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AMP‐activated protein kinase α2 is an essential signal in the regulation of insulin‐stimulated fatty acid uptake in control‐fed and high‐fat‐fed mice
AMP-activated protein kinase α2 is essential for controlling insulin-driven fat uptake in normal and high-fat diet mice
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Abstract
Low AMPKα2 activity in insulin-resistant mice increased basal fatty acid uptake by 147%.
- In control diet mice, low AMPKα2 activity increased basal fatty acid oxidation by 28% and prevented insulin-mediated changes.
- High-fat diet abolished insulin's typical effects on fatty acid uptake and oxidation in both wild-type and dominant negative mice.
- In high-fat diet-fed mice, low AMPKα2 activity elevated SIRT1 activity and reduced Protein Tyrosine Phosphatase 1B expression and Akt phosphorylation.
- High-fat diet increased adipose tissue levels of interleukin-6 and tumor necrosis factor α in wild-type mice, but not in dominant negative mice.
- Skeletal muscle levels of interleukin-15 were decreased in dominant negative mice under both diet conditions.
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