# Akt1 deficiency does not affect fiber type composition or mitochondrial protein expression in skeletal muscle of male mice

## TL;DR

This study shows that Akt1 deficiency in male mice affects muscle size but not fiber type or mitochondrial function.

## Contribution

The study reveals that Akt1 regulates muscle fiber size but not fiber type or mitochondrial content in skeletal muscle.

## Key findings

- Akt1 deficiency reduces body and muscle weight and fiber cross-sectional area.
- Akt1 loss does not alter ACLY phosphorylation or mitochondrial protein expression.
- Muscle fiber type composition remains unchanged in Akt1 knockout mice.

## Abstract

Insulin‐like growth factor‐1‐induced activation of ATP citrate lyase (ACLY) improves muscle mitochondrial function through an Akt‐dependent mechanism. In this study, we examined whether Akt1 deficiency alters skeletal muscle fiber type and mitochondrial function by regulating ACLY‐dependent signaling in male Akt1 knockout (KO) mice (12–16 weeks old). Akt1 KO mice exhibited decreased body weight and muscle wet weight, with reduced cross‐sectional areas of slow‐ and fast‐type muscle fibers. Loss of Akt1 did not affect the phosphorylation status of ACLY in skeletal muscle. The skeletal muscle fiber type and expression of mitochondrial oxidative phosphorylation complex proteins were unchanged in Akt1 KO mice compared with the wild‐type control. These observations indicate that Akt1 is important for the regulation of skeletal muscle fiber size, whereas the regulation of muscle fiber type and muscle mitochondrial content occurs independently of Akt1 activity.