Genetic Predictors of Weight Loss and Weight Regain After Intensive Lifestyle Modification, Metformin Treatment, or Standard Care in the Diabetes Prevention Program

Delahanty, Linda M.; Pan, Qing; Jablonski, Kathleen A.; Watson, Karol E.; McCaffery, Jeanne M.; Shuldiner, Alan R.; Kahn, Steven E.; Knowler, William C.; Florez, José C.; Franks, Paul W.

doi:10.2337/dc11-1328

Cited by 106 publications

(128 citation statements)

References 11 publications

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“…Interestingly, it has been shown that physical inactivity was associated with a BMI increase (1.95 ± 0.3 kg/m 2 ) in homozygous A-allele carriers compared with homozygous T-allele carriers (Andreasen et al 2008). The FTO genotype has also been shown to interact with weight loss (Delahanty et al 2012), and the A-allele seems to complicate weight maintenance in severe obese patients (Woehning et al 2013). Studies also show that the A-allele is associated with increased energy intake (Speakman et al 2008), but this could not be confirmed in the present study.…”

Section: Discussionmentioning

confidence: 99%

Gender-specific genetic associations of polymorphisms in ACE, AKR1C2, FTO and MMP2 with weight gain over a 10-year period

et al. 2014

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Weight gain, when it leads to overweight or obesity, is nowadays one of the major health problems. ACE, FTO, AKR1C2, TIMP4 and MMP2 genes have been implicated in previous studies on weight regulation. This study investigated the contribution of polymorphisms in these five candidate genes to the risk of weight gain over a 10-year time period. Two groups were selected from participants of the Doetinchem cohort study who were followed over a 10-year period: A stable weight group (±2 kg/10 year; n = 259) and a weight gainers group who increased their body weight by roughly 10 % ([8 kg/ 10 year; n = 237). Starting BMI was between 20 and 35 kg/m 2 and baseline age between 20 and 45 years. Selected SNPs and insert/deletion in candidate genes were measured in each group. In men, the allelic distribution of FTO rs9939609 (v 2 p = 0.005), ACE rs4340 (v 2 p = 0.006) and AKR1C2 rs12249281 (v 2 p = 0.019) differed between the weight stable and weight gainers group. Interaction between FTO rs9939609 and ACE rs4340 was observed. In women, the allelic distribution of MMP2 rs1132896 differed between the weight stable and weight gainers group (v 2 p = 0.00001). The A-allele of FTO was associated with a 1.999 higher risk of gaining weight in men (OR 1.99, p = 0.020), while in women, the C-allele of MMP2 was associated with a 2.509 higher risk of weight gain (OR 2.50, p = 0.001) over the 10-year period. We found that FTO in men and MMP2 in women are associated with weight gain over a 10-year follow-up period.

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Section: Discussionmentioning

confidence: 99%

Gender-specific genetic associations of polymorphisms in ACE, AKR1C2, FTO and MMP2 with weight gain over a 10-year period

et al. 2014

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“…Low-fat diets (Sonestedt et al, 2009) and embarking on a Mediterranean diet (Razquin et al, 2010) may also ' protect against ' FTO -related obesity, and some have suggested that education (Corella et al, 2010) and breast-feeding may also be protective (Dedoussis et al, 2011). There is also evidence that high genetic risk in terms of common variants could mitigate against weight loss via bariatric surgery (Still et al, 2011), caloric restriction (Matsuo et al, 2011), or within a diabetes prevention programme (Delahanty et al, 2012).…”

Section: The Search For ' Obesity Genes 'mentioning

confidence: 99%

Fat brains, greedy genes, and parent power: A biobehavioural risk model of child and adult obesity

Carnell

Kim

Pryor

2012

International Review of Psychiatry

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We live in a world replete with opportunities to overeat highly calorifi c, palatable foods -yet not everyone becomes obese. Why? We propose that individuals show differences in appetitive traits (e.g. food cue responsiveness, satiety sensitivity) that manifest early in life and predict their eating behaviours and weight trajectories. What determines these traits? Parental feeding restriction is associated with higher child adiposity, pressure to eat with lower adiposity, and both strategies with less healthy eating behaviours, while authoritative feeding styles coincide with more positive outcomes. But, on the whole, twin and family studies argue that nature has a greater infl uence than nurture on adiposity and eating behaviour, and behavioural investigations of genetic variants that are robustly associated with obesity (e.g. FTO) confi rm that genes infl uence appetite. Meanwhile, a growing body of neuroimaging studies in adults, children and high risk populations suggests that structural and functional variation in brain networks associated with reward, emotion and control might also predict appetite and obesity, and show genetic infl uence. Together these different strands of evidence support a biobehavioural risk model of obesity development. Parental feeding recommendations should therefore acknowledge the powerful -but modifi able -contribution of genetic and neurological infl uences to children ' s eating behaviour.

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“…In addition, 49 loci associated with body fat distribution (waist-to-hip ratio adjusted for BMI) were identified [3] . The first evidence for a role of genetic predisposition in weight loss and weight regain came from a study by Delahanty et al [4] , which showed that several gene variants were associated with short-and long-term weight loss and weight regain. Based on a meta-analysis of available studies, Xiang et al [5] concluded that individuals carrying the homozygous fat mass and obesity-associated (FTO) obesity-predisposing allele lose more weight by means of diet or lifestyle interventions than noncarriers.…”

Section: Introductionmentioning

confidence: 99%

Genetic Predictors of ≥5% Weight Loss by Multidisciplinary Advice to Severely Obese Subjects

Aller¹,

Mariman²,

Bouwman³

et al. 2017

Lifestyle Genomics

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Background:Weight loss success is determined by genetic factors, which may differ according to treatment strategy. Methods: From a multidisciplinary obesity treatment program involving dietary advice, psychological counseling, and increased physical activity, 587 subjects (68% female; 46.1 ± 12.4 years; BMI 39.9 ± 6.3) were recruited. At baseline, a blood sample was drawn for DNA isolation. Genotypes were determined for 30 polymorphisms in 25 candidate genes. The association between genotypes and weight loss was assessed after 3 months (short-term) and after 12 months of treatment (long-term). Weight loss was categorized as ≥ 5% or <5% of initial weight. Results: The G/G genotype of PLIN1 (rs2289487) and PLIN1 (rs2304795), the T/T genotype of PLIN1 (rs1052700), and the C/C genotype of MMP2 predicted ≥ 5% weight loss in the first 3 months. The C/G-G/G genotype of PPARγ (rs1801282) and the T/C genotype of TIMP4 (rs3755724) predicted ≥ 5% weight loss after 12 months. Subjects with the combination of PPARγ (rs1801282) C/G-G/G and TIMP4 (rs3755724) T/C lost even more weight. Conclusion: Polymorphisms in genes related to regulation of fat storage and structural adaptation of the adipocytes are predictors for weight loss success with different genes being relevant for short-term and long-term weight loss success.

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Genetic Predictors of Weight Loss and Weight Regain After Intensive Lifestyle Modification, Metformin Treatment, or Standard Care in the Diabetes Prevention Program

Cited by 106 publications

References 11 publications

Gender-specific genetic associations of polymorphisms in ACE, AKR1C2, FTO and MMP2 with weight gain over a 10-year period

Gender-specific genetic associations of polymorphisms in ACE, AKR1C2, FTO and MMP2 with weight gain over a 10-year period

Fat brains, greedy genes, and parent power: A biobehavioural risk model of child and adult obesity

Genetic Predictors of ≥5% Weight Loss by Multidisciplinary Advice to Severely Obese Subjects

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