Pancreatic adipose tissue infiltration, parenchymal steatosis and beta cell function in humans.
OBJECTIVE
This study aimed to perform a comprehensive analysis of interlobular, intralobular and parenchymal pancreatic fat in order to assess their respective effects on beta cell function.


METHODS
Fifty-six participants (normal glucose tolerance [NGT] (n = 28), impaired fasting glucose (IFG) and/or impaired glucose tolerance (IGT) (n = 14) and patients with type 2 diabetes (n = 14)) underwent a frequent-sampling OGTT and non-invasive magnetic resonance imaging (MRI; whole-body and pancreatic) and proton magnetic resonance spectroscopy ((1)H-MRS; liver and pancreatic fat). Total pancreatic fat was assessed by a standard 2 cm(3) (1)H-MRS method, intralobular fat by 1 cm(3) (1)H-MRS that avoided interlobular fat within modified DIXON (mDIXON) water images, and parenchymal fat by a validated mDIXON-MRI fat-fraction method.


RESULTS
Comparison of (1)H-MRS techniques revealed an inhomogeneous distribution of interlobular and intralobular adipose tissue, which increased with decreasing glucose tolerance. mDIXON-MRI measurements provided evidence against uniform steatosis, revealing regions of parenchymal tissue void of lipid accumulation in all participants. Total (r = 0.385, p < 0.01) and intralobular pancreas adipose tissue infiltration (r = 0.310, p < 0.05) positively associated with age, but not with fasting or 2 h glucose levels, BMI or visceral fat content (all p > 0.5). Furthermore, no associations were found between total and intralobular pancreatic adipose tissue infiltration and insulin secretion or beta cell function within NGT, IFG/IGT or patients with type 2 diabetes (all p > 0.2).


CONCLUSIONS
The pancreas does not appear to be another target organ for abnormal endocrine function because of ectopic parenchymal fat storage. No relationship was found between pancreatic adipose tissue infiltration and beta cell function, regardless of glucose tolerance status.
Institute for Clinical Diabetology, German Diabetes Center, Leibniz Center for Diabetes Research at Heinrich Heine University, Auf`m Hennekamp 65, 40225, Düsseldorf, Germany.
Paul
P
Begovatz
Chrysi
C
Koliaki
Katharina
K
Weber
Klaus
K
Strassburger
Bettina
B
Nowotny
Peter
P
Nowotny
Karsten
K
Müssig
Jürgen
J
Bunke
Giovanni
G
Pacini
Julia
J
Szendrödi
Michael
M
Roden
D000273:Adipose Tissue / Q000000981:diagnostic imaging / Q000473:pathology*; D000328:Adult; D000375:Aging / Q000378:metabolism; D001786:Blood Glucose / Q000378:metabolism; D015992:Body Mass Index; D005234:Fatty Liver / Q000000981:diagnostic imaging / Q000378:metabolism / Q000473:pathology; D005260:Female; D018149:Glucose Intolerance / Q000378:metabolism; D006801:Humans; D007328:Insulin / Q000378:metabolism; D050417:Insulin-Secreting Cells / Q000378:metabolism / Q000473:pathology*; D050356:Lipid Metabolism; D008297:Male; D008875:Middle Aged; D010179:Pancreas / Q000000981:diagnostic imaging / Q000378:metabolism / Q000473:pathology*; D010182:Pancreatic Diseases / Q000000981:diagnostic imaging / Q000473:pathology*; D014463:Ultrasonography
D001786:Blood Glucose; D007328:Insulin