Metabolism & Basic Biology of Aging

Scientist looking at research and laboratory equipment

Research in our Metabolism & Basic Biology of Aging directive focuses on understanding cellular and molecular processes that contribute to age-related diseases.

Scientists in this directive investigate a variety of factors including dietary components, physical activity, immune responses, intestinal homeostasis, the microbiome, cellular dysfunction, and senescence, and the key metabolic and molecular processes by which those factors impact age-related health.

Examples of our work

Research Summary: Predicting the Onset of Mobility Loss and Impact of Physical Activity
Mobility declines with age, contributing to loss of independence and quality of life in older adults; but the biological drivers of this loss of function are largely unknown. Work in our Metabolism & Basic Biology of Aging directive explored the links between mobility declines in older adults and biomarkers of cellular senescence (a stress response that can contribute to a variety of age-related diseases), as part of a large clinical trial, conducted in part at the HNRCA. Our scientists found that several factors secreted by senescent cells were predictive of mobility loss, and that high levels of physical activity decreased both biomarkers of senescence and risk of disability. These results provide evidence of a link between senescence and mobility decline in older adults and identify physical activity as a possible mitigating intervention.

Research Summary: Targeting an intestinal enzyme to help protect against obesity
Obesity remains a major public health challenge and understanding its underlying metabolic mechanisms is important to help address it. Work in our Metabolism & Basic Biology of Aging directive found that the enzyme acyl CoA synthetase 5 (ACSL5) produced in the small intestine, is involved in the development of diet-induced obesity. When we fed mice lacking the intestinal enzyme ACSL5 a diet that typically causes obesity, the mice did not become obese. They ate less of the diet because they had increased blood levels of the satiation hormones, glucagon-like peptide 1 and peptide yy, which are produced in the intestine. These findings suggest that targeting intestinal ACSL5 expression through dietary strategies may help protect against the development of obesity.

Research Team