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M J Weidemann

Publications and source records attributed to M J Weidemann.

78 records · Page 5Linked to original sources
PubMed1966

Oxidative phosphorylation accompanying oxidation of short-chain fatty acids by rat-liver mitochondria.

1. The factors concerned in the estimation of P/O ratios when fatty acids are oxidized by rat-liver mitochondria have been assessed. 2. The oxidation of butyrate, hexanoate and octanoate is accompanied by ATP synthesis. At low concentrations of the fatty acids, P/O ratios approximately 2.5 are obtained. 3. Oxidative phosphorylation is uncoupled, respiratory control ratios are lowered and respiration is inhibited when the concentration of the fatty acid in the incubating medium is raised (to 5-10mm); octanoate is a more potent uncoupler than either hexanoate or butyrate. 4. Serum albumin and carnitine, either singly or in combination, protect the mitochondria from the effect exerted by the fatty acids. 5. The rate of oxidation of short-chain fatty acids in the presence of ADP is increased in the presence of carnitine.

Adenosine Triphosphatases↗
PubMed1966

The effect of hexokinase and tricarboxylic acid-cycle intermediates on fatty acid oxidation and formation of ketone bodies by rat-liver mitochondria.

1. The oxidation of butyrate, hexanoate and octanoate by rat-liver mitochondria suspended in a tris-potassium chloride medium in the presence of malate and serum albumin has been investigated. 2. The oxidation of butyrate to acetoacetate was markedly decreased by the addition of a system competitive for ATP (hexokinase-glucose). 3. Serum albumin or tricarboxylic acid-cycle intermediates prevented the inhibition by hexokinase and in their presence a greater proportion of the oxygen consumption was contributed by the tricarboxylic acid cycle. The results suggest that the energy supply for fatty acid activation is either compartmentalized in a spatial or kinetic sense or there exists a special activating mechanism not involving ATP. 4. Malate and other tricarboxylic acid-cycle intermediates caused substantial reduction (to beta-hydroxybutyrate) of the acetoacetate formed during the oxidation of butyrate, hexanoate and octanoate.

Animals↗
PubMed1966

Transport and metabolism of fatty acids by isolated rumen epithelium.

1. The metabolism of even-numbered saturated (acetic acid to stearic acid) and unsaturated (oleic acid and linolenic acid) fatty acids by diaphragms of isolated rumen epithelium has been investigated. 2. When fatty acids are presented to the papillae surface, ketone bodies are released from the opposite (muscle) side of the tissue. 3. When the concentration of octanoate or decanoate is increased to a critical value, which varies inversely with the chain length of the fatty acid, the respiration of the tissue is inhibited and ketone body synthesis is diminished. Under these conditions unmetabolized fatty acid crosses the tissue down a concentration gradient. 4. The inhibitions by octanoate and decanoate are more marked when the fatty acid is presented to both surfaces of the rumen epithelium. 5. During the oxidation of octanoate and decanoate at non-inhibitory concentrations, small quantities of shorter chain fatty acids, including acetate, are produced.

Acetates↗
PubMed1966

The fate of isotopic carbon in kidney cortex synthesizing glucose from lactate.

1. When slices of kidney cortex are incubated with lactate and acetoacetate, lactate is almost quantitatively converted into glucose whereas acetoacetate provides a major part of the fuel of respiration. 2. In apparent contrast with these findings a large fraction of (14)C-labelled acetoacetate appears in glucose and a large fraction of (14)C-labelled lactate appears in the carbon dioxide. 3. The findings can be explained by: (a) the participation of oxaloacetate as an intermediate of both gluconeogenesis and respiration; (b) the fact that the carbon dioxide formed in the course of one turn of the tricarboxylic acid cycle is exclusively derived from oxaloacetate. 4. As a result there is a ;crossing over' of the carbon of the substrate of respiration to the pathway of gluconeogenesis and of the carbon of the glucogenic precursors to the pathway of respiration. 5. In the given situation the fate of the label does not allow predictions to be made about the net fate of the labelled metabolites. 6. The implications of the findings on the interpretation of isotopic data are discussed.

Acetoacetates↗