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Adipogenic and lipogenic gene expression pathways represent the integrated molecular circuits that govern the formation of fat cells (adipogenesis) and the synthesis of fatty acids (lipogenesis). Adipogenesis is a highly orchestrated process involving the sequential activation of transcription factors, most notably Peroxisome Proliferator-Activated Receptor gamma (PPAR-gamma) and CCAAT/enhancer-binding proteins (C/EBPs), which drive the differentiation of mesenchymal stem cells into mature adipocytes (Farmer, 2006, PMID: 16772468). Lipogenesis is the metabolic pathway that converts excess carbohydrates into fatty acids via enzymes such as Acetyl-CoA Carboxylase (ACC) and Fatty Acid Synthase (FASN), primarily regulated by Sterol Regulatory Element-Binding Protein 1c (SREBP-1c) (Horton et al., 2002, PMID: 11448928). These pathways are critical for energy homeostasis, but their chronic overactivation leads to obesity, insulin resistance, and non-alcoholic steatohepatitis (NASH) (Samuel & Shulman, 2012, PMID: 22325970). Therapeutic strategies often focus on modulating specific components, such as using Thiazolidinediones to activate PPAR-gamma for insulin sensitization or ACC inhibitors to reduce hepatic lipid accumulation (Goel et al., 2021, PMID: 33820417).
Modulation of key transcriptional regulators such as PPAR-gamma and SREBP-1c, or inhibition of rate-limiting enzymes like Acetyl-CoA Carboxylase (ACC) and Fatty Acid Synthase (FASN), to regulate adipocyte maturation and de novo lipogenesis.
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