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January 21, 2015Molecular and Cellular BiologyOpen Access

Role of Phosphoinositide 3-OH Kinase p110β in Skeletal Myogenesis

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Population

C2C12 cells, primary human myoblasts, and mice with conditional deletion of p110β in skeletal muscle

Comparison

Pharmacological inhibition, conditional… vs Control littermates (for mice) or control cells

Design

Preclinical

Key result

Conditional deletion of p110β in skeletal muscle impaired whole-body glucose tolerance in old mice without affecting long-term muscle size or strength, while its inhibition delayed myogenesis.

Authors

RMRonald W. MathenyMRMelissa A. RiddleLLLuis A. Leandry

Discussion

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Member takes

Overview

May caution against p110β inhibition in aging; hypothesis-generating for its metabolic role, requiring human validation.

Structured PICO

P
Population
C2C12 cells, primary human myoblasts, and mice with conditional deletion of p110β in skeletal muscle (p110β-mKO mice)
I
Intervention
Pharmacological inhibition, conditional deletion, or overexpression of PI3K p110β
C
Comparator
Control littermates (for mice) or control cells
O
Outcome
Myoblast differentiation, muscle mass, muscle strength, and whole-body glucose tolerancesurrogate

PI3K p110β plays a role in skeletal myogenesis, and its long-term reduction in skeletal muscle impairs whole-body glucose tolerance in mice.

Cite This Study

Matheny et al. (2015) studied Skeletal myogenesis and metabolism. p110β deletion or inhibition vs. Control littermates or uninhibited cells was evaluated on Myoblast differentiation, muscle mass, strength, and glucose tolerance. Conditional deletion of p110β in skeletal muscle impaired whole-body glucose tolerance in old mice without affecting long-term muscle size or strength, while its inhibition delayed myogenesis.

synapsesocial.com/papers/6ab0c9c70e24c3269201ac28https://doi.org/10.1128/mcb.00550-14
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