Research

Role of Brown Fat in the Pathogenesis of Fatty Acid Oxidation Disorders

Mutations in the acyl-CoA dehydrogenase (ACAD) enzyme family are the most common cause of fatty acid oxidation disorder. This project investigates defective body temperature regulation in ACAD knockout mice. In mice and human neonates a unique organ called brown adipose tissue (BAT) converts the energy released by fatty acid oxidation into body heat. ACAD knockout mice are unable to maintain body temperature when placed into a chilled environment, suggestive of poor BAT function.

This research has shown that short-chain acyl-CoA dehydrogenase (SCAD) knockout mice have reduced levels of UCP1, the protein that mediates heat production in BAT. However, the animals have a normal thermogenic response to norepinephrine injections. Despite reduced UCP1, SCAD-/- BAT is able to function similar to wildtype BAT. It is hypothesized that intolerance to cold exposure in SCAD-deficient animals is related to an inability to shiver, rather than dystunctional BAT. This hypothesis will be tested in future studies.

Principal Investigator
Eric Goetzman, PhD

Last Update
August 14, 2010
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Last Update
August 14, 2010
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