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Sarcopenia and Type 2 Diabetes: A Bidirectional Relationship

Sarcopenia is characterised by age-related reductions in skeletal muscle strength, mass, and functional ability. Importantly, sarcopenia is a multifactorial condition associated with metabolic alterations, including poor glucose disposal, insulin resistance, decreased metabolic rate and, thus, type 2 diabetes (T2D). Developing non-pharmaceutical guidelines for the prevention and treatment of both diseases when they coexist is essential to optimise patient health and reduce premature mortality within this patient population. This review aimed to examine 1) the pathophysiological link between sarcopenia and T2D, and 2) lifestyle interventions with the potential to mitigate both sarcopenia and T2D.

Sarcopenia is characterised by age-related reductions in skeletal muscle strength, mass, and functional ability. Importantly, sarcopenia is a multifactorial condition associated with metabolic alterations, including poor glucose disposal, insulin resistance, decreased metabolic rate and, thus, type 2 diabetes (T2D). Developing non-pharmaceutical guidelines for the prevention and treatment of both diseases when they coexist is essential to optimise patient health and reduce premature mortality within this patient population.

This review aimed to examine 1) the pathophysiological link between sarcopenia and T2D, and 2) lifestyle interventions with the potential to mitigate both sarcopenia and T2D.

Key learnings:

Individuals with T2D have a 2–3x higher prevalence of sarcopenia. Both conditions are engaged in a bidirectional relationship through shared pathophysiological mechanisms, including reduced glycemic control, oxidative stress, increased adiposity, and micro- and macrovascular complications. For instance, age-related dysfunctions in skeletal muscle are associated with the heightened production of reactive oxygen species. This impairs insulin signalling and disrupts glucose uptake, thereby promoting hyperglycemia. In patients with established T2D, chronic hyperglycemia, excessive intramuscular advanced glycation product (AGE) production, and T2D-associated neuropathy disturb muscle energetics and promote the development of sarcopenia. Similarly, higher intermuscular adipose tissue content contributes to insulin resistance in older adults but may also trigger sarcopenia-associated muscle fibrosis. Interventions with demonstrated therapeutic efficacy for both conditions include resistance and aerobic exercise, as well as dietary protein, omega-3 fatty acid, creatine monohydrate, and vitamin D supplementation.

Reviewed by: S. Duarte

Authors: Beaudart C, Demonceau C, Reginster J et al.

Published in: Journal of Cachexia, Sarcopenia and Muscle 2023

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