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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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- It remains essential to decipher some of the pathological mechanisms that link obesity with deterio rating human health. Insulin resistance, due to enhanced free fatty acid substrate delivery, results in disrupted glucose homeostasis and altered mitochondrial oxidative capacity, which is a characteristic feature of an obese state. In fact, as a major site for regulating glucose homeostasis and energy pro duction in response to insulin, the skeletal muscle has become an interesting target tissue to understand the impact of lipid overload on the development of insulin resistance and impaired mitochondrial respiratory function. In addition to systematically retrieving the discussed data, the current review brings an essential perspective in understanding the relevance of experimental models of lipid overload such as high fat diets in understanding the pathological link between insulin resistance and pathological changes in mitochondrial oxidative capacity. Importantly, inclusion of evidence from transgenic model highlights some of the unique molecular targets that are implicated in the development of insulin resistance and inefficient mitochondrial respiration processes within an obese state. Importantly, saturation with lipid products such as ceramides and diacylglycerols, especially within the skeletal muscle, appears to be instrumental in paving the path leading to worsening of metabolic complications. These metabolic consequences mostly interfere with the efficiency of the mitochondrial electron transport chain, leading to overproduction of toxic reactive oxygen species. Therefore, therapeutic agents that reverse the effects of lipid overload by improving insulin sensitivity and mitochondrial oxidative capacity are crucial for the management or even treatment of metabolic diseases.
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