Royal jelly ameliorates diet-induced obesity and glucose intolerance by promoting brown adipose tissue thermogenesis in mice. (January 2018)

• Record Type: Journal Article
• Authors: Yoneshiro, Takeshi; Kaede, Ryuji; Nagaya, Kazuki; Aoyama, Julia; Saito, Mana; Okamatsu-Ogura, Yuko; Kimura, Kazuhiro; Terao, Akira
• Is Part Of: Obesity research & clinical practice. Volume 12(2018)Supplement 1
• Page Start: 127
• Page End: 137
• Publication Date: 2018-01
• Subjects: Royal jelly -- Brown adipose tissue -- Obesity -- Diabetes mellitus -- Hepatic steatosis; Obesity -- Research -- Periodicals; Obesity -- Treatment -- Periodicals; Obesity -- Periodicals; Obésité -- Recherche -- Périodiques; Obésité -- Traitement -- Périodiques; Obesity -- Research; Obesity -- Treatment; Electronic journals; Periodicals; 616.398
• DOI: 10.1016/j.orcp.2016.12.006
• Languages: English
• ISSNs: 1871-403X

Abstract

Summary: 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.