Royal jelly ameliorates diet-induced obesity and glucose intolerance by promoting brown adipose tissue thermogenesis in mice

Jan 17, 2017Obesity research & clinical practice

Royal jelly reduces diet-related obesity and blood sugar problems by boosting heat production in brown fat of mice

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Abstract

Dietary royal jelly (RJ) suppressed high-fat diet-induced accumulation of white adipose tissue and hepatic triglycerides in mice.

RJ supplementation improved insulin sensitivity as indicated by reduced hyperglycemia and lower HOMA-IR scores.
RJ increased gene and protein expressions of thermogenic markers in brown adipose tissue without altering overall food intake.
No significant changes in locomotor activity were observed with RJ or honey bee larva powder supplementation.
RJ did not induce browning of white adipose tissue, suggesting its effects are primarily through metabolic thermogenesis in brown fat.

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INTRODUCTION: Identification of thermogenic food ingredients is potentially a useful strategy for the prevention of obesity and related metabolic disorders. It has been reported that royal jelly (RJ) supplementation improves insulin sensitivity; however, its impacts on energy expenditure and adiposity remain elusive. We investigated anti-obesity effects of RJ supplementation and their relation to physical activity levels and thermogenic capacities of brown (BAT) and white adipose tissue (WAT).

METHODS: C57BL/6J mice were fed under four different experimental conditions for 17 weeks: normal diet (ND), high fat diet (HFD), HFD with 5% RJ, and HFD with 5% honey bee larva powder (BL). Spontaneous locomotor activity, hepatic triglyceride (TG) content, and blood parameters were examined. Gene and protein expressions of thermogenic uncoupling protein 1 (UCP1) and mitochondrial cytochrome c oxidase subunit IV (COX-IV) in BAT and WAT were investigated by qPCR and Western blotting analysis, respectively.

RESULTS: Dietary RJ, but not BL, suppressed HFD-induced accumulations of WAT and hepatic TG without modifying food intake. Consistently, RJ improved hyperglycemia and the homeostasis model assessment-insulin resistance (HOMA-IR). Although dietary RJ and BL unchanged locomotor activity, gene and protein expressions of UCP1 and COX-IV in BAT were increased in the RJ group compared to the other experimental groups. Neither the RJ nor BL treatment induced browning of WAT.

CONCLUSION: Our results indicate that dietary RJ ameliorates diet-induced obesity, hyperglycemia, and hepatic steatosis by promoting metabolic thermogenesis in BAT in mice. RJ may be a novel promising food ingredient to combat obesity and metabolic disorders.

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Royal jelly ameliorates diet-induced obesity and glucose intolerance by promoting brown adipose tissue thermogenesis in mice

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