Polymorphism in the PPARgamma2 and beta2-adrenergic genes and diet lipid effects on body composition, energy expenditure and eating behavior of obese women

Rosado, Eliane Lopes; Bressan, Josefina; Martins, Marta Fonseca; Cecon, Paulo R.; Martínéz, J. Alfredo

doi:10.1016/j.appet.2007.04.003

Cited by 29 publications

(29 citation statements)

References 49 publications

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“…These data indicate that CART À1336 delA, PPARG2 1431 C4T and IGF2 Apal A4G may be involved in adaptations in thermogenesis independent of body composition. 7 The present finding that PPARG2 1431 C4T increased postprandial REE, together with an earlier report showing that individuals with the Pro12Ala polymorphism of PPARG2 had an increased postprandial REE and higher satiety, 26 suggest that PPARG2 polymorphisms may play a role in postprandial REE. The association between IGF2 Apal A4G and postprandial REE became statistically nonsignificant when further adjusted for postprandial plasma insulin concentration.…”

Section: Postprandial Reesupporting

confidence: 47%

Several obesity- and nutrient-related gene polymorphisms but not FTO and UCP variants modulate postabsorptive resting energy expenditure and fat-induced thermogenesis in obese individuals: the NUGENOB Study

et al. 2009

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Background: Part of the heterogeneity of the obesity phenotype may originate from genetic differences between obese individuals that may influence energy expenditure (EE). Objective: To examine if common single-nucleotide polymorphisms (SNPs) in genes related to obesity-associated phenotypes are associated with postabsorptive resting energy expenditure (REE) and postprandial REE in obese individuals. Design and methods: Postabsorptive REE and 3-h postprandial REE (liquid test meal containing 95% fat, energy content 50% of estimated REE) were measured in 743 obese individuals from eight clinical centres in seven European countries. The analysis assessed the association of genotypes of 44 SNPs in 28 obesity-related candidate genes with postabsorptive REE and postprandial REE taking into consideration the influence of body composition, habitual physical activity, insulin sensitivity, circulating thermogenic hormones and metabolites. Results: After adjustment for fat-free mass (FFM), age, sex and research centre, SNPs in CART, GAD2, PCSK1, PPARG3, HSD11B1 and LIPC were significantly associated with postabsorptive REE. SNPs in GAD2, HSD11B1 and LIPC remained significantly associated with postabsorptive REE after further adjustment for fat mass (FM). SNPs in CART, PPARG2 and IGF2 were significantly associated with postprandial REE after similar adjustments. These associations with postprandial REE remained significant after further adjustment for FM. FTO, UCP2 and UCP3 variants were not associated with postabsorptive or postprandial REE. Conclusions: Several gene polymorphisms associated with obesity-related phenotypes but not FTO and UCP variants may be responsible for some of the inter-individual variability in postabsorptive REE and fat-induced thermogenesis unaccounted for by FFM, FM, age and sex. The association between FTO and obesity that has been reported earlier may not be mediated directly through modulation of EE in obese individuals.

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Section: Postprandial Reesupporting

confidence: 47%

Several obesity- and nutrient-related gene polymorphisms but not FTO and UCP variants modulate postabsorptive resting energy expenditure and fat-induced thermogenesis in obese individuals: the NUGENOB Study

et al. 2009

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“…For example, increasing evidence suggests that genetic factors are associated with behavioral phenotypes such as satiety (71), energy expenditure, and affective response to physical activity (31). Identification of these specific biological processes may enable general behavioral phenotypes (e.g., calories per day) to be "unpacked" and in so doing could provide new targets for tailoring novel intervention approaches.…”

Section: Potential Advantages Of Using Genetic Information To Encouramentioning

confidence: 99%

The Behavioral Response to Personalized Genetic Information: Will Genetic Risk Profiles Motivate Individuals and Families to Choose More Healthful Behaviors?

McBride

Koehly

Sanderson

et al. 2010

Annu. Rev. Public Health

219

220

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This report describes the use of information emerging from genetic discovery to motivate risk-reducing health behaviors. Most research to date has evaluated the effects of information related to rare genetic variants on screening behaviors, in which genetic risk feedback has been associated consistently with improved screening adherence. The limited research with common genetic variants suggests that genetic information, when based on single-gene variants with low-risk probabilities, has little impact on behavior. The effect on behavioral outcomes of more realistic testing scenarios in which genetic risk is based on numerous genetic variants is largely unexplored. Little attention has been directed to matching genetic information to the literacy levels of target audiences. Another promising area for research is consideration of using genetic information to identify risk shared within kinship networks and to expand the influence of behavior change beyond the individual.

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“…PPARG also appears to affect food intake through heightened satiety (Rosado et al, 2007) and reduced fat intake, where the 12Ala variant was associated with reduced saturated fatty acid intake in adolescent girls (Dedoussis et al, 2009). In addition, PPARG genotype may infl uence child eating behaviour through variation in short-term energy compensation, a direct measure of satiety expression.…”

Section: Peroxisome Proliferator-activated Receptor Gene and Eating Bmentioning

confidence: 99%

Obesity and eating behaviour in children and adolescents: Contribution of common gene polymorphisms

Cecil

Dalton

Finlayson

et al. 2012

International Review of Psychiatry

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The prevalence of childhood obesity is increasing in many countries and confers risks for early type 2 diabetes, cardiovascular disease and metabolic syndrome. In the presence of potent ' obesogenic ' environments not all children become obese, indicating the presence of susceptibility and resistance. Taking an energy balance approach, susceptibility could be mediated through a failure of appetite regulation leading to increased energy intake or via diminished energy expenditure. Evidence shows that heritability estimates for BMI and body fat are paralleled by similar coeffi cients for energy intake and preferences for dietary fat. Twin studies implicate weak satiety and enhanced food responsiveness as factors determining an increase in BMI. Single gene mutations, for example in the leptin receptor gene, that lead to extreme obesity appear to operate through appetite regulating mechanisms and the phenotypic response involves overconsumption and a failure to inhibit eating. Investigations of robustly characterized common gene variants of fat mass and obesity associated ( FTO ), peroxisome proliferator-activated receptor ( PPARG ) and melanocortin 4 receptor ( MC4R ) which contribute to variance in BMI also infl uence the variance in appetite factors such as measured energy intake, satiety responsiveness and the intake of palatable energy-dense food. A review of the evidence suggests that susceptibility to childhood obesity involving specifi c allelic variants of certain genes is mediated primarily through food consumption (appetite regulation) rather than through a decrease in activity-related energy expenditure. This conclusion has implications for early detection of susceptibility, and for prevention and management of childhood obesity.

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Polymorphism in the PPARgamma2 and beta2-adrenergic genes and diet lipid effects on body composition, energy expenditure and eating behavior of obese women

Cited by 29 publications

References 49 publications

Several obesity- and nutrient-related gene polymorphisms but not FTO and UCP variants modulate postabsorptive resting energy expenditure and fat-induced thermogenesis in obese individuals: the NUGENOB Study

Several obesity- and nutrient-related gene polymorphisms but not FTO and UCP variants modulate postabsorptive resting energy expenditure and fat-induced thermogenesis in obese individuals: the NUGENOB Study

The Behavioral Response to Personalized Genetic Information: Will Genetic Risk Profiles Motivate Individuals and Families to Choose More Healthful Behaviors?

Obesity and eating behaviour in children and adolescents: Contribution of common gene polymorphisms

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