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Diabetes Care Publish Ahead of Print published online ahead of print July 31, 2007
DOI: 10.2337/dc07-0326

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Original Research

Pancreatic Fat Content and ß-cell Function in Men With and Without Type 2 Diabetes

Maarten E. Tushuizen, MD1, Mathijs C. Bunck, MD1, Petra J. Pouwels, PhD2, Saskia Bontemps, MSc1, Jan Hein T. van Waesberghe, MD, PhD3, Roger K. Schindhelm, MD, PhD1, Andrea Mari, PhD4, Robert J. Heine, MD, PhD, FRCP1 and Michaela Diamant, MD, PhD1

1Department of Endocrinology/Diabetes Center
2Department of Physics & Medical Technology
3Department of Radiology; VU University Medical Center, Amsterdam, The Netherlands
4Institute of Biomedical Engineering, National Research Council, Padova, Italy

m.diamant{at}vumc.nl

ABSTRACT

Objective:Insulin resistance, associated with increased lipolysis, results in a high exposure of non-adipose tissues to lipids. Experimental data indicate that fatty infiltration of pancreatic islets may also contribute to ß-cell dysfunction, but whether this occurs in humans in vivo is unknown.

Research Design and Methods:Using proton magnetic resonance spectroscopy and oral glucose tolerance tests, we studied the association of pancreatic lipid accumulation in vivo and various aspects of ß-cell function in 12 insulin-naïve type 2 diabetic and 24 age- and BMI-matched non-diabetic males.

Results:Patients versus controls had higher HbA1c, fasting plasma glucose, insulin and triglyceride levels, lower HDL-C, but similar waist circumference. Median (interquartile range) pancreatic fat content in patients and controls was 20.4 (13.4-43.6) and 9.7 (7.0-20.2)%, respectively (P=0.032). Pancreatic fat correlated negatively with ß-cell function parameters, including the insulinogenic index adjusted for insulin resistance, early glucose-stimulated insulin secretion, ß-cell glucose sensitivity, rate sensitivity (all P<0.05), but not potentiation. However, these associations were significantly affected by the diabetic state, such that a significant association of pancreatic fat with ß-cell dysfunction was only present in the non-diabetic group (all P<0.01), suggesting that once diabetes occurs, factors additional to pancreatic fat account for further ß-cell function decline. In controls, the association of pancreatic fat and ß-cell function remained significant after correction for BMI, fasting plasma glucose and triglycerides (P=0.006).

Conclusions:These findings indicate that pancreatic lipid content may contribute to ß-cell dysfunction and possibly to the subsequent development of type 2 diabetes in susceptible humans.


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Y. Saisho, A. E. Butler, and P. C. Butler
Pancreatic Fat Content and {beta}-Cell Function in Men With and Without Type 2 Diabetes: Response to Tushuizen et al.
Diabetes Care, May 1, 2008; 31(5): e38 - e38.
[Full Text] [PDF]


Home page
Diabetes CareHome page
M. E. Tushuizen, M. C. Bunck, P. J. Pouwels, and M. Diamant
Pancreatic Fat Content and {beta}-Cell Function in Men With and Without Type 2 Diabetes: Response to Saisho, Butler, and Butler
Diabetes Care, May 1, 2008; 31(5): e39 - e39.
[Full Text] [PDF]




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