The genetics of obesity: practical implications

Hebebrand, Johannes; Sommerlad, C.; Geller, Frank; Görg, T; Hinney, Anke

doi:10.1038/sj.ijo.0801689

Cited by 46 publications

(29 citation statements)

References 66 publications

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“…38 Parental BMI was not associated with the therapeutic outcome in the current study; however, sib-sib BMI correlations have consistently been higher than parent-offspring correlations. 37 Another explanation, however, might be that the presence of an obese sibling not attending the program and thus sticking to his/her eating and sedentary habits may discourage the index child in his/her efforts to change that behavior.…”

Section: Discussionmentioning

confidence: 99%

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Treating childhood obesity: Family background variables and the child's success in a weight‐control intervention

Pott

Albayrak

Pauli‐Pott

2009

Intl J Eating Disorders

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Objective: To analyze whether caregiver and family characteristics predict success in a family-based lifestyle intervention program for children and adolescents.Method: Participants were 111 overweight and obese children (7-15 years) who attended a family-based weightreduction program. Body mass index (BMI) and BMI standard deviation scores (BMI-SDS) of index child, and BMI of family members, family adversity characteristics, depression, and attachment attitudes of the primary caregiver were assessed.Results: Risk of nonresponse ( 5% reduction of BMI-SDS or dropout) was elevated in older children, cases with obese sibling(s), maternal depression, and avoidant attachment attitude. In a logistic regression analysis, maternal depression, attachment attitude, and age of index child explained common variance whereas the presence of obese siblings explained unique variance in nonresponding.Discussion: To meet the specific needs of all participating families and to prevent the discouraging experience of failure in weight-control interventions, our data suggest that special support should be provided to adolescents with obese siblings, and cases of maternal depression, and avoidant attachment attitude. V V C 2009 by Wiley Periodicals, Inc.

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Section: Discussionmentioning

confidence: 99%

“…37 Because an obese sibling predicted a poor outcome, we hypothesize that, in these cases, genetic factors account for an obesity phenotype less amenable to weight reduction programs. Indeed, in a recent study, we were able to show that children with a specific insulininduced gene 2 genotype fared less well in such a program.…”

Section: Discussionmentioning

confidence: 99%

Treating childhood obesity: Family background variables and the child's success in a weight‐control intervention

Pott

Albayrak

Pauli‐Pott

2009

Intl J Eating Disorders

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“…Obesity and associated metabolic alterations are growing problems in public health [2,7,8]. Although a positive energy balance is likely to be a final common pathway for obesity, changes in eating behaviour and genetic susceptibility are factors that have emerged recently [2,9].…”

Section: Introductionmentioning

confidence: 99%

A possible role of neuropeptide Y, agouti-related protein and leptin receptor isoforms in hypothalamic programming by perinatal feeding in the rat

et al. 2004

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Aim/hypothesis: Perinatal overfeeding predisposes humans and rats to obesity and diabetes in later life. One classical model for studying the effect of early feeding is manipulation of the size of rat litters. Rats growing up in small litters gain more weight than rats growing up in normal-sized litters. Interestingly, these obese rats maintain this phenotype in adulthood. Conversely, rats raised in large litters show a delay in growth and a decrease in body weight. The aim of this work was to assess the hypothalamic control mechanisms of food intake regulated by perinatal feeding. Methods: Leptin levels were analysed using RIA. Leptin receptor mRNA levels were analysed using RT-PCR. Neuropeptide mRNA levels were analysed using in situ hybridisation. Results: Perinatally overfed neonatal male rats exhibited hyperleptinaemia and a decrease in hypothalamic mRNA levels of the long isoform of the leptin receptor (OB-Rb), explaining their leptin resistance. Moreover, this obese model showed an increase in the mRNA expression of cocaine-and amphetamine-regulated transcript, neuropeptide Y and agouti-related protein in the hypothalamic arcuate nucleus (ARC). In contrast, perinatally underfed neonatal male rats with hypoleptinaemia showed an increase in hypothalamic mRNA of the short isoforms of the leptin receptor. Furthermore, they exhibited an increase in expression of neuropeptide Y and agoutirelated protein in the ARC. Conclusions/interpretation: Rats overfed during early postnatal life show a leptinresistant state mediated by down-regulation of the hypothalamic OB-Rb. These data, together with the increased expression of neuropeptide Y and agouti-related protein in specific neurons in the ARC, might indicate the existence of regulated programming in this nucleus and may provide a new aetiopathogenic concept in susceptibility to obesity.

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“…[1][2][3][4][5][6][7][8][9][10][11][12] Several mutations of the MC4R, mainly one nonsense (Tyr-35-Stop) and three frameshift mutations (732-733insGATT, 631-634delCTCT, 47-48insG) can be considered loss-of-function mutations and are associated with dominant inheritance of obesity. Functional studies showed that many of the missense muations also lead to a loss of function of the MC4R.…”

Section: Introductionmentioning

confidence: 99%

A novel nonsense mutation in the melanocortin-4 receptor associated with obesity in a Spanish population

et al. 2003

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BACKGROUND:In recent years, several groups have reported dominant inheritance of obesity conferred by missense, nonsense and frameshift mutations in the melanocortin 4 receptor gene (MC4R). Hence, MC4R is involved in the most common monogenic form of human obesity described so far. OBJECTIVES: In this context, we screened a Spanish population, composed of obese subjects and normal weight controls, for mutations in the MC4-R by single-strand conformational polymorphism (SSCP). SUBJECTS AND METHODS: Overall 313 individuals, 159 obese subjects (body mass index: BMI: 37.6 kg/m 2 , 95% CI: 36.7-38.5 kg/m 2 ) and 154 normal weight control subjects (BMI: 22.3 kg/m 2 , 95% CI: 22.0-22.6 kg/m 2 ) were screened for MC4-R mutations. RESULTS: We detected a novel nonsense mutation at codon 16 of the MC4-R in an obese female (BMI: 30.0 kg/m 2 ) and a previously described missense mutation (Val-253-Ile) located within the sixth trans-membrane domain of the MC4-R in a normal weight individual (BMI: 19.0 kg/m 2 ). The polymorphism Val-103-Ile was detected in one obese individual, while four subjects (two cases and two controls) with the polymorphism Ile-251-Leu were found. CONCLUSIONS: We have identified a novel nonsense mutation (Trp-16-Stop) that, based on previously described frameshift and nonsense mutations, most likely results in dominantly inherited obesity. Within this Spanish population, the frequency of the Ile-251-Leu polymorphism of the MC4R was similar in obese and control subjects (about 1.3%), while the polymorphism Val-103-Ile was only detected in an obese individual (0.6%).

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The genetics of obesity: practical implications

Cited by 46 publications

References 66 publications

Treating childhood obesity: Family background variables and the child's success in a weight‐control intervention

Treating childhood obesity: Family background variables and the child's success in a weight‐control intervention

A possible role of neuropeptide Y, agouti-related protein and leptin receptor isoforms in hypothalamic programming by perinatal feeding in the rat

A novel nonsense mutation in the melanocortin-4 receptor associated with obesity in a Spanish population

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