ArticleNutrition & metabolism2012
Nutritional regulation of genome-wide association obesity genes in a tissue-dependent manner.
Article in Nutrition & metabolism, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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23 citing papers in PubMed, 46 citations in OpenAlex.
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- Incorporating methylation genome information improves prediction accuracy for drug treatment responses.BMC genetics · 2018Article
- Obesity-associated geneProceedings of the National Academy of Sciences of the United States of America · 2017Article
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- Birth weight modifies the association between central nervous system gene variation and adult body mass index.Journal of human genetics · 2016Article
- Dissecting diabetes/metabolic disease mechanisms using pluripotent stem cells and genome editing tools.Molecular metabolism · 2015Review
- Influence of lifestyle on the FAIM2 promoter methylation between obese and lean children: a cohort study.BMJ open · 2015Article
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- SH2B1 regulation of energy balance, body weight, and glucose metabolism.World journal of diabetes · 2014Review
- Neuroadaptations in the striatal proteome of the rat following prolonged excessive sucrose intake.Neurochemical research · 2014Article
- The KCTD family of proteins: structure, function, disease relevance.Cell & bioscience · 2013Article
- Association of the FTO obesity risk variant rs8050136 with percentage of energy intake from fat in multiple racial/ethnic populations: the PAGE study.American journal of epidemiology · 2013Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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backgroundGenome-wide association studies (GWAS) have recently identified several new genetic variants associated with obesity. The majority of the variants are within introns or between genes, suggesting they affect gene expression, although it is not clear which of the nearby genes they affect. Understanding the regulation of these genes will be key to determining the role of these variants in the development of obesity and will provide support for a role of these genes in the development of obesity.
methodsWe examined the expression of 19 GWAS obesity genes in the brain and specifically the hypothalamus, adipose tissue and liver of mice by real-time quantitative PCR. To determine whether these genes are nutritionally regulated, as may be expected for genes affecting obesity, we compared tissues from fasting and non-fasting animals and tissues from mice consuming a high fat high sucrose diet in comparison to standard rodent chow.
resultsWe found complex, tissue-dependent patterns of nutritional regulation of most of these genes. For example, Bat2 expression was increased ~10-fold in the brain of fed mice but was lower or unchanged in the hypothalamus and adipose tissue. Kctd15 expression was upregulated in the hypothalamus, brain and adipose tissue of fed mice and downregulated by high fat feeding in liver, adipose tissue and the hypothalamus but not the remainder of the brain. Sh2b1 expression in the brain and Faim2 expression in adipose tissue were specifically increased >20-fold in fed mice. Tmem18 expression in adipose tissue but not the brain was reduced 80% by high fat feeding. Few changes in the expression of these genes were observed in liver.
conclusionsThese data show nutritional regulation of nearly all these GWAS obesity genes, particularly in the brain and adipose tissue, and provide support for their role in the development of obesity. The complex patterns of nutritional and tissue-dependent regulation also highlight the difficulty that may be encountered in determining how the GWAS genetic variants affect gene expression and consequent obesity risk in humans where access to tissues is constrained.
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Registered trials
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