Curcumin induces brown fat-like phenotype in 3T3-L1 and primary white adipocytes

Numerous natural products available over the counter are commonly consumed by healthy, sub-healthy or ill people for the treatment and prevention of various chronic diseases. Among them, a few dietary polyphenols, including the curry compound curcumin, have been attracting the most attention from biomedical researchers and drug developers. Unlike many so-called "good drug candidates", curcumin and several other dietary polyphenols do not have a single known therapeutic target or defined receptor. In addition, the bioavailability of these polyphenols is usually very low due to their poor absorption in the gut. These recently debated features have created enormous difficulties for drug developers. In this review, I do not discuss how to develop curcumin, other dietary polyphenols or their derivatives into pharmaceutical agents. Instead, I comment on how curcumin and dietary polyphenol research has enriched our knowledge of insulin signaling, including the presentation of my perspectives on how these studies will add to our understanding of the famous hepatic insulin function paradox.

Obesity and its associated metabolic syndrome continue to be a health epidemic in westernized societies and is catching up in the developing world. Despite such increases, little headway has been made to reverse adverse weight gain in the global population. Few medical options exist for the treatment of obesity which points to the necessity for exploration of anti-obesity therapies including pharmaceutical and nutraceutical compounds. Defects in brown adipose tissue, a major energy dissipating organ, has been identified in the obese and is hypothesized to contribute to the overall metabolic deficit observed in obesity. Not surprisingly, considerable attention has been placed on the discovery of methods to activate brown adipose tissue. A variety of plant-derived, natural compounds have shown promise to regulate brown adipose tissue activity and enhance the lipolytic and catabolic potential of white adipose tissue. Through activation of the sympathetic nervous system, thyroid hormone signaling, and transcriptional regulation of metabolism, natural compounds such as capsaicin and resveratrol may provide a relatively safe and effective option to upregulate energy expenditure. Through utilizing the energy dissipating potential of such nutraceutical compounds, the possibility exists to provide a therapeutic solution to correct the energy imbalance that underlines obesity.

BackgroundOverweight and obesity are widespread chronic disorders defined as excessive fat accumulation, and are major risk factors for several chronic diseases including type 2 diabetes, coronary heart disease, high blood pressure and fatty liver. Changes in lifestyle such as increased physical activity and a healthy diet can be crucial tools for treating obesity. Intake of rose hip, the fruit of several plants belonging to the Rosaceae family, has been shown to reduce body fat mass and prevent body weight gain. Thus, the aim of the study was to elucidate potential mechanisms through which rose hip inhibit diet-induced obesity.MethodsC57BL/6 J mice were fed a high fat diet with (RH) or without (CTR) rose hip supplementation for three months. In vivo indirect calorimetry was monitored, as well as gene expression and protein levels of different adipose depots.ResultsAlthough no differences in energy intake were found compared to the CTR group, RH prevented body weight gain and lowered blood glucose, insulin and cholesterol levels. Indirect calorimetry showed that RH-fed mice have significantly higher EE during the dark phase, despite comparable voluntary activity. Moreover, when challenged with treadmill running, RH-fed mice exhibited higher metabolic rate. Therefore, we hypothesized that RH could stimulate the brown adipose tissue (BAT) thermogenic capacity or may induce browning of the white adipose tissue (WAT). Compared to the CTR group, gene expression and protein levels of some brown and “brite” markers, together with genes able to promote brown adipocyte differentiation and thermogenesis (such as ucp1, tbx15, bmp7, and cidea), as well as phosphorylation of AMPK, was increased in WAT (but not in BAT) of RH-fed mice.ConclusionsTaken together these results indicate that dietary rose hip prevents body weight gain by increasing whole body EE and inducing browning of WAT. Thus, it has potential therapeutic implication for treatment of obesity and related metabolic disorders.