What question did this study set out to answer?

To determine whether isoform-specific impairment of Akt1 and Akt2 activation contributes to in vivo insulin resistance in major insulin-target tissues.

May 1, 2000DiabetesOpen Access

Divergent regulation of Akt1 and Akt2 isoforms in insulin target tissues of obese Zucker rats.

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Authors

YKY B KimBeth Israel Deaconess Medical Center OPOdile D. PeroniBeth Israel Deaconess Medical Center TFT F FrankeNew York University

Discussion

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Implication

Animal study demonstrates tissue-specific impairment of Akt1 and Akt2 activation in obese Zucker rats, suggesting distinct isoform-level mechanisms in insulin resistance.

Key Points

To determine whether isoform-specific impairment of Akt1 and Akt2 activation contributes to in vivo insulin resistance in major insulin-target tissues.
Administered acute intravenous insulin (10 U/kg for 2.5 min) to insulin-resistant obese Zucker rats and lean littermates.
Measured protein expression, phosphorylation, and kinase activity of Akt1 and Akt2, alongside PI3K activity and IRS-1 levels in muscle, liver, and adipose tissue.
Evaluated insulin-stimulated glucose transport and concentration-dependent signaling sensitivity in isolated adipocytes.
In obese rats versus lean controls, insulin-stimulated Akt1 activity decreased by 30% in muscle and 21% in adipose tissue but increased by 37% in liver; Akt2 activity decreased by 29% in muscle and 37% in liver but increased by 24% in adipose tissue.
Akt2 protein levels fell 56% in muscle and 35% in liver without changes in Akt1 expression, while PI3K activity associated with IRS-1 or phosphotyrosine declined by 67% to 86% across all tissues.
Maximal insulin-stimulated glucose transport decreased by 70% in obese adipocytes despite normal sensitivity and increased activation of Akt2.

Cite This Study

Kim et al. (2000) studied this question.

synapsesocial.com/papers/69dd54da80eea7d3f699b91c https://doi.org/10.2337/diabetes.49.5.847

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May 1, 2000DiabetesOpen Access

Divergent regulation of Akt1 and Akt2 isoforms in insulin target tissues of obese Zucker rats.

View Full Paper

Ask AI

Bookmark

Authors

YKY B KimBeth Israel Deaconess Medical Center OPOdile D. PeroniBeth Israel Deaconess Medical Center TFT F FrankeNew York University

Discussion

Member takes

Implication

Animal study demonstrates tissue-specific impairment of Akt1 and Akt2 activation in obese Zucker rats, suggesting distinct isoform-level mechanisms in insulin resistance.

Key Points

To determine whether isoform-specific impairment of Akt1 and Akt2 activation contributes to in vivo insulin resistance in major insulin-target tissues.
Administered acute intravenous insulin (10 U/kg for 2.5 min) to insulin-resistant obese Zucker rats and lean littermates.
Measured protein expression, phosphorylation, and kinase activity of Akt1 and Akt2, alongside PI3K activity and IRS-1 levels in muscle, liver, and adipose tissue.
Evaluated insulin-stimulated glucose transport and concentration-dependent signaling sensitivity in isolated adipocytes.
In obese rats versus lean controls, insulin-stimulated Akt1 activity decreased by 30% in muscle and 21% in adipose tissue but increased by 37% in liver; Akt2 activity decreased by 29% in muscle and 37% in liver but increased by 24% in adipose tissue.
Akt2 protein levels fell 56% in muscle and 35% in liver without changes in Akt1 expression, while PI3K activity associated with IRS-1 or phosphotyrosine declined by 67% to 86% across all tissues.
Maximal insulin-stimulated glucose transport decreased by 70% in obese adipocytes despite normal sensitivity and increased activation of Akt2.

Cite This Study

Kim et al. (2000) studied this question.

synapsesocial.com/papers/69dd54da80eea7d3f699b91c https://doi.org/10.2337/diabetes.49.5.847

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