Abstract
The phytochemical oxyresveratrol has been shown to exert diverse biological activities including prevention of obesity. However, the exact reason underlying the anti-obese effects of oxyresveratrol is not fully understood. Here, we investigated the effects and mechanism of oxyresveratrol in adipocytes and high-fat diet (HFD)-fed obese mice. Oxyresveratrol suppressed lipid accumulation and expression of adipocyte markers during the adipocyte differentiation of 3T3-L1 and C3H10T1/2 cells. Administration of oxyresveratrol in HFD-fed obese mice prevented body-weight gains, lowered adipose tissue weights, improved lipid profiles, and increased glucose tolerance. The anti-obese effects were linked to increases in energy expenditure and higher rectal temperatures without affecting food intake, fecal lipid content, and physical activity. The increased energy expenditure by oxyresveratrol was concordant with the induction of thermogenic genes including Ucp1, and the reduction of white adipocyte selective genes in adipose tissue. Furthermore, Foxo3a was identified as an oxyresveratrol-induced gene and it mimicked the effects of oxyresveratrol for induction of thermogenic genes and suppression of white adipocyte selective genes, suggesting the role of Foxo3a in oxyresveratrol-mediated anti-obese effects. Taken together, these data show that oxyresveratrol increases energy expenditure through the induction of thermogenic genes in adipose tissue and further implicates oxyresveratrol as an ingredient and Foxo3a as a molecular target for the development of functional foods in obesity and metabolic diseases.
Highlights
Energy imbalance whereby calories consumed exceed calories expended causes obesity and abnormal excess fat accumulation [1]
While brown adipocytes can be derived from progenitors that express myogenic factor (Myf5), paired box (Pax7), and engrailed (En1) in the dermomyotome, beige adipocytes are derived from precursor cells that express platelet-derived growth factor–β (PDGF-β), smooth muscle actin (SMA), and myosin heavy chain 11 (Myh11) [13]
These results show that oxyresveratrol increases energy expenditure by acting on the stimulation of thermogenesis and further implicating its potential use in treating obesity and metabolic diseases
Summary
Energy imbalance whereby calories consumed exceed calories expended causes obesity and abnormal excess fat accumulation [1]. Phytochemicals including berberine, butein, capsaicin, resveratrol, and curcumin can increase energy expenditure through the stimulation of thermogenic brown or beige adipocytes Various molecular targets such as 5’ adenosine monophosphate-activated protein kinase (AMPK), Prdm, TRPV1, and beta-adrenergic pathway are regulated by these phytochemicals for their thermogenic responses [14]. This suggests that phytochemically induced thermogenic adipocytes may be useful to combat human metabolic diseases and further present molecular targets for WAT browning and energy expenditure. We further identified Foxo3a as an oxyresveratrol-regulated new thermogenic regulator in adipocytes These results show that oxyresveratrol increases energy expenditure by acting on the stimulation of thermogenesis and further implicating its potential use in treating obesity and metabolic diseases
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