# Efficacy of Human Recombinant Growth Hormone in Females of a Non-Obese Hyperglycemic Mouse Model after Birth with Low Birth Weight

## TL;DR

This study shows that growth hormone improves insulin resistance in female mice born with low birth weight by increasing type 1 muscle fibers and enhancing liver mitochondrial function.

## Contribution

The study demonstrates a novel therapeutic effect of GH on insulin resistance in a non-obese hyperglycemic mouse model with low birth weight.

## Key findings

- GH treatment improved the insulin resistance index in the Ischemia-GH group compared to the Ischemia group.
- GH increased the percentage of type 1 muscle fibers and altered muscle fiber type.
- GH reduced oxidative stress and increased ATP production in the liver, indicating improved mitochondrial function.

## Abstract

We examined whether the administration of growth hormone (GH) improves insulin resistance in females of a non-obese hyperglycemic mouse model after birth with low birth weight (LBW), given that GH is known to increase muscle mass. The intrauterine Ischemia group underwent uterine artery occlusion for 15 min on day 16.5 of gestation. At 4 weeks of age, female mice in the Ischemia group were divided into the GH-treated (Ischemia-GH) and non-GH-treated (Ischemia) groups. At 8 weeks of age, the glucose metabolism, muscle pathology, and metabolome of liver were assessed. The insulin resistance index improved in the Ischemia-GH group compared with the Ischemia group (p = 0.034). The percentage of type 1 muscle fibers was higher in the Ischemia-GH group than the Ischemia group (p < 0.001); the muscle fiber type was altered by GH. In the liver, oxidative stress factors were reduced, and ATP production was increased in the Ischemia-GH group compared to the Ischemia group (p = 0.014), indicating the improved mitochondrial function of liver. GH administration is effective in improving insulin resistance by increasing the content of type 1 muscle fibers and improving mitochondrial function of liver in our non-obese hyperglycemic mouse model after birth with LBW.