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The fat mass and obesity-associated gene (FTO) is linked to higher plasma levels of the hunger hormone ghrelin and lower serum levels of the satiety hormone leptin in older adults
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Functional Pharmacology.ORCID iD: 000-0002-8911-4068
Uppsala University, Science for Life Laboratory, SciLifeLab. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Molecular Medicine.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Biochemial structure and function. (Clinical Chemistry)
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2014 (English)In: Diabetes, ISSN 0012-1797, E-ISSN 1939-327X, Vol. 63, no 11, 3955-3959 p.Article in journal (Refereed) Published
Abstract [en]

The mechanisms through which common polymorphisms in the fat mass and obesity-associated gene (FTO) drive the development of obesity in humans are poorly understood. By using C: ross-sectional data from 985 elderly (50% females) who participated at age 70 years in the Prospective Investigation of the Vasculature in Uppsala Seniors, circulating levels of ghrelin and leptin were measured after an overnight fast. In addition, subjects were genotyped for FTO rs17817449 (AA, n=345 (35%); AC/CA, n=481 (48.8%); CC, n=159 (16.1%). Linear regression analyses controlling for sex, self-reported physical activity level, fasting plasma glucose, and body mass index were utilized. A positive relationship between the number of FTO C risk alleles and plasma ghrelin levels was found (P=0.005; relative plasma ghrelin difference between CC and AA carriers = ∼9%). In contrast, serum levels of the satiety enhancing hormone leptin were inversely linked to the number of FTO C risk alleles (P=0.001; relative serum leptin difference between CC and AA carriers = ∼11%). These associations were also found when controlling for waist circumference. The present findings suggest that FTO may facilitate weight gain in humans by shifting the endocrine balance from the satiety hormone leptin toward the hunger promoting hormone ghrelin.

Place, publisher, year, edition, pages
2014. Vol. 63, no 11, 3955-3959 p.
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Public Health, Global Health, Social Medicine and Epidemiology
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URN: urn:nbn:se:uu:diva-228726DOI: 10.2337/db14-0470ISI: 000343966100043PubMedID: 24898142OAI: oai:DiVA.org:uu-228726DiVA: diva2:734729
Available from: 2014-07-21 Created: 2014-07-21 Last updated: 2017-12-05Bibliographically approved

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Benedict, ChristianAxelsson, TomasLarsson, AndersIngelsson, ErikLind, LarsSchiöth, Helgi B

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Benedict, ChristianAxelsson, TomasLarsson, AndersIngelsson, ErikLind, LarsSchiöth, Helgi B
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Functional PharmacologyScience for Life Laboratory, SciLifeLabMolecular MedicineBiochemial structure and functionMolecular epidemiologyCardiovascular epidemiology
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Diabetes
Public Health, Global Health, Social Medicine and Epidemiology

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