Kumar M V, Sunvold G D, Scarpace P J
Geriatric Research, Education and Clinical Center, Department of Veterans Affairs Medical Center, Gainesville, FL 32608-1197, USA.
J Lipid Res. 1999 May;40(5):824-9.
All-trans-retinoic acid (RA), an active metabolite of vitamin A, induces the gene expression of uncoupling protein 1 (UCP1) in brown adipose tissue (BAT) and suppresses leptin gene expression in white adipose tissue (WAT) when given as an acute dose. These contrasting effects of RA leave in doubt the overall effect of chronic RA or vitamin A supplementation on energy homeostasis. To investigate the effects of dietary vitamin A supplementation on leptin and UCP1 gene expression, rats were fed either a normal diet (2.6 retinol/kg diet) or a vitamin A-supplemented diet (129 mg retinol/kg diet) for 8 weeks, and adiposity, serum leptin levels, leptin mRNA levels in perirenal WAT, UCP1 and UCP2 mRNA levels in BAT, and beta3-adrenergic receptor mRNA levels in BAT and WAT were examined. Rats on both diets gained a similar amount of weight, but there was a small 9% decrease in the adiposity index in the vitamin A-supplemented rats. Dietary vitamin A supplementation increased UCP1 gene expression in BAT by 31%, but suppressed leptin gene expression by 44% and serum leptin levels by 65%. UCP2 and beta3-adrenergic receptor gene expression in BAT and perirenal WAT were unchanged by the vitamin A diet. These data suggest that dietary vitamin A has a role in regulating energy homeostasis by enhancing UCP1 gene expression and decreasing serum leptin levels.
全反式维甲酸(RA)是维生素A的一种活性代谢产物,急性给药时可诱导棕色脂肪组织(BAT)中解偶联蛋白1(UCP1)的基因表达,并抑制白色脂肪组织(WAT)中瘦素基因的表达。RA的这些相反作用使得慢性RA或补充维生素A对能量稳态的总体影响存疑。为了研究饮食中补充维生素A对瘦素和UCP1基因表达的影响,将大鼠分别喂食正常饮食(2.6微克视黄醇/千克饮食)或补充维生素A的饮食(129毫克视黄醇/千克饮食)8周,然后检测肥胖程度、血清瘦素水平、肾周WAT中瘦素mRNA水平、BAT中UCP1和UCP2 mRNA水平以及BAT和WAT中β3-肾上腺素能受体mRNA水平。两种饮食的大鼠体重增加量相似,但补充维生素A的大鼠肥胖指数略有下降,下降了9%。饮食中补充维生素A使BAT中UCP1基因表达增加31%,但使瘦素基因表达降低44%,血清瘦素水平降低65%。维生素A饮食对BAT和肾周WAT中UCP2和β3-肾上腺素能受体基因表达没有影响。这些数据表明,饮食中的维生素A通过增强UCP1基因表达和降低血清瘦素水平在调节能量稳态中发挥作用。