Fumeron F, Durack-Bown I, Betoulle D, Cassard-Doulcier A M, Tuzet S, Bouillaud F, Melchior J C, Ricquier D, Apfelbaum M
Institut National de la Santé et de la Recherche Médical U286, Faculté Xavier Bichat, Paris, France.
Int J Obes Relat Metab Disord. 1996 Dec;20(12):1051-4.
To investigate whether the genetic polymorphisms of the uncoupling protein (UCP) and beta 3 adrenergic receptor (beta 3 AR) were associated with differences of weight loss in obese patients submitted to a low calorie diet.
Longitudinal, clinical intervention study of a 25% restriction in energy intake with respect to genotypes.
163 patients with a body mass index above 27.
Body weight and body mass index at baseline and after 2.5 months, genotypes by polymerase chain reaction followed by enzymatic digestion.
For the UCP polymorphism, two alleles, 1 and 2 were identified with respective frequencies of 0.27 and 0.73. The allele 1 was associated with lower body weight loss after diet: 4,6,5.7 and 7.1 kg for the 1-1, 1-2 and 2-2 genotypes respectively (P < 0.05). No difference in weight loss was found according to the beta 3 AR Trp64Arg mutation.
A genetic variant of the UCP gene is associated with a resistance to low calorie diet. This result, together with previous data on body weight gain, supports the hypothesis of a role of UCP and brown adipose tissue in the body weight regulation in humans. The importance of the Trp64Arg mutation of the beta 3 AR in the resistance to low calorie diet is still to demonstrate.
研究解偶联蛋白（UCP）和β3肾上腺素能受体（β3AR）的基因多态性是否与接受低热量饮食的肥胖患者体重减轻的差异相关。
关于基因型的能量摄入限制25%的纵向临床干预研究。
163名体重指数高于27的患者。
基线时和2.5个月后的体重和体重指数，通过聚合酶链反应随后酶切来确定基因型。
对于UCP基因多态性，鉴定出两个等位基因，1和2，其频率分别为0.27和0.73。等位基因1与饮食后较低的体重减轻相关：1-1、1-2和2-2基因型的体重减轻分别为4.6、5.7和7.1千克（P<0.05）。根据β3AR Trp64Arg突变未发现体重减轻有差异。
UCP基因的一个遗传变异与低热量饮食抵抗相关。这一结果，连同先前关于体重增加的数据支持UCP和棕色脂肪组织在人类体重调节中起作用的假说。β3AR的Trp64Arg突变在低热量饮食抵抗中的重要性仍有待证实。
