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Related Experiment Video

Updated: Jul 15, 2026

Phosphorus-31 Magnetic Resonance Spectroscopy: A Tool for Measuring In Vivo Mitochondrial Oxidative Phosphorylation Capacity in Human Skeletal Muscle

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Published on: January 19, 2017

Skeletal muscle mitochondrial dysfunction & diabetes.

Raghavakaimal Sreekumar¹, K Sreekumaran Nair

¹Endocrinology Division, Mayo Clinic, Rochester, MN 55905, USA. nair.sree@mayo.edu

The Indian Journal of Medical Research

|May 15, 2007

Summary

Skeletal muscle insulin resistance, a hallmark of type 2 diabetes, is linked to mitochondrial dysfunction. Insulin treatment improves mitochondrial gene expression in diabetics, indicating insulin

Area of Science:

Metabolic diseases
Mitochondrial function
Skeletal muscle physiology

Background:

Skeletal muscle insulin resistance is central to type 2 diabetes pathophysiology.
Muscle mitochondrial dysfunction is observed in type 2 diabetes, aging, and offspring of diabetic individuals.
The causal relationship between insulin resistance and mitochondrial dysfunction remains unclear.

Purpose of the Study:

To investigate the role of insulin in regulating skeletal muscle mitochondrial function and biogenesis.
To determine if insulin resistance precedes or follows mitochondrial dysfunction in type 2 diabetes.

Main Methods:

Gene array analysis of muscle biopsy samples from type 2 diabetic patients and controls.
Insulin infusion studies to assess mitochondrial gene expression and ATP production.

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Comparison of mitochondrial ATP production in response to varying insulin levels.

Main Results:

Altered OXPHOS gene expression in type 2 diabetes normalizes with insulin treatment.
Insulin infusion increases muscle mitochondrial gene transcripts and ATP production.
Type 2 diabetic patients show impaired mitochondrial ATP production response to insulin compared to controls.

Conclusions:

Insulin is a key regulator of skeletal muscle mitochondrial biogenesis.
Insulin resistance in type 2 diabetes is associated with impaired mitochondrial response to insulin.
Reduced substrate utilization may contribute to mitochondrial dysfunction in diabetic individuals.