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Pancreatic fat is negatively associated with insulin secretion in individuals with impaired fasting glucose and/or impaired glucose tolerance: a nuclear magnetic resonance study
Author(s) -
Heni Martin,
Machann Jürgen,
Staiger Harald,
Schwenzer Nina F.,
Peter Andreas,
Schick Fritz,
Claussen Claus D.,
Stefan Norbert,
Häring HansUlrich,
Fritsche Andreas
Publication year - 2010
Publication title -
diabetes/metabolism research and reviews
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.307
H-Index - 110
eISSN - 1520-7560
pISSN - 1520-7552
DOI - 10.1002/dmrr.1073
Subject(s) - medicine , endocrinology , impaired glucose tolerance , insulin resistance , insulin , impaired fasting glucose , diabetes mellitus , adipose tissue , pancreas , glucose tolerance test , type 2 diabetes , beta cell , islet
Background The pathogenesis of type 2 diabetes is characterized by insulin resistance and β‐cell dysfunction. Pancreatic fat load may add to the development of β‐cell dysfunction. The aim was to thoroughly quantify the fat content of pancreas sections (caput, corpus, and cauda) and to compare the impact of pancreatic, intrahepatic, and visceral fat on insulin secretion in humans. Methods Fifty‐one subjects were subjected to an oral glucose tolerance test (OGTT) with glucose, insulin, and C‐peptide measurements [28 subjects displayed normal glucose tolerance, 23 impaired fasting glycemia (IFG)] and/or impaired glucose tolerance (IGT)], and also to whole‐body magnetic resonance imaging (MRI), pancreas MRI, and liver magnetic resonance spectroscopy (MRS). Results After adjustment for gender and age, the mean pancreatic fat content was positively associated with body mass index (BMI), visceral adipose tissue (VAT), and waist circumference (all p ≤ 0.0013). The mean pancreatic fat content was negatively associated with OGTT‐based measures of insulin secretion (all p ≤ 0.03). Analysis of the subgroups of glucose tolerance showed that this was restricted to subjects with IGT and/or IFG. Visceral fat also represented a determinant of β‐cell function in individuals with IGT and/or IFG (all p ≤ 0.02), whereas intrahepatic fat did not. In a stepwise multivariate regression analysis, pancreatic fat turned out to be a stronger determinant of impaired insulin secretion than visceral fat. Conclusions Pancreatic fat is negatively associated with insulin secretion in subjects with IGT/IFG and, therefore, might represent an additional pathogenetic factor leading to β‐cell dysfunction. Copyright © 2010 John Wiley & Sons, Ltd.