Overview
- Washington University researchers report that peroxisomes, via the enzyme ACOX2, generate heat in brown fat as an alternative to mitochondrial UCP1.
- Loss of ACOX2 in mouse brown fat reduced local heat output, impaired cold tolerance, worsened insulin sensitivity, and increased weight gain on a high-fat diet.
- Overexpressing ACOX2 increased brown-fat thermogenesis, improved cold tolerance, enhanced insulin sensitivity, and limited diet-induced obesity.
- Cold exposure increased peroxisome numbers in brown fat, with a stronger rise in UCP1-deficient mice, and heat was verified using a fluorescent sensor and infrared imaging.
- The Sept. 17 Nature paper links ACOX2 activity to branched fatty acids found in diet and produced by gut microbes, outlines exploratory diet or drug strategies, and discloses a provisional patent by the authors.