A1 Refereed original research article in a scientific journal
The Obesity Risk SNP (rs17782313) near the MC4R Gene Is Not Associated with Brain Glucose Uptake during Insulin Clamp-A Study in Finns
Authors: Rebelos Eleni, Honka Miikka-Juhani, Ekblad Laura, Bucci Marco, Hannukainen Jarna C., Silva Lilian Fernandes, Virtanen Kirsi A., Nummenmaa Lauri, Nuutila Pirjo
Publisher: MDPI
Publication year: 2021
Journal: Journal of Clinical Medicine
Journal name in source: JOURNAL OF CLINICAL MEDICINE
Journal acronym: J CLIN MED
Article number: ARTN 1312
Volume: 10
Issue: 6
Number of pages: 8
DOI: https://doi.org/10.3390/jcm10061312
Self-archived copy’s web address: https://research.utu.fi/converis/portal/detail/Publication/59734534
The melanocortin system is involved in the control of adiposity through modulation of food intake and energy expenditure. The single nucleotide polymorphism (SNP) rs17782313 near the MC4R gene has been linked to obesity, and a previous study using magnetoencephalography has shown that carriers of the mutant allele have decreased cerebrocortical response to insulin. Thus, in this study, we addressed whether rs17782313 associates with brain glucose uptake (BGU). Here, [F-18]-fluorodeoxyglucose positron emission tomography (PET) data from 113 Finnish subjects scanned under insulin clamp conditions who also had the rs17782313 determined were compiled from a single-center cohort. BGU was quantified by the fractional uptake rate. Statistical analysis was performed with statistical parametric mapping. There was no difference in age, BMI, and insulin sensitivity as indexed by the M value between the rs17782313-C allele carriers and non-carriers. Brain glucose uptake during insulin clamp was not different by gene allele, and it correlated with the M value, in both the rs17782313-C allele carriers and non-carriers. The obesity risk SNP rs17782313 near the MC4R gene is not associated with brain glucose uptake during insulin clamp in humans, and this frequent mutation cannot explain the enhanced brain glucose metabolic rates in insulin resistance.
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