Mitochondrial respiration is decreased in skeletal muscle of patients with type 2 diabetes
Open accessAbstract
We tested the hypothesis of a lower respiratory capacity per mitochondrion in skeletal muscle of type 2 diabetic patients compared with obese subjects. Muscle biopsies obtained from 10 obese type 2 diabetic and 8 obese nondiabetic male subjects were used for assessment of 3-hydroxy-Acyl-CoA-dehydrogenase (HAD) and citrate synthase activity, uncoupling protein (UCP)3 content, oxidative stress measured as 4-hydroxy-2-nonenal (HNE), fiber type distribution, and respiration in isolated mitochondria. Respiration was normalized to citrate synthase activity (mitochondrial content) in isolated mitochondria. Maximal ADP-stimulated respiration (state 3) with pyruvate plus malate and respiration through the electron transport chain (ETC) were reduced in type 2 diabetic patients, and the proportion of type 2X fibers were higher in type 2 diabetic patients compared with obese subjects (all P < 0.05). There were no differences in respiration with palmitoyl-l-carnitine plus malate, citrate synthase activity, HAD activity, UCP3 content, or oxidative stress measured as HNE between the groups. In the whole group, state 3 respiration with pyruvate plus malate and respiration through ETC were negatively associated with A1C, and the proportion of type 2X fibers correlated with markers of insulin resistance (P < 0.05). In conclusion, we provide evidence for a functional impairment in mitochondrial respiration and increased amount of type 2X fibers in muscle of type 2 diabetic patients. These alterations may contribute to the development of type 2 diabetes in humans with obesity.
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Maximal respiration is lower in isolated mitochondria from muscle of type 2 diabetics.
“Measurements on isolated mitochondria show that maximal respiration is lower in muscle from type 2 diabetics (8).”
The present results are in accordance with some but not all studies assessing mitochondrial function in insulin resistance and type 2 diabetes.
“These findings are in accordance with some (9,28) but not all (8,10) studies assessing mitochondrial function in insulin resistance and type 2 diabetes.”
Most earlier studies did not report aerobic fitness measurements.
“In addition, most of the earlier studies did not report aerobic fitness measurements (8,9,28), whereas one study did match the control and diabetic subjects for whole-body aerobic power (Vo2max) (10).”
Three studies have reported mitochondrial function ex vivo in a diabetic population with conflicting results.
“So far, three studies have reported mitochondrial function ex vivo in a diabetic population (13–15), with conflicting results.”
From Lower intrinsic ADP-stimulated mitochondrial respiration underlies in vivo mitochondrial dysfunction in muscle of male type 2 diabetic patients (2008) · cites this paper as [13]
Ex vivo studies on mitochondrial function in type 2 diabetic patients appear less conclusive, and in these studies in vivo mitochondrial function was not assessed.
“Ex vivo studies on mitochondrial function in type 2 diabetic patients appear less conclusive (13–15); however, in these studies, in vivo mitochondrial function was not assessed.”
From Lower intrinsic ADP-stimulated mitochondrial respiration underlies in vivo mitochondrial dysfunction in muscle of male type 2 diabetic patients (2008) · cites this paper as [13]
Other studies have shown no significant reductions in citrate synthase in obesity, T2DM, or nondiabetic subjects with a family history of T2DM.
“Other studies, however, have shown no significant reductions in citrate synthase in obesity (4, 5, 25), T2DM (26), or nondiabetic subjects with a family history of T2DM (16).”
Diabetes is characterised by reduced mitochondrial electron transport chain activity.
“Diabetes is also characterised by reduced mitochondrial electron transport chain activity,50 which results in energetic inefficiency.”
From Age-related and disease-related muscle loss: The effect of diabetes, obesity, and other diseases (2014) · cites this paper as [50]
Development of insulin resistance has been associated with a reduction in mitochondrial content and impaired mitochondrial respiratory function.
“the development of insulin resistance has been associated with a reduction in mitochondrial content and impaired mitochondrial respiratory function [14,15].”
From Exercise mitigates sleep-loss-induced changes in glucose tolerance, mitochondrial function, sarcoplasmic protein synthesis, and diurnal rhythms (2021) · cites this paper as [15]
Reductions in citrate synthase activity and mitochondrial respiratory function have been reported in type 2 diabetes patients compared with obese non-diabetics.
“reductions in citrate synthase activity (a surrogate marker for mitochondrial content [16]) and mitochondrial respiratory function has also been reported in T2D patients, compared to obese non-diabetics, suggesting a link between mitochondrial changes and the development of insulin resistance and T2D [14,15].”
From Exercise mitigates sleep-loss-induced changes in glucose tolerance, mitochondrial function, sarcoplasmic protein synthesis, and diurnal rhythms (2021) · cites this paper as [15]
Insulin resistance and reductions in glucose tolerance have previously been linked to altered mitochondrial characteristics.
“Insulin resistance and reductions in glucose tolerance have previously been linked to altered mitochondrial characteristics [14,15,54]”
From Exercise mitigates sleep-loss-induced changes in glucose tolerance, mitochondrial function, sarcoplasmic protein synthesis, and diurnal rhythms (2021) · cites this paper as [15]
Biochemical studies have reported decreased activity of a variety of mitochondrial enzymes in type 2 diabetic subjects, supporting an intrinsic functional mitochondrial defect.
