In a new study, researchers found that liver metabolism is disrupted in people with obesity-related type 2 diabetes, which contributes to high blood sugar and muscle loss—also known as skeletal muscle atrophy.
The research was conducted by a team at Monash University.
Using human trials as well as mouse models, the team found the liver metabolism of the amino acid alanine is altered in people with obesity-related type 2 diabetes.
By selectively silencing enzymes that break down alanine in liver cells, high blood sugar and muscle loss can be reversed by the restoration of skeletal muscle protein synthesis, a critical determinant of muscle size and strength.
The researchers found the altered liver metabolism directly affects muscle size and strength.
The mechanism behind this is driven by elevated levels of the hormones cortisol and glucagon which enhance the cycling of amino acids between liver and skeletal muscle, causing muscles to become smaller and weaker.
Along with metabolic dysfunction and related complications, an often overlooked co-morbidity of obesity is skeletal muscle atrophy, which causes frailty, and is related to reduced life-quality and death.
The team says that the aging-related diseases of skeletal muscle loss and type 2 diabetes are very prevalent.
The new findings demonstrate that the liver is a critical control point for muscle protein metabolism; a discovery that is quite surprising.
These findings highlight the need to examine the role of skeletal muscle atrophy in type 2 diabetes more closely in human clinical populations.
The study solidifies the long-known metabolic biochemistry staple, the glucose-alanine cycle, as a fundamental part of the metabolism in health and disease.
The study is published in Nature Metabolism. One author of the study is Dr. Adam Rose.
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