SEMINAR
UC Berkeley
Aging is characterized by a decline in healthspan, negatively affecting whole-body energy metabolism and ultimately increasing the organism's susceptibility to cancer, metabolic and neurodegenerative diseases. Because the aging process is strongly affected by environmental factors in invertebrate models where canonical sensory perception can acutely influence normal aging, we explored whether neural circuits that detect sensory stimuli were implicated in transducing nutrient availability and metabolic status to facilitate glucose homeostatic processes. We report the discovery of a novel neuroendocrine circuit that regulates metabolic health and longevity conserved from C.elegans nematodes to mice. Deletion of transient receptor potential cation channel subfamily V member 1 (TRPV1) pain receptors contained in sensory neurons originating from the Dorsal Root Ganglia extends mouse longevity by improving metabolic flexibility through ameliorated insulin secretion with age. This discovery provides evidence that upon aging, pain-sensitive sensory neurons release excessive amount of neuropeptidic signals that largely contribute to the onset of metabolic decline. These findings open new therapeutic possibilities to improve longevity, metabolic health and a novel pharmacological approach to treat insulin secretory defects associated with type 2 diabetes.
Host: Prof. Lluis Fajas