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Mitochondrial function in skeletal muscle is normal and unrelated to insulin action in young men born with low birth weight.
J Clin Endocrinol Metab. 2008 Oct; 93(10):3885-92.JC

Abstract

OBJECTIVE

Low birth weight (LBW) is an independent risk factor of insulin resistance and type 2 diabetes. Recent studies suggest that mitochondrial dysfunction and impaired expression of genes involved in oxidative phosphorylation (OXPHOS) may play a key role in the pathogenesis of insulin resistance in aging and type 2 diabetes. The aim of this study was to determine whether LBW in humans is associated with mitochondrial dysfunction in skeletal muscle.

METHODS

Mitochondrial capacity for ATP synthesis was assessed by (31)phosphorus magnetic resonance spectroscopy in forearm and leg muscles in 20 young, lean men with LBW and 26 matched controls. On a separate day, a hyperinsulinemic euglycemic clamp with excision of muscle biopsies and dual-energy x-ray absorptiometry scanning was performed. Muscle gene expression of selected OXPHOS genes was determined by quantitative real-time PCR.

RESULTS

The LBW subjects displayed a variety of metabolic and prediabetic abnormalities, including elevated fasting blood glucose and plasma insulin levels, reduced insulin-stimulated glycolytic flux, and hepatic insulin resistance. Nevertheless, in vivo mitochondrial function was normal in LBW subjects, as was the expression of OXPHOS genes.

CONCLUSIONS

These data support and expand previous findings of abnormal glucose metabolism in young men with LBW. In addition, we found that the young, healthy men with LBW exhibited hepatic insulin resistance. However, the study does not support the hypothesis that muscle mitochondrial dysfunction per se is the underlying key metabolic defect that explains or precedes whole body insulin resistance in LBW subjects at risk for developing type 2 diabetes.

Authors+Show Affiliations

Steno Diabetes Center, Niels Steensens Vej 1, 2820 Gentofte, Denmark. chbe@steno.dkNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Controlled Clinical Trial
Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

18628517

Citation

Brøns, Charlotte, et al. "Mitochondrial Function in Skeletal Muscle Is Normal and Unrelated to Insulin Action in Young Men Born With Low Birth Weight." The Journal of Clinical Endocrinology and Metabolism, vol. 93, no. 10, 2008, pp. 3885-92.
Brøns C, Jensen CB, Storgaard H, et al. Mitochondrial function in skeletal muscle is normal and unrelated to insulin action in young men born with low birth weight. J Clin Endocrinol Metab. 2008;93(10):3885-92.
Brøns, C., Jensen, C. B., Storgaard, H., Alibegovic, A., Jacobsen, S., Nilsson, E., Astrup, A., Quistorff, B., & Vaag, A. (2008). Mitochondrial function in skeletal muscle is normal and unrelated to insulin action in young men born with low birth weight. The Journal of Clinical Endocrinology and Metabolism, 93(10), 3885-92. https://doi.org/10.1210/jc.2008-0630
Brøns C, et al. Mitochondrial Function in Skeletal Muscle Is Normal and Unrelated to Insulin Action in Young Men Born With Low Birth Weight. J Clin Endocrinol Metab. 2008;93(10):3885-92. PubMed PMID: 18628517.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Mitochondrial function in skeletal muscle is normal and unrelated to insulin action in young men born with low birth weight. AU - Brøns,Charlotte, AU - Jensen,Christine B, AU - Storgaard,Heidi, AU - Alibegovic,Amra, AU - Jacobsen,Stine, AU - Nilsson,Emma, AU - Astrup,Arne, AU - Quistorff,Bjørn, AU - Vaag,Allan, Y1 - 2008/07/15/ PY - 2008/7/17/pubmed PY - 2008/12/17/medline PY - 2008/7/17/entrez SP - 3885 EP - 92 JF - The Journal of clinical endocrinology and metabolism JO - J Clin Endocrinol Metab VL - 93 IS - 10 N2 - OBJECTIVE: Low birth weight (LBW) is an independent risk factor of insulin resistance and type 2 diabetes. Recent studies suggest that mitochondrial dysfunction and impaired expression of genes involved in oxidative phosphorylation (OXPHOS) may play a key role in the pathogenesis of insulin resistance in aging and type 2 diabetes. The aim of this study was to determine whether LBW in humans is associated with mitochondrial dysfunction in skeletal muscle. METHODS: Mitochondrial capacity for ATP synthesis was assessed by (31)phosphorus magnetic resonance spectroscopy in forearm and leg muscles in 20 young, lean men with LBW and 26 matched controls. On a separate day, a hyperinsulinemic euglycemic clamp with excision of muscle biopsies and dual-energy x-ray absorptiometry scanning was performed. Muscle gene expression of selected OXPHOS genes was determined by quantitative real-time PCR. RESULTS: The LBW subjects displayed a variety of metabolic and prediabetic abnormalities, including elevated fasting blood glucose and plasma insulin levels, reduced insulin-stimulated glycolytic flux, and hepatic insulin resistance. Nevertheless, in vivo mitochondrial function was normal in LBW subjects, as was the expression of OXPHOS genes. CONCLUSIONS: These data support and expand previous findings of abnormal glucose metabolism in young men with LBW. In addition, we found that the young, healthy men with LBW exhibited hepatic insulin resistance. However, the study does not support the hypothesis that muscle mitochondrial dysfunction per se is the underlying key metabolic defect that explains or precedes whole body insulin resistance in LBW subjects at risk for developing type 2 diabetes. SN - 0021-972X UR - https://www.unboundmedicine.com/medline/citation/18628517/Mitochondrial_function_in_skeletal_muscle_is_normal_and_unrelated_to_insulin_action_in_young_men_born_with_low_birth_weight_ L2 - https://academic.oup.com/jcem/article-lookup/doi/10.1210/jc.2008-0630 DB - PRIME DP - Unbound Medicine ER -