Muscle ATP defect in diabetes-prone offspring
Lean insulin-resistant offspring of type 2 diabetic parents showed blunted insulin-stimulated muscle ATP synthesis versus matched controls.
Source
Decreased insulin-stimulated ATP synthesis and phosphate transport in muscle of insulin-resistant offspring of type 2 diabetic parents
Study at a glance
- Design
- Other — Clamp + 31P MRS group comparison of IR offspring vs controls; no randomized intervention
- N
- N=14 · 7 IR offspring vs 7 controls, from the paper’s “What Did the Researchers Do and Find?” section in the stored full text
- Population
- Young lean sedentary adults with or without parental type 2 diabetes history
- Outcome
- Insulin-stimulated muscle ATP synthesis and phosphate transport (31P MRS)
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What they did
Healthy lean sedentary IR offspring with family diabetes history and matched controls underwent hyperinsulinemic-euglycemic clamps with 31P MRS of muscle ATP synthesis and phosphate transport.
What they found
Insulin raised muscle ATP flux ~90% in controls but only ~5% in IR offspring, supporting early mitochondrial dysfunction before overt diabetes.
The limits
What it doesn't show
Whether fixing ATP synthesis prevents diabetes, and findings may not generalize beyond young lean high-risk offspring.
Key terms
- Insulin resistance
- Reduced tissue response to insulin, a precursor state for type 2 diabetes.
- ATP synthesis
- Mitochondrial production of ATP measured here as muscle flux.
- Hyperinsulinemic-euglycemic clamp
- Gold-standard method holding glucose steady while infusing insulin.
- 31P MRS
- Magnetic resonance spectroscopy of phosphorus metabolites in vivo.
- IR offspring
- Insulin-resistant children/grandchildren of people with type 2 diabetes.
- IMCL
- Intramyocellular lipid content linked to mitochondrial and insulin phenotypes.
Flashcards
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Quiz yourself
IR offspring ATP response to insulin was about:
Common questions
Who were IR offspring?
Seven lean healthy young adults with multi-generation type 2 diabetes family history.
What was the key ATP finding?
Insulin stimulated ATP flux ~90% in controls vs ~5% in IR offspring.
Why is this clinically relevant?
Suggests mitochondrial ATP defects appear early in diabetes pathogenesis.
Was this an animal study?
No—human volunteers studied with clamps and MRS.
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