QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Purchase Article View Shopping Cart Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Brady, L. J. Articles by Hoppel, C. L. Search for Related Content PubMed PubMed Citation Articles by Brady, L. J. Articles by Hoppel, C. L.

Effect of Diet and Starvation on Hepatic Mitochondrial Function in the Rat¹

Veterans Administration Medical Center and Departments of Pharmacology and Medicine, Case Western Reserve University, Cleveland, OH 44106

The purpose of the present study was to assess the effect of diet and starvation on mitochondrial function. Diet did not affect hepatic mitochondrial oxidation of lipid or nonlipid substrates when expressed as nanogram atoms of oxygen consumed per minute per milligram mitochondrial protein. Furthermore, diet did not affect mitochondrial palmitoylcarnitine utilization rate, mitochondrial ketoacid production, or mitochondrial carnitine palmitoyltransferase specific activity. When the data for palmitoylcarnitine utilization were expressed per gram liver, the rates were significantly lower in rats fed the high fat diet of Schemmel et al. (J. Nutr. 110: 1041–1048, 1970). DNA content (milligrams/gram) indicated that cell size rather than cell number contributed to greater total liver weight in rats fed the Schemmel high fat diet. In both stock diet-fed controls and rats fed the Schemmel high fat diet, mitochondrial protein per gram liver decreased with duration of starvation. Mitochondrial carnitine palmitoyltransferase was unchanged by diet or starvation. Thus, neither diet nor diet followed by starvation altered hepatic mitochondrial capacity to oxidize lipid substrates.

KEY WORDS: • mitochondria • high fat diet • fatty acid oxidation • ketoacid production • carnitine palmitoyltransferase

¹ Supported by National Institutes of Health grants AM 15804 and AM 07329 and by the Veterans Administration.

² Dr. Brady was a fellow of the American Heart Association, Northeast Ohio Chapter, while this work was carried out.

Manuscript received 7 April 1983.