Journal of Lipid Research, Vol. 7, 56-61, January 1966
Copyright © 1966 by Lipid Research, Inc.

Factors influencing the utilization of ketone bodies by mouse adipose tissue

Richard W. Hanson and Zigmund Z. Ziporin

U. S. Army Medical Research and Nutrition Laboratory, Fitzsimons General Hospital, Denver, Colorado

Factors influencing the utilization of ketone bodies by mouse adipose tissue in vitro were studied. Epididymal fat pads can oxidize dl--hydroxybutyrate-3-¹⁴C and acetoacetate-3-¹⁴C to ¹⁴CO₂ as well as convert these compounds to fatty acid-¹⁴C. An increased output of ¹⁴CO₂ from -hydroxybutyrate-3-¹⁴C was noted in response to glucose plus insulin, succinate, oxaloacetate, l-asparate, and l-malate. Fatty acid synthesis from -hydroxybutyrate was enhanced by glucose plus insulin, l-aspartate, l-malate, oxaloacetate, and citrate.

Nicotinamide stimulated the oxidation of -hydroxybutyrate but not of acetoacetate to CO₂, and did not affect fatty acid synthesis from either ketone body. Nicotinamide increased NAD⁺ and NADP⁺ levels in epididymal fat pads without affecting the concentration of NADH and NADPH. "Superlipogenesis" caused by fasting the mice for 48 hr and re-feeding them for 24 hr sharply enhanced CO₂ output and lipogenesis from -hydroxybutyrate. The activities of glucose-6-phosphate dehydrogenase, 6-phosphogluconic dehydrogenase, NADP-malic dehydrogenase, and citrate cleavage enzyme from mouse adipose tissue were increased during "superlipogenesis." Free fatty acid release by epididymal fat pads in vitro was slightly increased by -hydroxybutyrate. The relationship of ketone body metabolism and lipogenesis in adipose tissue is discussed.

Supplementary key words adipose tissue • ketone bodies • metabolism • oxidation • conversion to fatty acid • lipogenesis • enzymes • NAD • NADP • nucleotide coenzymes • nicotinamide • free fatty acid release • mouse

Submitted on May 13, 1965
Accepted on July 16, 1965

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