Muscle mitochondrial ATP synthesis and glucose transport/phosphorylation in type 2 diabetes
2007

Muscle Mitochondrial ATP Synthesis and Glucose Transport in Type 2 Diabetes

Sample size: 31 publication Evidence: moderate

Author Information

Author(s): Szendroedi Julia, Schmid Albrecht I, Chmelik Marek, Toth Christian, Brehm Attila, Krssak Martin, Nowotny Peter, Wolzt Michael, Waldhausl Werner, Roden Michael

Primary Institution: Department of Internal Medicine 3, University of Vienna, Vienna, Austria

Hypothesis

Alterations in insulin action and mitochondrial function should be present even in nonobese patients with well-controlled type 2 diabetes mellitus (T2DM).

Conclusion

Patients with well-controlled T2DM feature slightly lower flux through muscle ATP synthesis, which occurs independently of glucose transport/phosphorylation and lipid deposition.

Supporting Evidence

  • Insulin sensitivity was lower in patients with T2DM compared to controls.
  • Muscle lipid contents were comparable across groups.
  • Hyperinsulinemia increased glucose-6-phosphate levels by 50% in all groups.
  • Patients with diabetes had 27% lower fasting ATP synthetic flux compared to younger controls.
  • Insulin stimulation increased ATP synthetic flux only in controls.

Takeaway

Even people with well-managed type 2 diabetes have some problems with how their muscles make energy, which isn't just about how they handle sugar or fat.

Methodology

The study used magnetic resonance spectroscopy to measure ATP synthesis and glucose transport in patients with T2DM and control groups.

Potential Biases

Potential bias due to the small sample size affecting the detection of associations.

Limitations

The study had a small sample size and did not measure muscle glycogen synthesis due to time restrictions.

Participant Demographics

Participants included nonobese patients with well-controlled T2DM and two control groups matched for age and body mass.

Statistical Information

P-Value

0.031

Confidence Interval

95% CI 39%–99%

Statistical Significance

p<0.05

Digital Object Identifier (DOI)

10.1371/journal.pmed.0040154

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