“Biochemical studies have reported a decrease in the activity of a variety of mitochondrial enzymes [122], also supporting an intrinsic functional mitochondrial defect in type 2 diabetic subjects.”
From Pathogenesis of insulin resistance in skeletal muscle (2010) · cites this paper as [122]
There is no evidence that reduced mitochondrial function is a primary factor in the pathophysiology of type 2 diabetes.
“Although the existence of mitochondrial abnormalities in patients with type 2 diabetes has been extensively reported during the last decade (1–5), there is no evidence that a reduced mitochondrial function is a primary factor in the pathophysiology of this disease.”
From Prolonged fasting identifies skeletal muscle mitochondrial dysfunction as consequence rather than cause of human insulin resistance (2010) · cites this paper as [5]
It has generally been assumed that a reduction in muscle mitochondrial function will result in reductions in whole-body fat oxidative capacity.
“it has generally been assumed that a reduction in muscle mitochondrial function will result in reductions in whole-body fat oxidative capacity (3–5,42,43).”
From Prolonged fasting identifies skeletal muscle mitochondrial dysfunction as consequence rather than cause of human insulin resistance (2010) · cites this paper as [5]
A few studies have observed ex vivo reduced mitochondrial capacity compared with age- and BMI-matched controls and corrected for mitochondrial density.
“In contrast, a few studies have observed an ex vivo reduced mitochondrial capacity whencomparedwith age- and BMI-matched controls and corrected for mitochondrial density (6, 24).”
From Physical activity is the key determinant of skeletal muscle mitochondrial function in type 2 diabetes (2012) · cites this paper as [24]
Not matching groups or including subjects with a wide VO2max range can substantially affect the results.
“Lack of matching (24) or inclusion of subjects with a broad range in VO 2max values (6) may largely influence the outcome.”
From Physical activity is the key determinant of skeletal muscle mitochondrial function in type 2 diabetes (2012) · cites this paper as [24]
The mitochondrial capacity to oxidize acetyl-CoA coming from glucose is conserved in insulin-resistant subjects even if mitochondrial defects have been reported in those individuals.
“Furthermore, the mitochondrial capacity to oxidize acetyl-CoA coming from glucose is conserved in insulin-resistant subjects even if mitochondrial defects have been reported in those individuals ([3](#r3), [25](#r25), [36](#r36), [37](#r37), [40](#r40), [42](#r42), [43](#r43), [48](#r48), [59](#r59)).”
From Metabolic flexibility and insulin resistance (2008) · cites this paper as [36]
Multiple mitochondrial abnormalities are present in type 2 diabetic and insulin-resistant individuals.
“These data and the evidence indicating multiple mitochondrial abnormalities in type 2 diabetic and insulin-resistant individuals ([3](#r3), [25](#r25), [36](#r36), [37](#r37), [40](#r40), [42](#r42), [43](#r43), [48](#r48), [59](#r59)) led to the hypothesis that lower mitochondrial capacity is associated with reduced resting lipid oxidation and therefore increased muscle lipid accumulation.”
From Metabolic flexibility and insulin resistance (2008) · cites this paper as [36]
Maximal ADP-stimulated respiration (state 3, malate and pyruvate as substrates) is decreased in mitochondria isolated from obese subjects with DM compared with obesity alone, and these differences persist after normalization to citrate synthase activity.
“Mogensen et al. (119) observed decreases in maximal ADP-stimulated respiration (state 3, malate and pyruvate as substrates) in mitochondria isolated from obese subjects with DM as compared with obesity alone; these differences persisted even after normalization to citrate synthase activity.”
From The role of mitochondria in the pathogenesis of type 2 diabetes (2010) · cites this paper as [119]
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- Authors
- Mogensen, M., Sahlin, K., Fernström, M., Glintborg, D., Vind, B. F., Beck-Nielsen, H., & Højlund, K.
- Affiliations
- University of Southern Denmark (DK)
- Stockholm University College of Physical Education and Sports, GIH, Stockholm, Sweden
- Odense University Hospital (DK)
- Department of Endocrinology, Diabetes Research Centre, Odense University Hospital, Odense, Denmark
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 2007-06-01
- Volume
- 56
- Issue
- 6
- Pages
- 1592-1599
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- OpenAlex
- W2093366966
- Cited by
- 573
- References
- 52
- Citations by year
- 2026: 11 · 2025: 14 · 2024: 29 · 2023: 36 · 2022: 38 · 2021: 28 · 2020: 33 · 2019: 28 · 2018: 28 · 2017: 21 · 2016: 24 · 2015: 22 · 2014: 25 · 2013: 38 · 2012: 44
- FWCI
- 15.25
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Diabetes (publishedVersion)
- PubMed (publishedVersion)
- University of Southern Denmark Research Portal (University of Southern Denmark) (submittedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Keywords
- type 2 diabetes, skeletal muscle, mitochondrial respiration, electron transport chain, fiber type distribution, insulin resistance, obesity, oxidative stress, UCP3, citrate synthase, 3-hydroxyacyl-CoA dehydrogenase, HbA1c
- MeSH terms
- Biopsy, Blood Glucose, Citrate (si)-Synthase, Diabetes Mellitus, Type 2, Electron Transport, Humans, Male, Middle Aged, Mitochondria, Muscle, Obesity, Oxygen Consumption, Reference Values, 3-Hydroxyacyl CoA Dehydrogenases, Muscle, Skeletal
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