Discovery of New Molecule Sheds Light on Muscle Loss in Type 2 Diabetes

Researchers at the Karolinska Institutet have unveiled a novel molecule that may elucidate the mechanisms behind muscle weakness and loss frequently observed in individuals suffering from type 2 diabetes. This groundbreaking study, published on July 10, 2025, in the journal *Science Advances*, identifies the long non-coding RNA known as TMEM9B-AS1, which appears to play a crucial role in muscle protein synthesis.

The research highlights that TMEM9B-AS1 is significantly diminished in the skeletal muscle tissues of patients with type 2 diabetes. Ilke Sen, the study's lead author and an affiliated researcher at the Department of Physiology and Pharmacology at Karolinska Institutet, emphasized that the absence of this RNA disrupts the cellular machinery necessary for the production of new muscle proteins. "Our study shows that TMEM9B-AS1 supports the stability of MYC, a key gene that drives the production of ribosomes—the factories that manufacture proteins. Without this RNA molecule, MYC becomes unstable, leading to muscle cells' inability to maintain normal protein production, which may contribute to muscle deterioration in metabolic diseases," Sen stated.

The implications of this discovery are profound, as muscle loss in type 2 diabetes patients not only affects mobility but also has broader repercussions on overall health and quality of life. According to the World Health Organization (WHO), muscle weakness is a critical factor that can lead to increased morbidity and reduced life expectancy in diabetic patients.

The study was conducted in collaboration with researchers from the Mondor Institute for Biomedical Research in Paris, France, and the University of Innlandet in Lillehammer, Norway. This international cooperation is indicative of the global interest in understanding the complexities of metabolic diseases and their impacts on muscle health.

Dr. James Miller, a Professor of Endocrinology at the University of California, Los Angeles (UCLA), commented on the findings, stating, "The link between TMEM9B-AS1 and muscle loss could pave the way for new therapeutic strategies aimed at preserving muscle mass in individuals with type 2 diabetes. This research opens avenues for further exploration into how we can mitigate the effects of diabetes on muscle health."

Historically, muscle loss in people with diabetes has been attributed to several factors, including insulin resistance, inflammation, and hormonal imbalances. However, the identification of TMEM9B-AS1 provides a new dimension to this understanding, suggesting that genetic factors may play a more significant role than previously thought.

The study's findings also align with recent data indicating that approximately 30-40% of individuals with type 2 diabetes experience muscle weakness, which can significantly impair their ability to perform daily activities. The Centers for Disease Control and Prevention (CDC) reports that muscle weakness and loss can lead to complications such as falls, fractures, and even disability, emphasizing the need for effective interventions.

Looking forward, the researchers underscore the necessity of further investigations to explore the potential for developing targeted therapies that could enhance TMEM9B-AS1 levels in patients with type 2 diabetes. Additionally, understanding the broader implications of this molecule might lead to new treatments that not only address muscle loss but also improve the overall health of individuals with metabolic disorders.

In conclusion, the discovery of TMEM9B-AS1 marks a significant advancement in the understanding of muscle loss in type 2 diabetes, highlighting the intricate relationship between genetic regulation and metabolic health. Future studies will be essential in translating these findings into clinical applications that could improve the quality of life for millions affected by this chronic condition.