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Am J Physiol Endocrinol Metab 291: E860-E866, 2006. First published May 16, 2006; doi:10.1152/ajpendo.00366.2005
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TRANSLATIONAL PHYSIOLOGY

Parenteral and enteral metabolism of anaplerotic triheptanoin in normal rats

Renée P. Kinman,1,2 Takhar Kasumov,2 Kathryn A. Jobbins,2 Katherine R. Thomas,2 Jillian E. Adams,2 Lisa N. Brunengraber,2 Gerd Kutz,3 Wolf-Ulrich Brewer,4 Charles R. Roe,5 and Henri Brunengraber2

Departments of 1Pediatrics and 2Nutrition, Case Western Reserve University, Cleveland, Ohio; 3Fachhochschule Lippe und Hoxter University of Applied Sciences, Detmold, Germany; 4Sasol GmbH, Witten, Germany; and 5Institute of Metabolic Disease, Baylor University Medical Center, Dallas, Texas

Submitted 5 August 2005 ; accepted in final form 8 May 2006

A new chronic treatment for inherited disorders of long-chain fatty acid oxidation involves administering up to one-third of dietary calories as triheptanoin, a medium-odd-chain triglyceride (Roe CR, Sweetman L, Roe DS, David F, and Brunengraber H. J Clin Invest 110: 259–269, 2002). Heptanoate and C5-ketone bodies derived from its partial oxidation in liver are precursors of anaplerotic propionyl-CoA in peripheral tissues. It was hypothesized that increasing anaplerosis in peripheral tissues would boost energy production. In the present study, we tested the potential of a triheptanoin emulsion as an intravenous nutrient. Normal rats were infused with triheptanoin intravenously or intraduodenally at up to 40% of caloric requirement. The blood concentration ratio (heptanoate/C5-ketone bodies) was high with intravenous and low with intraduodenal triheptanoin infusion. During intravenous infusion of triheptanoin, lipolysis was stimulated but appeared compensated by fatty acid reesterification. During intraduodenal infusion of triheptanoin, lipolysis was not stimulated. Our data support the hypothesis that intravenous triheptanoin could be used to treat decompensated patients with long-chain fatty acid oxidation disorders.

heptanoate; C5-ketone bodies; fatty acid oxidation disorders; anaplerosis


Address for reprint requests and other correspondence: H. Brunengraber, Dept. of Nutrition, Case Western Reserve University, Euclid Ave., Cleveland, OH 44106-4954 (e-mail: hxb8{at}case.edu)




This article has been cited by other articles:


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C. R. Roe, B-Z Yang, H. Brunengraber, D. S. Roe, M. Wallace, and B. K. Garritson
Carnitine palmitoyltransferase II deficiency: Successful anaplerotic diet therapy
Neurology, July 22, 2008; 71(4): 260 - 264.
[Abstract] [Full Text] [PDF]


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