Short-chain fatty acids (SCFAs), especially acetate, propionate and butyrate, are the end products from the intestinal microbial fermentation of dietary fibers and resistant starch. It has been well documented that plasma and colonic SCFAs are associated with metabolic syndromes. Recently, the involvement of SCFAs in energy homeostasis regulation has been extensively studied. The importance of SCFAs on energy metabolism has highlighted the potential of modulating SCFAs as a nutritional target to prevent and counteract metabolism disorders and its associated diseases such as obesity and type 2 diabetes. Here, we summarize the current knowledge about the biological properties of SCFAs with their impact on the energy homeostasis.

To evaluate the anti‐obesity effects of chlorogenic acid (CGA), the mice were fed a high‐fat diet (HFD) upon chlorogenic acid treatment for 6 weeks. The results showed administration of chlorogenic acid (150 mg per kg per day) remarkably promoted body loss, reduced lipid levels in plasma and altered mRNA expression of lipogenesis and lipolysis related genes in adipose tissue. Moreover, chlorogenic acid also reversed the HFD‐induced gut microbiota dysbiosis, including significantly inhibiting the growth of Desulfovibrionaceae, Ruminococcaceae, Lachnospiraceae, Erysipelotrichaceae, and raising the growth of Bacteroidaceae, Lactobacillaceae. Overall, the amelioration of HFD‐induced gut microbiota dysbiosis by chlorogenic acid may contribute, at least partially, to its beneficial effects on ameliorating HFD‐induced obesity.

T supplementation was well tolerated and improved body composition but had no effect on functional performance. T supplementation improved upper body strength only in nonexercisers compared with placebo.

Short-chain fatty acids play crucial roles in a range of physiological functions. However, the effects of short-chain fatty acids on brown adipose tissue have not been fully investigated. We examined the role of acetate, a short-chain fatty acid formed by fermentation in the gut, in the regulation of brown adipocyte metabolism. Our results show that acetate up-regulates adipocyte protein 2, peroxisomal proliferator-activated receptor-γ coactivator-1α, and uncoupling protein-1 expression and affects the morphological changes of brown adipocytes during adipogenesis. Moreover, an increase in mitochondrial biogenesis was observed after acetate treatment. Acetate also elicited the activation of ERK and cAMP response element-binding protein, and these responses were sensitive to G(i/o)-type G protein inactivator, Gβγ-subunit inhibitor, phospholipase C inhibitor, and MAPK kinase inhibitor, indicating a role for the G(i/o)βγ/phospholipase C/protein kinase C/MAPK kinase signaling pathway in these responses. These effects of acetate were mimicked by treatment with 4-chloro-α-(1-methylethyl)-N-2-thiazolylbenzeneacetamide, a synthetic G protein-coupled receptor 43 (GPR43) agonist and were impaired in GPR43 knockdown cells. Taken together, our results indicate that acetate may have important physiological roles in brown adipocytes through the activation of GPR43.

ObjectivesCartonectin is a novel adipokine of the C1q complement/TNF-related protein (CTRP) superfamily, with glucose lowering effects, anti-inflammatory and cardio-protective properties. We sought to investigate circulating cartonectin concentrations in subjects with type 2 diabetes mellitus (T2DM) as well as age and BMI matched control subjects. We also examined the effects of a 2 hour 75 g oral glucose tolerance test (OGTT) on serum cartonectin concentrations in T2DM subjects.DesignCross-sectional study [newly diagnosed (first discovery, not on any treatments) T2DM (n = 47) and control (n = 63) subjects]. Serum cartonectin was measured by ELISA.ResultsSerum cartonectin concentrations were significantly lower in patients with T2DM compared to controls (P<0.05). Furthermore, serum cartonectin was significantly negatively correlated with glucose and CRP, and significantly positively correlated with leptin, in all subjects (n = 110). When subjected to multiple regression analysis, none of these variables were predictive of serum cartonectin (P>0.05). There were no significant correlations in T2DM subjects (n = 47). In control subjects (n = 63), serum cartonectin was significantly negatively correlated with CRP, and significantly positively correlated with insulin, HOMA-IR and leptin. However, when subjected to multiple regression analysis, none of these variables were predictive of serum cartonectin (P>0.05). Finally, serum cartonectin concentrations were significantly lower in T2DM subjects after a 2 hour 75 g OGTT (P<0.01).ConclusionsCartonectin may serve as a novel biomarker for the prediction and early diagnosis of T2DM patients. Furthermore, cartonectin and/or pharmacological agents that increase circulating cartonectin levels can represent a new therapeutic field in the treatment of T2DM patients. Further research is needed to clarify these points.

Background Polyphenols are a class of plant secondary metabolites with a variety of physiological functions. Polyphenols and their intestinal metabolites could greatly affect host energy metabolism via multiple mechanisms. Objective The objective of this review was to elaborate the role of intestinal microecology in the regulatory effects of dietary polyphenols and their metabolites on energy metabolism. Methods In this review, we illustrated the potential mechanisms of energy metabolism regulated by the crosstalk between polyphenols and intestinal microecology including intestinal microbiota, intestinal epithelial cells, and mucosal immune system. Results Polyphenols can selectively regulate the growth of susceptible microorganisms (eg. reducing the ratio of Firmicutes to Bacteroides, promoting the growth of beneficial bacteria and inhibiting pathogenic bacteria) as well as alter bacterial enzyme activity. Moreover, polyphenols can influence the absorption and secretion of intestinal epithelial cells, and alter the intestinal mucosal immune system. Conclusion The intestinal microecology play a crucial role for the regulation of energy metabolism by dietary polyphenols.

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Background Inducible brown adipocytes called beige adipocytes are found in white adipose tissue (WAT) depots. They express functional UCP1 and have thermogenic fat-burning capacities as also found in classical brown adipocytes in response to various stimuli. Beige adipocytes may also secrete certain factors that affect WAT function and systemic metabolism. Therefore, a white-to-brown fat conversion could be a novel therapeutic avenue for tackling obesity and metabolic disorders. Scope and Approach In this review, we examine the evidence supporting the concept that the anti-obesity action attributed to polyphenols might be contributed by their stimulation of WAT browning, and discuss the possible underlying mechanisms involved in this action. Key Findings and Conclusions Current evidence, mostly derived from animal models, strongly supports that dietary polyphenols may play roles in the browning of WAT. Studies also show multiple signaling pathways, receptors, and transcription factors have been associated with the browning effects of dietary polyphenols. In conclusion, polyphenol compounds and their principal metabolites may contribute to counteracting human obesity via promoting WAT browning.