Obesity is an escalating global health challenge, driven by adipose tissue dysfunction characterized by adipocyte hypertrophy, chronic low-grade inflammation and impaired insulin signaling, which together promote insulin resistance, dyslipidemia, hepatic steatosis and cardiovascular disease. Chlorogenic acid (CGA), a dietary phenolic phytochemical abundant in coffee, tea, fruits and vegetables, has attracted considerable interest as a modulator of adipocyte biology and metabolism. This review summarizes in vitro and in vivo evidence of the effects of CGA on adipogenesis, lipid metabolism, thermogenesis, inflammation and glucose homeostasis. In vitro studies employing murine and human adipocyte and progenitor cell models demonstrate that CGA attenuates adipocyte differentiation and lipid accumulation via downregulation of adipogenic transcription factors (PPARγ, C/EBPα) and lipogenic enzymes (FASN, ACC, SREBP 1c), alongside activation of AMPK, Shp2–Erk1/2 and Wnt–β catenin signaling. Several reports further show that CGA promotes browning of white adipocytes and enhances thermogenic and mitochondrial gene expression. Complementary in vivo studies in diet-induced obesity and diabetes models reveal that CGA reduces body weight gain, adiposity, adipocyte size and hepatic steatosis, improves lipid profiles, glucose tolerance and insulin sensitivity, and exerts anti-inflammatory and antioxidant effects in metabolic tissues. Collectively, current preclinical evidence supports CGA as a multifaceted modulator of adipose tissue function and whole-body metabolic homeostasis; however, rigorously designed, long-term clinical trials are required to establish its efficacy and safety in humans.
Sehra et al. (Sat,) studied this question.
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