Liver ATP synthesis is lower and relates to insulin sensitivity in patients with type 2 diabetes - PubMed (original) (raw)
Liver ATP synthesis is lower and relates to insulin sensitivity in patients with type 2 diabetes
Albrecht Ingo Schmid et al. Diabetes Care. 2011 Feb.
Abstract
Objective: Steatosis associates with insulin resistance and may even predict type 2 diabetes and cardiovascular complications. Because muscular insulin resistance relates to myocellular fat deposition and disturbed energy metabolism, we hypothesized that reduced hepatic ATP turnover (fATP) underlies insulin resistance and elevated hepatocellular lipid (HCL) contents.
Research design and methods: We measured hepatic fATP using (31)P magnetic resonance spectroscopy in patients with type 2 diabetes and age- and body mass-matched controls. Peripheral (M and M/I) and hepatic (suppression of endogenous glucose production) insulin sensitivity were assessed with euglycemic-hyperinsulinemic clamps.
Results: Diabetic individuals had 29% and 28% lower peripheral and hepatic insulin sensitivity as well as 42% reduced fATP than controls. After adjusting for HCL, fATP correlated positively with peripheral and hepatic insulin sensitivity but negatively with waist circumference, BMI, and fasting plasma glucose. Multiple regression analysis identified waist circumference as an independent predictor of fATP and inorganic phosphate (P(I)) concentrations, explaining 65% (P = 0.001) and 56% (P = 0.003) of the variations. Hepatocellular P(I) primarily determined the alterations in fATP.
Conclusions: In patients with type 2 diabetes, insulin resistance relates to perturbed hepatic energy metabolism, which is at least partly accounted for by fat depots.
Figures
Figure 1
Liver MR data of one patient with type 2 diabetes. A: Axial slice through the liver (gradient echo, prone position). The grid corresponds to the chemical shift imaging matrix. The voxels surrounded by the bold white line were selected for quantification. The MR spectrum corresponding to the “×” in the image is shown on the right panel. B: MR spectra from the saturation transfer experiment (solid line). The ATP resonance is completely suppressed, and the PI signal is lower than in the baseline control experiment (dashed line).
Figure 2
Correlations with hepatocellular ATP production (fATP) with (A) hepatic insulin resistance (EGP suppression; all: r = 0.77, P = 0.002; type 2 diabetic subjects: r = 0.79, P = 0.01; controls: r = 0.54, P = 0.17), (B) waist circumference (all: r = −0.78, P = 0.001; type 2 diabetic subjects: r = 0.57, P = 0.11; controls: r = 0.68, P = 0.064), (C) HCL contents (all: r = −0.51, P = 0.038; type 2 diabetic subjects r = −0.20, P = 0.61; controls: r = 0.62, P = 0.10), (D) hepatic concentrations of PI (all: r = 0.77, P = 0.0003; type 2 diabetic subjects: r = 0.57, P = 0.11; controls: r = 0.68, P = 0.064) across all participants (type 2 diabetic subjects: ●, controls: △).
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References
- Angulo P. Nonalcoholic fatty liver disease. N Engl J Med 2002;346:1221–1231 - PubMed
- Roden M. Mechanisms of Disease: hepatic steatosis in type 2 diabetes—pathogenesis and clinical relevance. Nat Clin Pract Endocrinol Metab 2006;2:335–348 - PubMed
- Bays H, Mandarino L, DeFronzo RA. Role of the adipocyte, free fatty acids, and ectopic fat in pathogenesis of type 2 diabetes mellitus: peroxisomal proliferator-activated receptor agonists provide a rational therapeutic approach. J Clin Endocrinol Metab 2004;89:463–478 - PubMed
- Loria P, Lonardo A, Targher G. Is liver fat detrimental to vessels? Intersections in the pathogenesis of NAFLD and atherosclerosis. Clin Sci (Lond) 2008;115:1–12 - PubMed
- Tilg H, Moschen A. Update on nonalcoholic fatty liver disease: genes involved in nonalcoholic fatty liver disease and associated inflammation. Curr Opin Clin Nutr Metab Care 2010;13:391–396 - PubMed
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