Adipose tissue is at the nexus of processes involved in healthspan and metabolic dysfunction. Progression of age-related fat tissue dysfunction follows different trajectories across different fat depots, with fat becoming redistributed from subcutaneous to intra-peritoneal depots and ultimately ectopic sites, such as liver, muscle, and bone marrow. This is associated with insulin resistance, hypertension, atherosclerosis, strokes, myocardial infarction, cancer, and cognitive dysfunction. ... Senescent cells in adipose tissue could have profound clinical consequences because of their pro-inflammatory secretory phenotype, the large amount of adipose tissue in humans, and its central metabolic role.
The loss of skeletal muscle is one of the most dramatic changes in the human body consequent to advancing age and is referred to as sarcopenia. It is a primary cause of age-related changes in muscle performance, functional status and metabolic homeostasis. In an effort to counter sarcopenia and its consequences, we have studied strategies to inhibit the muscle-enriched TGF-β superfamily member, myostatin. The purpose of this seminar is to demonstrate how antibody-directed approaches to myostatin have not only increased muscle mass in mouse models of aging and disease, but improved physical function and whole-body metabolism. Ultimately, strategies to disrupt myostatin may provide a means to extend healthspan.
A number of researchers have been working on ways to manipulate muscle growth through myostatin-connected mechanisms. For example:
The researchers tried to use one protein called follistatin to impede the action of another, myostatin, that's known to inhibit muscle growth. They injected the gene for follistatin into the right legs of six healthy monkeys and after eight weeks, their right legs had grown and were larger than their left legs. "We created a stronger muscle," said Brian Kaspar, the principal investigator for Nationwide's research institute. "We also showed that the muscle generated more force."