| Literature DB >> 6631531 |
Abstract
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.Entities:
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Year: 1983 PMID: 6631531 DOI: 10.1093/jn/113.11.2129
Source DB: PubMed Journal: J Nutr ISSN: 0022-3166 Impact factor: 4.798