Raboel 2009 J Clin Endocrinol Metabol

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RabΓΈl R, HΓΈjberg PM, Almdal T, Boushel R, Haugaard SB, Madsbad S, Dela F (2009) Effect of hyperglycemia on mitochondrial respiration in type 2 diabetes. J Clin Endocrinol Metabol 94:1372-78.

Β» PMID: 19141588 ; Open Access

Raboel R, Hoejberg 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 Β± 2.5 yr (mean Β± SE); body mass index, 30.2 Β± 1.1 kg/m2 ] in poor glycemic control were treated with insulin aspart and NPH insulin for a median period of 46 d (range, 31–59). Mitochondrial respiration and citrate synthase activity (a marker of mitochondrial content) were measured before and after treatment. Eleven healthy subjects (age, 53.3 Β± 2.7 yr; body mass index, 30.6 Β± 1.1 kg/m2) were included as controls.

Results: Hemoglobin A1c (9.1 Β± 0.5 to 7.5 Β± 0.3%; P < 0.001) and fasting plasma glucose (12.7 Β± 1.1 to 6.5 Β± 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.

β€’ O2k-Network Lab: DK Copenhagen Dela F, SE Stockholm Boushel RC, CA Vancouver Boushel RC, DK Copenhagen Larsen S

Cited by

Gnaiger 2020 BEC MitoPathways
Gnaiger E (2020) Mitochondrial pathways and respiratory control. An introduction to OXPHOS analysis. 5th ed. Bioenerg Commun 2020.2. https://doi.org/10.26124/bec:2020-0002

Labels: MiParea: Respiration, Exercise physiology;nutrition;life style, mt-Medicine, Patients  Pathology: Diabetes 

Organism: Human  Tissue;cell: Skeletal muscle  Preparation: Permeabilized tissue  Enzyme: Complex I  Regulation: ADP, Ion;substrate transport, Substrate  Coupling state: LEAK, OXPHOS  Pathway: N, NS  HRR: Oxygraph-2k 

BEC 2020.2 

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