Additive effects of the mutations in the beta3-adrenergic receptor and uncoupling protein-1 genes on weight loss and weight maintenance in Finnish women

J Clin Endocrinol Metab. 1998 Dec;83(12):4246-50. doi: 10.1210/jcem.83.12.5339.

Abstract

This study examined whether the Trp64Arg mutation in the beta3-adrenergic receptor (beta3AR) and the A-->G mutation in the uncoupling protein-1 (UCP-1) genes have associations with weight loss and subsequent weight maintenance. Seventy-seven obese (body mass index range, 29-46 kg/m2), clinically healthy, premenopausal women were studied. A 12-wk weight reduction by very low calorie diet (VLCD) was followed by a 40-wk weight maintenance phase. The subjects were divided into four groups according to their beta3AR and UCP-1 genotype: no mutation (control; n=37), only Trp64Arg mutation in the beta3AR gene (n=12), only A-->G mutation in the UCP-1 gene (n=23), and both mutations (n=5). Subjects with both mutations had a lower weight reduction during VLCD than the controls [-10.5+/-0.6 (+/-SEM) vs. -14.0+/-0.5 kg; P=0.051, by ANOVA]. During the maintenance phase, weight in subjects with both mutations increased by 5.8+/-1.5 kg, but remained unchanged in the controls (-0.5+/-0.8 kg; P=0.041). The changes in weight in subjects with only one of the mutation were close to the results in the controls. Resting energy expenditure, adjusted for fat mass, fat-free mass, and maximal aerobic power, did not change differently between the groups throughout the study. The results suggest that a combination of the Trp64Arg mutation in the beta3AR and the A-->G mutation in the UCP-1 genes may be associated with faster weight gain after a VLCD.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Amino Acid Sequence
  • Base Sequence
  • Body Weight / physiology*
  • Carrier Proteins / genetics*
  • Energy Intake
  • Energy Metabolism / physiology
  • Female
  • Finnland
  • Humans
  • Ion Channels
  • Membrane Proteins / genetics*
  • Mitochondrial Proteins
  • Mutation / genetics
  • Mutation / physiology*
  • Receptors, Adrenergic, beta / genetics*
  • Uncoupling Protein 1
  • Weight Loss / physiology

Substances

  • Carrier Proteins
  • Ion Channels
  • Membrane Proteins
  • Mitochondrial Proteins
  • Receptors, Adrenergic, beta
  • UCP1 protein, human
  • Uncoupling Protein 1