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Lack of association of liver fat with model parameters of β-cell function in men with impaired glucose tolerance and type 2 diabetes

¹ Department of Endocrinology/Diabetes Centre² Department of Physics and Medical Technology³ Institute of Biomedical EngineeringNational Research Council, I-35127, Padova, Italy

(Correspondence should be addressed to M Diamant who is now at Department of Endocrinology/Diabetes Centre, VU University Medical Centre, PO Box 7057, 1007 MB Amsterdam, The Netherlands; Email: m.diamant{at}vumc.nl)

Objective: Hepatic steatosis and obesity are components of the metabolic syndrome and risk factors for developing type 2 diabetes (T2DM). We studied how liver fat and body fat distribution relate to various aspects of β-cell function.

Methods: In 12 men with T2DM, 10 men with impaired glucose tolerance (IGT), and 14 age- and body mass index-matched controls, we measured body fat distribution and liver fat by magnetic resonance imaging and spectroscopy. An oral glucose tolerance test was performed to calculate insulin secretory rate (ISR) by C-peptide deconvolution, and β-cell function using a mathematical model that describes ISR as a function of absolute glucose levels (insulin secretory tone and glucose sensitivity), the glucose rate of change (rate sensitivity), and a potentiation factor.

Results: Waist circumference and the various body fat compartments did not differ among groups. IGT had the highest total and late phase insulin secretion (P<0.001), whereas patients had the lowest insulinogenic index adjusted for insulin resistance (P=0.006). In spite of the hypersecretion, IGT had β-cell glucose sensitivity, rate sensitivity, and potentiation similar to controls. Liver fat content was highest in diabetic patients (P=0.004) and showed the strongest association with total and late phase of insulin secretion in the IGT group (r=0.657, P=0.039 and r=0.732, P=0.016 respectively). Model β-cell function variables showed no association with liver fat or body fat compartments.

Conclusions: These data suggest that, in spite of the association of central adiposity and liver fat with T2DM risk, additional, hitherto unknown factors may contribute to β-cell dysfunction in susceptible humans.