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Adipogenesis and lipogenesis pathways are the fundamental biological processes governing the development of adipose tissue and the synthesis of lipids. Adipogenesis involves the differentiation of precursor cells into mature adipocytes, a process orchestrated by a hierarchical network of transcription factors, most notably peroxisome proliferator-activated receptor gamma (PPARγ) and the CCAAT/enhancer-binding protein (C/EBP) family [4, 11]. Lipogenesis, particularly de novo lipogenesis, is the metabolic pathway that converts excess carbohydrates into fatty acids and triglycerides through enzymes such as ATP-citrate lyase (ACLY), acetyl-CoA carboxylase (ACC), and fatty acid synthase (FAS) [6, 16]. These pathways are central to maintaining energy balance, but their dysregulation is a hallmark of metabolic disorders, including obesity, type 2 diabetes, and non-alcoholic fatty liver disease (NAFLD) [2, 19]. Therapeutic interventions often target these pathways to improve insulin sensitivity or reduce ectopic fat accumulation, using agents like thiazolidinediones or novel lipogenesis inhibitors [3, 6]. However, modulating these pathways presents challenges, such as managing the risk of weight gain, fluid retention, or potential lipotoxicity in non-adipose tissues [3, 14, 19].
Modulation of adipocyte differentiation through PPAR-gamma activation and inhibition of de novo fatty acid synthesis via ACC, FAS, and ACLY inhibition [2, 3, 6].
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