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SHR Neuro Cancer Cardio Lipid Metab Microb

Fritsch, M; Koliaki, C; Livingstone, R; Phielix, E; Bierwagen, A; Meisinger, M; Jelenik, T; Strassburger, K; Zimmermann, S; Brockmann, K; Wolff, C; Hwang, JH; Szendroedi, J; Roden, M.
Time course of postprandial hepatic phosphorus metabolites in lean, obese, and type 2 diabetes patients.
Am J Clin Nutr. 2015; 102(5): 1051-1058. Doi: 10.3945/ajcn.115.107599 [OPEN ACCESS]
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Leading authors Med Uni Graz: Fritsch Maria
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Abstract:: Impaired energy metabolism is a possible mechanism that contributes to insulin resistance and ectopic fat storage. We examined whether meal ingestion differently affects hepatic phosphorus metabolites in insulin-sensitive and insulin-resistant humans. Young, lean, insulin-sensitive humans (CONs) [mean ± SD body mass index (BMI; in kg/m(2)): 23.2 ± 1.5]; insulin-resistant, glucose-tolerant, obese humans (OBEs) (BMI: 34.3 ± 1.7); and type 2 diabetes patients (T2Ds) (BMI: 32.0 ± 2.4) were studied (n = 10/group). T2Ds (61 ± 7 y old) were older (P < 0.001) than were OBEs (31 ± 7 y old) and CONs (28 ± 3 y old). We quantified hepatic γATP, inorganic phosphate (Pi), and the fat content [hepatocellular lipids (HCLs)] with the use of (31)P/(1)H magnetic resonance spectroscopy before and at 160 and 240 min after a high-caloric mixed meal. In a subset of volunteers, we measured the skeletal muscle oxidative capacity with the use of high-resolution respirometry. Whole-body insulin sensitivity (M value) was assessed with the use of hyperinsulinemic-euglycemic clamps. OBEs and T2Ds were similarly insulin resistant (M value: 3.5 ± 1.4 and 1.9 ± 2.5 mg · kg(-1) · min(-1), respectively; P = 0.9) and had 12-fold (P = 0.01) and 17-fold (P = 0.002) higher HCLs, respectively, than those of lean persons. Despite comparable fasting hepatic γATP concentrations, the maximum postprandial increase of γATP was 6-fold higher in OBEs (0.7 ± 0.2 mmol/L; P = 0.03) but only tended to be higher in T2Ds (0.6 ± 0.2 mmol/L; P = 0.09) than in CONs (0.1 ± 0.1 mmol/L). However, in the fasted state, muscle complex I activity was 53% lower (P = 0.01) in T2Ds but not in OBEs (P = 0.15) than in CONs. Young, obese, nondiabetic humans exhibit augmented postprandial hepatic energy metabolism, whereas elderly T2Ds have impaired fasting muscle energy metabolism. These findings support the concept of a differential and tissue-specific regulation of energy metabolism, which can occur independently of insulin resistance. This trial was registered at clinicaltrials.gov as NCT01229059. © 2015 American Society for Nutrition.
Find related publications in this database (using NLM MeSH Indexing): Adenosine Triphosphate - metabolism; Adult -; Aged -; Allostasis -; Biopsy -; Body Mass Index -; Calorimetry, Indirect -; Cohort Studies -; Diabetes Mellitus, Type 2 - blood; Diabetes Mellitus, Type 2 - complications; Diabetes Mellitus, Type 2 - metabolism; Diabetes Mellitus, Type 2 - pathology; Electron Transport Complex I - metabolism; Energy Metabolism -; Female -; Humans -; Insulin Resistance -; Liver - metabolism; Magnetic Resonance Spectroscopy -; Male -; Middle Aged -; Muscle, Skeletal - enzymology; Muscle, Skeletal - metabolism; Muscle, Skeletal - pathology; Obesity - blood; Obesity - complications; Obesity - metabolism; Obesity - pathology; Postprandial Period -; Quadriceps Muscle - enzymology; Quadriceps Muscle - metabolism; Quadriceps Muscle - pathology
Find related publications in this database (Keywords): hepatic steatosis; mitochondrial function; mixed-meal test; phosphorus magnetic resonance spectroscopy; type 2 diabetes