Raboel 2009 J Clin Endocrinol Metabol: Difference between revisions
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|enzymes=Complex I | |enzymes=Complex I | ||
|diseases=Diabetes | |diseases=Diabetes | ||
|topics=ADP, Ion | |topics=ADP, Ion;substrate transport, Substrate | ||
|instruments=Oxygraph-2k | |instruments=Oxygraph-2k | ||
|discipline=Biomedicine | |discipline=Biomedicine | ||
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Revision as of 15:28, 12 August 2013
Rabol R, Hojberg PMV, Almdal T, Boushel RC, Haugaard SB, Madsbad S, Dela F (2009) Effect of hyperglycemia on mitochondrial respiration in type 2 diabetes. J Clin Endocrinol Metabol 94: 1372-1378. |
Rabol R, Hojberg PMV, Almdal T, Boushel RC, Haugaard SB, Madsbad S, Dela F (2009) J Clin Endocrinol Metabol
Abstract: Aim: Skeletal muscle mitochondrial content is reduced in type 2 diabetes mellitus (T2DM). Whether hyperglycemia inhibits mitochondrial biogenesis and/or function is unknown. This study examined the effect of different levels of glycemia on skeletal muscle mitochondrial function in patients with T2DM.
Patients and Methods: Eleven patients with T2DM [9 males, 2 females; age, 52.8 ยฑ 2.5 yr (mean ยฑ SE); body mass index, 30.2 ยฑ 1.1 kg/m2 ] in poor glycemic control were treated with insulin aspart and NPH insulin for a median period of 46 d (range, 31โ59). Mitochondrial respiration and citrate synthase activity (a marker of mitochondrial content) were measured before and after treatment. Eleven healthy subjects (age, 53.3 ยฑ 2.7 yr; body mass index, 30.6 ยฑ 1.1 kg/m2) were included as controls.
Results: Hemoglobin A1c (9.1 ยฑ 0.5 to 7.5 ยฑ 0.3%; P < 0.001) and fasting plasma glucose (12.7 ยฑ 1.1 to 6.5 ยฑ 0.3 mmol/liter; P < 0.001) were reduced after treatment. Mitochondrial respiration per milligram muscle was lower in T2DM compared to controls [substrates for complex I, 24% lower (P < 0.05); substrates for complex I+II, 17% lower (P < 0.05)]. Mitochondrial respiration and citrate synthase activity did not differ before and after improvements in glycemic control, but mitochondrial respiration correlated with fasting plasma glucose before (r2 = 0.53; P < 0.05) but not after treatment [r2 = 0.0024; not significant (NS)]. Mitochondrial respiration normalized to mitochondrial content did not differ between control subjects and patients with T2DM.
Discussion: Mitochondrial respiration and content was not improved after significant improvements in glycemic control. However, severe hyperglycemia inhibited respiration reversibly, but moderate hyperglycemia and mitochondrial function were not correlated.
โข O2k-Network Lab: DK_Copenhagen_Dela F, DK_Copenhagen_Boushel RC
Labels: MiParea: Respiration, Exercise physiology;nutrition;life style, mt-Medicine
Pathology: Diabetes
Organism: Human Tissue;cell: Skeletal muscle Preparation: Intact Organism"Intact Organism" is not in the list (Intact organism, Intact organ, Permeabilized cells, Permeabilized tissue, Homogenate, Isolated mitochondria, SMP, Chloroplasts, Enzyme, Oxidase;biochemical oxidation, ...) of allowed values for the "Preparation" property., Permeabilized tissue Enzyme: Complex I Regulation: ADP, Ion;substrate transport, Substrate
HRR: Oxygraph-2k