Relation of weight maintenance and dietary restraint to peroxisome proliferator–activated receptor γ2, glucocorticoid receptor, and ciliary neurotrophic factor polymorphisms

Vogels, N.; Mariman, E.C.M.; Bouwman, Freek G.; Kester, A.D.M.; Diepvens, K.; Westerterp-Plantenga, Margriet S.

doi:10.1093/ajcn/82.4.740

Cited by 47 publications

(30 citation statements)

References 44 publications

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“…They observed that both carrying the Ala allele and the amount of fat oxidation reduction were predictors of weight regain. This finding was confirmed by Vogels et al [50], who identified proportionally more Ala-allele carriers among subjects with unsuccessful (23.5%) than with successful (9.5%) weight maintenance. The Ala variant of the protein has lower binding affinity for the promoter element of target genes, which is accompanied by a lower transactivation [77], in that case fat oxidation.…”

Section: Genetic Predispositionsupporting

confidence: 65%

“…On the other hand, conflicting findings have been reported as well. Vogels et al [50] measured the leptin drop in successful and non-successful weight maintainers after weight loss by a 6-week VLCD. The unsuccessful group (n = 99) lost 7.2 kg body weight (4.6 kg fat mass) and regained 4.9 kg within 1 year, whereas the successful group (n = 21) lost a comparable 7.6 kg body weight (4.9 kg fat mass) and lost an additional 1.8 kg.…”

Section: Module 2: Energy Regulation By Metabolic Hormonesmentioning

confidence: 99%

“…In a study with 120 subjects who lost 8% of body weight on a 6-week VLCD, it was found that subjects with the G/G genotype as compared to those with the G/C and C/C genotypes had a significantly higher baseline BMI, a decreased disinhibition/emotional eating, and had significantly less feelings of hunger during weight loss. After a 1-year follow-up, the G/G genotype turned out to be a predictor of weight maintenance [50]. …”

Section: Genetic Predispositionmentioning

confidence: 99%

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Human Biology of Weight Maintenance after Weight Loss

Mariman

2012

Lifestyle Genomics

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One year after losing weight, most people have regained a significant part of the lost weight. As such, weight regain after weight loss has a negative impact on human health. The risk for weight regain is determined by psychosocial and behavioral factors as well as by various physiological and molecular parameters. Here, the latter intrinsic factors are reviewed and assembled into four functional modules, two related to the energy balance and two related to resistance against weight loss. Reported genetic factors do not reveal additional functional processes. The modules form nodes in a network describing the complex interactions of intrinsically determined weight maintenance. This network indicates that after an initial weight loss persons with a high baseline fat mass will most easily succeed in maintaining weight, because they can lose fat without raising stress in adipocytes and at the same time spare fat-free mass. However, continued weight loss and weight maintenance requires extra measures like increased physical activity, limited energy intake and a fat-free sparing composition of the diet. Eventually, this network may help to design novel therapeutic measures based on preventing the return effect of specific plasma factors or by preventing the accumulation of adipocyte cellular stress.

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Section: Genetic Predispositionsupporting

confidence: 65%

Section: Module 2: Energy Regulation By Metabolic Hormonesmentioning

confidence: 99%

Section: Genetic Predispositionmentioning

confidence: 99%

See 1 more Smart Citation

Human Biology of Weight Maintenance after Weight Loss

Mariman

2012

Lifestyle Genomics

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“…Some of the current strategies to improve weight maintenance are focused on comparing the genetic make up and potential interactions with the dietary intake [20,[32][33][34] . However, only a few investigations have evaluated the predictive role of nutrigenomics on weight regulation and weight cycling [19] .…”

Section: Discussionmentioning

confidence: 99%

“…So, in order to dismiss this heterogeneity, body weight changes, concretely those related to the maintenance period, were considered taking into account the cut-off point of the 10% body weight loss re- gain. Thus, subjects were categorized into 2 distinct groups (WMS and WRS) according to either high or low weight change during the 6-month weight-maintenance period [20,34] . Firstly, we analyzed the influence of weight maintenance in the anthropometrical variables, which revealed no differences before and after the LCD.…”

