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- Traditionally recognised as the energy reservoir and main site of adaptive thermogenesis, white and brown adipose tissues are complex endocrine organs regulating systemic energy metabolism via the secretion of bioactive molecules, termed “adipokines” and “batokines”, respectively. Due to its significant role in regulating whole-body energy metabolism and other physiological processes, adipose tissue has been increasingly explored as a feasible therapeutic target for obesity. Flavonoids are one of the most significant plant polyphenolic compounds holding a great potential as therapeutic agents for combating obesity. However, understanding their mechanisms of action remains largely insufficient to formulate therapeutic theories. This review critically discusses scientific evidence highlighting the role of flavonoids in ameliorating obesity-related metabolic complications, including adipose tissue dysfunction, inflammation, insulin resistance, hepatic steatosis, and cardiovascular comorbidities in part by modulating the release of adipokines and batokines. Further discussion advocates for the use of therapeutics targeting these bioactive molecules as a potential avenue for developing effective treatment for obesity and its adverse metabolic diseases such as type 2 diabetes.
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- Enlargement of adipose tissue through hypertrophy is a key hallmark of obesity. Our previous study demonstrated that chronic obesity induces brown adipose tissue hypertrophy and altered batokine gene expression patterns in vivo. The present study further explored and verified the pathophysiological and molecular changes implicated in brown adipocyte hypertrophy by exposing T37i cells to 0.25, 0.5, 0.75, and 1 mM of palmitic acid for 48 h. The results showed that palmitic acid-induced intracellular lipid accumulation and lipolysis. Gene expression analysis demonstrated that palmitic acid downregulated genes responsible for glucose and lipid metabolism, such as AdipoQ and PIk3r1, while upregulating Cpt1A, a mitochondrial fatty acid transporter, and Tnf-α, a pro-inflammatory cytokine. Moreover, palmitic acid downregulated brown adipocyte transcriptional factors and thermogenic markers, including Prdm16, Pparg, Cidea, Dio2, Sirt1, and Ucp1. Gene expression of batokines involved in regulating substrate metabolism (Fgf21), angiogenesis (Nrg4 and VegfA), and immune cell recruitment (Metrnl, Gdf15, and Cxcl14) were altered by palmitic acid. This data has demonstrated that palmitic acid contributes to the hypertrophy and whitening of brown adipocytes by inhibiting brown adipocyte differentiation and altering batokines expression patterns.
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