Yoshida Mei, Hayashi Kaori, Watadani Risa, Okano Yoshiyasu, Tanimura Keiya, Kotoh Jun, Sasaki Daiki, Matsumoto Kozo, Maeda Akihiko
Department of Animal Medical Sciences, Faculty of Life Sciences, Kyoto Sangyo University, Motoyama, Kamigamo, Kita-ku, Kyoto 603-8555, Japan.
J Vet Med Sci. 2017 Feb 14;79(2):299-307. doi: 10.1292/jvms.16-0458. Epub 2016 Nov 26.
The study examined whether royal jelly (RJ) can prevent obesity and ameliorate hyperglycemia in type 2 diabetes. This study utilized obese/diabetic KK-Ay mice. RJ (10 mg/kg) was administered by oral gavage. Body weight, plasma glucose and insulin levels were measured. mRNA and protein levels were determined using quantitative reverse transcription polymerase chain reaction and western blotting, respectively. Four weeks of RJ administration improved hyperglycemia and partially suppressed body weight gain, although the latter effect did not reach statistical significance. In addition, RJ administration did not improve insulin resistance. RJ administration suppressed the mRNA expression of glucose-6-phosphatase (G6Pase), a key enzyme of gluconeogenesis, in the liver. Simultaneously, RJ administration induced adiponectin (AdipoQ) expression in abdominal fat, adiponectin receptor-1 (AdipoR1) expression in the liver and phosphorylated AMP-activated protein kinase (pAMPK) expression, which suppressed G6Pase levels in the livers of KK-Ay mice. pAMPK levels were also increased in skeletal muscle, but glucose transporter-4 (Glut4) translocation was not increased in the RJ supplementation group. The improvement in hyperglycemia due to long-term RJ administration may be because of the suppression of G6Pase expression through the upregulation of AdipoQ and AdipoR1 mRNA and pAMPK protein expressions.
该研究考察了蜂王浆（RJ）是否能预防肥胖并改善2型糖尿病患者的高血糖状况。本研究使用了肥胖/糖尿病KK-Ay小鼠。通过灌胃给予RJ（10毫克/千克）。测量体重、血糖和胰岛素水平。分别使用定量逆转录聚合酶链反应和蛋白质印迹法测定mRNA和蛋白质水平。给予RJ四周改善了高血糖状况，并部分抑制了体重增加，尽管后一种效果未达到统计学意义。此外，给予RJ并未改善胰岛素抵抗。给予RJ抑制了肝脏中糖异生关键酶葡萄糖-6-磷酸酶（G6Pase）的mRNA表达。同时，给予RJ诱导腹部脂肪中脂联素（AdipoQ）表达、肝脏中脂联素受体-1（AdipoR1）表达以及磷酸化的AMP激活蛋白激酶（pAMPK）表达，从而抑制了KK-Ay小鼠肝脏中的G6Pase水平。骨骼肌中的pAMPK水平也有所升高，但在补充RJ的组中葡萄糖转运蛋白-4（Glut4）的转位并未增加。长期给予RJ导致高血糖状况改善可能是由于通过上调AdipoQ和AdipoR1 mRNA以及pAMPK蛋白表达来抑制G6Pase表达。
