Genipin is the major active component of Gardeniae fructus and has been shown to ameliorate diabetes and
insulin resistance in rat models. In this study, we first investigated the effect of
genipin on
obesity and the related lipid metabolism mechanisms in diet-induced obese rats. Our results showed that
genipin reduced
body weight, food intake, and visceral fat mass; ameliorated
dyslipidemia,
glucose intolerance,
insulin intolerance, adipocyte
hypertrophy, and hepatic steatosis; and reduced serum
tumor necrosis factor-α level in diet-induced obese rats. Quantitative real-time reverse-transcription polymerase chain reaction results further illustrated that
genipin promoted lipolysis and β-oxidation of
fatty acid by upregulating gene expressions of
hormone-sensitive lipase and adipose
triglyceride lipase in white adipose tissue (WAT) and
peroxisome proliferator-activated receptor-α and
carnitine palmitoyltransferase 1α in hepatic tissue. Moreover,
genipin promoted browning of WAT by upregulating the
mRNA and
protein levels of
uncoupling protein 1 and PRD1-BF1-RIZ1 homologous domain containing 16 in WAT. Additionally,
genipin inhibited gene expressions of
activin receptor-like kinase 7,
tumor necrosis factor-α, and interlukin-6 in WAT. These results indicated that
genipin had a potential therapeutic role in
obesity, in which regulation of lipid mobilization and browning of WAT were involved.