Association between brain-derived neurotrophic factor Val66Met and obesity in children and adolescents

Škledar, Marijana; Nikolac, Matea; Dodig-Ćurković, Katarina; Ćurković, Mario; Borovečki, Fran; Pivac, Nela

doi:10.1016/j.pnpbp.2011.08.003

Cited by 57 publications

(50 citation statements)

References 37 publications

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“…The variant commonly occurs with high frequency in humans, and association of the met allele with a higher body mass index implied potential involvement of the variant in obesity (25,36). Use of mice with the human BDNF val66met knock-in in both alleles (BDNF…”

Section: M/mmentioning

confidence: 99%

“…The BDNF val66met SNP occurs in a high frequency in humans with 20-30% of the U.S. population and nearly 70% of Asians carrying the met on either one or both alleles (22,23). The rs6265 SNP is linked to eating disorders and obesity in children and adults, and also deficits in memory function (24)(25)(26)(27). Moreover, mice harboring the human val66met SNP in both alleles (BDNF…”

Section: Introductionmentioning

confidence: 99%

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Inhibition of the CD36 receptor reduces visceral fat accumulation and improves insulin resistance in obese mice carrying the BDNF-Val66Met variant

Yang

Park

Cho

2018

Journal of Biological Chemistry

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Running title: CD36 inhibition improves metabolic dysfunction in obese miceKey words: CD36, diabetes, insulin resistance, obese, salvianolic acid B AbstractObesity-induced metabolic dysfunctions increase risk of vascular diseases including type II diabetes and stroke. While managing obesity is an interest to address the worldwide health problem, how genetic variability affects human obesity development and specific targets for obesity-related metabolic disease have not been thoroughly studied. A single nucleotide polymorphism (SNP) in the brain derived neurotropic factor (BDNF) gene that results in the substitution of a valine to a methionine at codon 66 (val66met) occurs with a high frequency in humans. This study addressed the effect of genetic variability in developing obesity and the efficacy of the inhibition of CD36, a multifunctional receptor implicated in obesity and insulin resistance, in wild-type mice and mice with the bdnf val66met variant. CD36 inhibition by salvionolic acid B (SAB) in diet-induced obese wild-type mice reduced visceral fat accumulation and improved insulin resistance. The benefit of SAB was aborted in CD36 knockout mice, showing the specificity of SAB. In addition, mice with the val66met variant in both alleles (BDNF M/M ) fed high-fat diet exhibited extreme obesity with increased CD36 gene and protein levels in macrophages. Chronic SAB treatment in BDNF M/M mice significantly decreased visceral fat accumulation and improved insulin resistance. Notably, the effect of SAB was greater in the extreme obese BDNF M/M mice compared to the wild-type mice. The study demonstrated a link between bdnf val66met and elevated CD36 expression, and suggested that CD36 inhibition may be a novel strategy to improve metabolic dysfunctions and to normalize risk factors for vascular diseases in the obese population.

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Section: M/mmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Inhibition of the CD36 receptor reduces visceral fat accumulation and improves insulin resistance in obese mice carrying the BDNF-Val66Met variant

Yang

Park

Cho

2018

Journal of Biological Chemistry

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“…BDNF has also been shown to affect NPY and POMC expression [425][426][427] , and the serotonin system within the hypothalamus 428 [434][435][436] . However, some studies report the reverse association linking the 66Met allele to obesity 437,438 , while others report no association 439 .…”

Section: Neurotrophin Involvement In Obesitymentioning

confidence: 99%

The role of genetic variation across IL-1β, IL-2, IL-6, and BDNF in antipsychotic-induced weight gain

Fonseka

Tiwari

Gonçalves

et al. 2015

The World Journal of Biological Psychiatry

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“…In contrast, only 20 % of WAGR patients with intact Bdnf alleles developed obesity. Finally, several studies have linked the functional BdnfVal66Met polymorphism to higher body mass index in humans (Beckers et al 2008;Skledar et al 2012;Speliotes et al 2010;Thorleifsson et al 2009). This highly prevalent mutation (Shimizu et al 2004) impedes activity-dependent secretion and signaling of BDNF (Chen et al 2006).…”

Section: Bdnfmentioning

confidence: 99%

Neurotrophins and the Regulation of Energy Balance and Body Weight

Rios

2014

Handbook of Experimental Pharmacology

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Complex interactions between the brain and peripheral tissues mediate the effective control of energy balance and body weight. Hypothalamic and hindbrain neural circuits integrate peripheral signals informing the nutritional status of the animal and in response regulate nutrient intake and energy utilization. Obesity and its many medical complications emerge from the dysregulation of energy homeostasis. Excessive weight gain might also arise from alterations in reward systems of the brain that drive consumption of calorie dense, palatable foods in the absence of an energy requirement. Several neurotrophins, most notably brain-derived neurotrophic factor, have been implicated in the molecular and cellular processes underlying body weight regulation. Here, we review investigations interrogating their roles in energy balance and reward centers of the brain impacting feeding behavior and energy expenditure.

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Association between brain-derived neurotrophic factor Val66Met and obesity in children and adolescents

Cited by 57 publications

References 37 publications

Inhibition of the CD36 receptor reduces visceral fat accumulation and improves insulin resistance in obese mice carrying the BDNF-Val66Met variant

Inhibition of the CD36 receptor reduces visceral fat accumulation and improves insulin resistance in obese mice carrying the BDNF-Val66Met variant

The role of genetic variation across IL-1β, IL-2, IL-6, and BDNF in antipsychotic-induced weight gain

Neurotrophins and the Regulation of Energy Balance and Body Weight

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