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Fritsch 2015 Am J Clin Nutr

From Bioblast
Publications in the MiPMap
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 (2015) Time course of postprandial hepatic phosphorus metabolites in lean, obese, and type 2 diabetes patients. Am J Clin Nutr 102:1051-8.

» PMID: 26423389

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 (2015) Am J Clin Nutr

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. Keywords: Hepatic steatosis, Mitochondrial function, Mixed-meal test, Phosphorus magnetic resonance spectroscopy, Type 2 diabetes

O2k-Network Lab: DE Duesseldorf Roden M


Labels: MiParea: Respiration, Exercise physiology;nutrition;life style, Patients  Pathology: Diabetes, Obesity 

Organism: Human  Tissue;cell: Skeletal muscle 


Coupling state: OXPHOS, ET  Pathway: N, NS  HRR: Oxygraph-2k 

2016-04