Open AccessBrain substrate metabolism and ß‐cell function in humans: A positron emission tomography study
Author(s) -
Rebelos Eleni,
Mari Andrea,
Bucci Marco,
Honka MiikkaJuhani,
Hannukainen Jarna C.,
Virtanen Kirsi A.,
Hirvonen Jussi,
Nummenmaa Lauri,
Heni Martin,
Iozzo Patricia,
Ferrannini Ele,
Nuutila Pirjo
Publication year - 2020
Publication title -
endocrinology, diabetes and metabolism
Language(s) - English
Resource type - Journals
ISSN - 2398-9238
DOI - 10.1002/edm2.136
Subject(s) - medicine , positron emission tomography , endocrinology , glucose clamp technique , glucose uptake , insulin , basal (medicine) , statistical parametric mapping , insulin resistance , diabetes mellitus , type 2 diabetes , fatty acid , carbohydrate metabolism , basal insulin , chemistry , insulin sensitivity , nuclear medicine , biochemistry , magnetic resonance imaging , radiology
Aims Recent clinical studies have shown enhanced brain glucose uptake during clamp and brain fatty acid uptake in insulin‐resistant individuals. Preclinical studies suggest that the brain may be involved in the control of insulin secretion. The aim of this study was to investigate whether brain metabolism assessed as brain glucose and fatty acid uptake is associated with the parameters of β‐cell function in humans. Materials and methods We analysed cross‐sectional data of 120 subjects across a wide range of BMI and insulin sensitivity. Brain glucose uptake (BGU) was measured during euglycaemic‐hyperinsulinaemic clamp (n = 67) and/or during fasting (n = 45) using [ 18 F]‐fluorodeoxyglucose (FDG) positron emission tomography (PET). In another group of subjects (n = 34), brain fatty acid uptake was measured using [ 18 F]‐fluoro‐6‐thia‐heptadecanoic acid (FTHA) PET during fasting. The parameters of β ‐ cell function were derived from OGTT modelling. Statistical analysis was performed with whole‐brain voxel‐based statistical parametric mapping. Results In non‐diabetics, BGU during euglycaemic hyperinsulinaemic clamp correlated positively with basal insulin secretion rate ( r = 0.51, P = .0008) and total insulin output ( r = 0.51, P = .0008), whereas no correlation was found in type 2 diabetics. BGU during clamp correlated positively with potentiation in non‐diabetics ( r = 0.33, P = .02) and negatively in type 2 diabetics ( r = −0.61, P = .02). The associations in non‐diabetics were not explained with whole‐body insulin sensitivity or BMI. No correlations were found between baseline (fasting) BGU and basal insulin secretion rate, whereas baseline brain fatty acid uptake correlated directly with basal insulin secretion rate ( r = 0.39, P = .02) and inversely with potentiation ( r = −0.36, P = .04). Conclusions Our study provides coherent, though correlative, evidence that, in humans, the brain may be involved in the control of insulin secretion independently of insulin sensitivity.