Section: Discussionmentioning

confidence: 99%

Expression of Two Inflammation-Related Genes (RIPK3 and RNF216) in Mononuclear Cells Is Associated with Weight-Loss Regain in Obese Subjects

Goyenechea

Crujeiras²,

Abete³

et al. 2009

Lifestyle Genomics

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Background/Aims: Nutrigenomics is providing molecular biomarkers concerning the assessment of diet-related diseases. We analyzed the expression of two interacting genes (RIPK3 and RNF216) in obese subjects receiving a low-calorie diet (LCD) and during the subsequent weight changes. Methods: Two groups of obese subjects (BMI 32.3 ± 5.5kg/m²; age 37.7 ± 7.1 years) were selected according to the 6-month weight-regain outcome after the weight-loss induced by an 8-week LCD (n = 12). Body composition and mRNA levels of RIPK3 and RNF216 in peripheral blood mononuclear cells (PBMC) were evaluated by qRT-PCR at three time-points (week 0, week 8 and week 32). Results: All subjects lost weight significantly (–5.8 ± 2.3%, p < 0.001) and were grouped depending on the successful weight-loss maintenance (weight-loss regain ≤10% or >10%). At baseline (week 0), no differences were observed in the mRNA levels between groups (p > 0.05). However, at the end of the LCD (week 8), association analysis revealed that higher mRNA levels in PBMC of RIPK3 and RNF216 were able to detect those individuals who are more prone to regain weight 6-month after the nutritional intervention (p < 0.05). Conclusions: Gene expression of RIPK3 and RNF216 in PBMC could identify those obese subjects, who will regain more weight after a successful initial weight loss. The mRNA levels of these genes could be suggested as nutrigenomic biomarkers for predicting the obesity treatment outcome.

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Interaction Between Pro12Ala Polymorphism of PPARγ2 and Diet on Adiposity Phenotypes

Lapice

Vaccaro

2014

Curr Atheroscler Rep

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The aim of this report is to perform a systematic review and qualitative synthesis of the literature to address whether, and to what extent, diet modulates the effects of the Pro12Ala polymorphism of peroxisome proliferator-activated receptor gamma 2 (PPARγ2) on body weight and other measures of adiposity. A systematic search of the literature was conducted, wherein both observational and experimental studies of adults were reviewed. Overall, the results of the observational studies show little consistency. Methodological differences in their design, conduct and analysis may largely account for the apparently discrepant findings. This notwithstanding, the main picture that emerges is that the energy content and composition of the diet may affect BMI, body composition and metabolic parameters in Ala allele carriers more than in Pro/Pro homozygotes. In most studies, carriers of the Ala allele with an obesogenic lifestyle (i.e. high-energy, high-carbohydrate and, to some extent, high-fat diets) are more obese than Pro homozygotes. Well-designed intervention studies with a sufficiently large sample size consistently show that carriers of the Ala allele are more prone to weight loss when exposed to a healthy lifestyle; however, these individuals do not seem to retain these benefits when returning to a sedentary lifestyle and inadequate dieting behaviours. Some key questions in this area of research have emerged. Carefully designed and adequately powered studies are needed, particularly involving the development and validation of standardized tools for the assessment of dietary exposure, including the use of biomarkers, to move the field forward.

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Relation of weight maintenance and dietary restraint to peroxisome proliferator–activated receptor γ2, glucocorticoid receptor, and ciliary neurotrophic factor polymorphisms

Abstract: The different genotypes of the PPARgamma2 and GRL genes contribute to WM, either directly (GRL) or indirectly (PPARgamma2 and GRL) via baseline body mass index and waist circumference, and to changes in Three-Factor Eating Questionnaire scores.

Cited by 47 publications

References 44 publications

Human Biology of Weight Maintenance after Weight Loss

Human Biology of Weight Maintenance after Weight Loss

Expression of Two Inflammation-Related Genes (RIPK3 and RNF216) in Mononuclear Cells Is Associated with Weight-Loss Regain in Obese Subjects

Interaction Between Pro12Ala Polymorphism of PPARγ2 and Diet on Adiposity Phenotypes

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