Literature DB >> 3041450

Sensitivity to overfeeding: the Quebec experiment with identical twins.

C Bouchard1, A Tremblay, J P Despres, E T Poehlman, G Theriault, A Nadeau, P Lupien, S Moorjani, J Dussault.   

Abstract

The role of the genotype in the response to short-term overfeeding was assessed by submitted six pairs of male monozygotic twins to a 4.2 MJ (1000 kcal) per day energy intake surplus for a period of 22 consecutive days. Individual differences in fat mass and fat-free mass gains were observed in response to overfeeding but they were not randomly distributed. Indeed, the within-pair resemblance in the response was striking when compared to the heterogeneity found among the pairs in adiposity and fat-free mass gains. The intrapair resemblance in the response to overfeeding as assessed by the intraclass coefficient computed with the individual changes, reached 0.88 for total fat mass and 0.76 for fat-free mass. A similar trend for a genetically determined pattern of adaptation to overfeeding was observed for resting metabolic rate (intraclass = 0.63), thermic effect of a meal (intraclass = 0.62), and energy cost of submaximal exercise (intraclass = 0.78) when the data were analysed in terms of changes in oxygen uptake. On the other hand, no major alterations in glucose and insulin response to a glucose load or a test meal, in cardio-pulmonary adaptation to submaximal exercise and in maximal exercise tolerance were found with overfeeding. In contrast, the response of suprailiac fat cell lipolysis (intraclass of about 0.7) and heparin releasable adipose tissue lipoprotein lipase (intraclass - 0.82) varied among individuals but was highly homogeneous within genotypes. Similarly, a genotype-overfeeding interaction effect was seen for serum triglycerides (intraclass = 0.69), HDL-cholesterol (intraclass = 0.85), and the HDL-cholesterol to total cholesterol ratio (intraclass = 0.82). Multiple correlation analyses suggest that much of the variance in the response of fat mass (R = 0.65) and fat-free mass (R = 0.81) is accounted for by alterations in the energy expenditure components assessed in the study. If one takes into account the measurement errors always present in such complex studies and the fact that only a limited fraction of the energy expenditure of activity was considered by design, one can conclude that the genotype determines to a large extent the response variation to short-term overfeeding. In particular, the genotype-overfeeding interaction effect for body composition changes seems to be mediated by the various energy expenditure components, themselves characterized by significant genotype-overfeeding interaction effects.(ABSTRACT TRUNCATED AT 400 WORDS)

Entities:  

Mesh:

Substances:

Year:  1988        PMID: 3041450

Source DB:  PubMed          Journal:  Prog Food Nutr Sci        ISSN: 0306-0632


  7 in total

1.  Body fat in identical twins reared apart: roles for genes and environment.

Authors:  R A Price; I I Gottesman
Journal:  Behav Genet       Date:  1991-01       Impact factor: 2.805

2.  Brain regulation of appetite in twins.

Authors:  Susan J Melhorn; Sonya Mehta; Mario Kratz; Vidhi Tyagi; Mary F Webb; Carolyn J Noonan; Dedra S Buchwald; Jack Goldberg; Kenneth R Maravilla; Thomas J Grabowski; Ellen A Schur
Journal:  Am J Clin Nutr       Date:  2016-01-06       Impact factor: 7.045

3.  Nongenetic influences of obesity on other cardiovascular disease risk factors: an analysis of identical twins.

Authors:  B Newman; J V Selby; C P Quesenberry; M C King; G D Friedman; R R Fabsitz
Journal:  Am J Public Health       Date:  1990-06       Impact factor: 9.308

4.  Decreased food intake following overfeeding involves leptin-dependent and leptin-independent mechanisms.

Authors:  Christy L White; Megan N Purpera; Kenny Ballard; Christopher D Morrison
Journal:  Physiol Behav       Date:  2010-04-10

5.  Do genetic modifiers of high-density lipoprotein cholesterol and triglyceride levels also modify their response to a lifestyle intervention in the setting of obesity and type-2 diabetes mellitus?: The Action for Health in Diabetes (Look AHEAD) study.

Authors:  Gordon S Huggins; George D Papandonatos; Bahar Erar; L Maria Belalcazar; Ariel Brautbar; Christie Ballantyne; Abbas E Kitabchi; Lynne E Wagenknecht; William C Knowler; Henry J Pownall; Rena R Wing; Inga Peter; Jeanne M McCaffery
Journal:  Circ Cardiovasc Genet       Date:  2013-07-16

Review 6.  Leptin resistance and the response to positive energy balance.

Authors:  Christopher D Morrison
Journal:  Physiol Behav       Date:  2008-04-12

Review 7.  Set points, settling points and some alternative models: theoretical options to understand how genes and environments combine to regulate body adiposity.

Authors:  John R Speakman; David A Levitsky; David B Allison; Molly S Bray; John M de Castro; Deborah J Clegg; John C Clapham; Abdul G Dulloo; Laurence Gruer; Sally Haw; Johannes Hebebrand; Marion M Hetherington; Susanne Higgs; Susan A Jebb; Ruth J F Loos; Simon Luckman; Amy Luke; Vidya Mohammed-Ali; Stephen O'Rahilly; Mark Pereira; Louis Perusse; Tom N Robinson; Barbara Rolls; Michael E Symonds; Margriet S Westerterp-Plantenga
Journal:  Dis Model Mech       Date:  2011-11       Impact factor: 5.758

  7 in total

北京卡尤迪生物科技股份有限公司 © 2022-2023.