ArticlePloS one2017
GNB3 overexpression causes obesity and metabolic syndrome.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 19 citations in OpenAlex.
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- Sertraline exposure during development may impact post-myocardial infarction survival in adult mice.Physiological reports · 2025Article
- Genetic interaction between oxidative stress and body mass index in a Spanish population.Redox biology · 2025Article
- Copy Number Variation and Selection Signal: Exploring the Domestication History and Phenotype Differences Between Duroc and the Chinese Native Ningxiang Pigs.International journal of molecular sciences · 2024Article
- Three Blind Moles: Molecular Evolutionary Insights on the Tempo and Mode of Convergent Eye Degeneration inGenes · 2023Article
- Metabolic Adverse Effects of Psychotropic Drug Therapy: A Systematic Review.European journal of investigation in health, psychology and education · 2023Review
- Integrated bioinformatics analysis and screening of hub genes in polycystic ovary syndrome.Endocrine · 2022Article
- Association of miRNA targetome variants in LAMC1 and GNB3 genes with colorectal cancer and obesity.Cancer medicine · 2022Article
- WGCNA Analysis of Important Modules and Hub Genes of Compound Probiotics Regulating Lipid Metabolism in Heat-Stressed Broilers.Animals : an open access journal from MDPI · 2022Article
- Review
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
The G-protein beta subunit 3 (GNB3) gene has been implicated in obesity risk; however, the molecular mechanism of GNB3-related disease is unknown. GNB3 duplication is responsible for a syndromic form of childhood obesity, and an activating DNA sequence variant (C825T) in GNB3 is also associated with obesity. To test the hypothesis that GNB3 overexpression causes obesity, we created bacterial artificial chromosome (BAC) transgenic mice that carry an extra copy of the human GNB3 risk allele. Here we show that GNB3-T/+ mice have increased adiposity, but not greater food intake or a defect in satiety. GNB3-T/+ mice have elevated fasting plasma glucose, insulin, and C-peptide, as well as glucose intolerance, indicating type 2 diabetes. Fasting plasma leptin, triglycerides, cholesterol and phospholipids are elevated, suggesting metabolic syndrome. Based on a battery of behavioral tests, GNB3-T/+ mice did not exhibit anxiety- or depressive-like phenotypes. GNB3-T/+ and wild-type animals have similar activity levels and heat production; however, GNB3-T/+ mice exhibit dysregulation of acute thermogenesis. Finally, Ucp1 expression is significantly lower in white adipose tissue (WAT) in GNB3-T/+ mice, suggestive of WAT remodeling that could lead to impaired cellular thermogenesis. Taken together, our study provides the first functional link between GNB3 and obesity, and presents insight into novel pathways that could be applied to combat obesity and type 2 diabetes.
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