MPI AGE seminar: "Sweet Physiology: Hyperglycemia Tolerance and the Molecular Basis of Metabolic Resilience in Nectar Bats"

About Dr. Camacho's talk:

Across mammals, chronic overconsumption of dietary sugar triggers insulin resistance and glucotoxicity. Nectar-feeding bats defy that rule. Nightly, they drink 1.5x of their body weight in liquid sugar, and individuals reach blood glucose >750 mg/dL without disease. Remarkably, relative to a similarly sized mouse, nectar bats live 5x longer: the human equivalent of reaching 400 years old. I have found that in skeletal muscle, the AKT branch of the insulin pathway is selectively blunted while a parallel MAPK/ERK branch stays active, a rewiring linked to longevity elsewhere. Losing AKT's brake on fat oxidation lets muscle keep burning fat while ERK-driven glycolysis handles the glucose. As such, nectar bats appear to have decoupled glucose disposal from the pathway that converts chronic sugar intake into disease.

My research combines functional genomics, lipidomics, and in vivo physiology in nectar and fruit bats with bat-derived cell models to ask how bats achieve insulin-independent glucose disposal, and what the elevated endocannabinoid AEA, tied to feeding reward, neuroprotection, and energy metabolism, is doing there: protecting tissue from hyperglycemic damage, or simply reflecting the reward circuitry behind an extreme sugar habit. Translating these pathways into mice and humans could reveal mechanisms of metabolic resilience.

This event is aimed at a specialist audience.