scholarly journals The effect of glucagon treatment and starvation of virgin and lactating rats on the rates of oxidation of octanoyl-l-carnitine and octanoate by isolated liver mitochondria

1980 ◽  
Vol 190 (2) ◽  
pp. 293-300 ◽  
Author(s):  
Victor A. Zammit
Keyword(s):  
Fatty Acids ◽  
Tricarboxylic Acid Cycle ◽  
Atp Synthesis ◽  
Liver Mitochondria ◽  
Oxidation Rates ◽  
Consumption Rates ◽  
Mitochondrial Oxidation ◽  
Elevated Rate ◽  
Isolated Liver ◽  
Chain Fatty Acids

1. Oxygen-consumption rates owing to oxidation of octanoate or octanoylcarnitine by isolated mitochondria from livers of fed, starved and glucagon-treated virgin or 12-day-lactating animals were measured under State-3 and State-4 conditions, in the presence or absence of l-malate and inhibitors of tricarboxylic acid-cycle activity (malonate and fluorocitrate). 2. Mitochondria from fed lactating animals had a slightly lower rate of octanoylcarnitine oxidation than did those of fed virgin animals, whereas the rates of octanoate oxidation were unaffected. 3. Starvation of virgin animals for 24h or 48h resulted in a large (70–100%) increase in mitochondrial octanoylcarnitine oxidation; rates of octanoate oxidation were either unaffected (24 and 48h starvation in the absence of malonate and fluorocitrate) or diminished by 30% (48h starvation in the presence of inhibitors). In lactating animals, 24h starvation resulted in a smaller increase in the rate of octanoylcarnitine oxidation than that obtained for mitochondria from virgin rats. 4. Glucagon treatment (by intra-abdominal injection) of fed virgin and lactating rats increased the rate of mitochondrial oxidation of both octanoylcarnitine and octanoate. Injection of glucagon into 48h-starved virgin rats did not increase further the already elevated rate of octanoylcarnitine oxidation, but reversed the inhibition of octanoate β-oxidation observed for these mitochondria in the presence of malonate and fluorocitrate. 5. It is suggested that glucagon activates octanoylcarnitine oxidation by increasing the activity of the carnitine/acylcarnitine transport system [Parvin & Pande (1979) J. Biol. Chem.254, 5423–5429] and that the increase in octanoate oxidation by mitochondria from glucagon-treated animals is caused by the increased rate of ATP synthesis in these mitochondria. 6. The results are discussed in relation to the increased capacity of the liver to oxidize long-chain fatty acids and carnitine esters of medium-chain fatty acids under conditions characterized by increased ketogenesis.

scholarly journals Comparative biochemistry of β-oxidation. An investigation into the abilities of isolated heart mitochondria of various animal species to oxidize long-chain fatty acids, including the C22:1 monoenes

1978 ◽  
Vol 174 (2) ◽  
pp. 379-386 ◽  
Author(s):  
H Osmundsen ◽  
J Bremer
Keyword(s):  
Fatty Acids ◽  
Animal Species ◽  
Species Differences ◽  
Isolated Heart ◽  
Tricarboxylic Acid Cycle ◽  
Heart Mitochondria ◽  
Long Chain Fatty Acids ◽  
Beta Oxidation ◽  
Long Chain ◽  
Chain Fatty Acids

Rates of acylcarnitine oxidation by isolated heart mitochondria from various animal species were measured polarographically, and by using a spectrophotometric assay [see Osmundsen & Bremer (1977) Biochem. J. 164, 621-633]. Polarographic measurements do not give a correct guide to abilities to beta-oxidize very-long-chain acylcarnitines, in particular C22:1 fatty acylcarnitines. 2. No significant species differences were detected in the abilities to beta-oxidize various C22:1 fatty acylcarnitines. Significant species differences were, however, detected when rates of beta-oxidation were correlated with rates of respiration brought about by very-long-chain acylcarnitines. We concluded that some aspects of oxidative metabolism (possibly the oxidation of tricarboxylic acid-cycle intermediates) are inhibited by very-long-chain fatty acids in some species (e.g. the rat and the cat but not in others (e.g. the pig and the rabbit). 3. It is proposed that the pattern of variation of rates of oxidation of various acylcarnitines (as measured spectrophotometrically) of various chain lengths can be used as a guide to the chain-length specificities of the acyl-CoA dehydrogenases of beta-oxidation (EC 1.3.99.3).

VARIATIONS IN LIPID INTAKE AND THEIR INFLUENCE ON RESPIRATION AND TRICARBOXYLIC ACID CYCLE ACTIVITY

1965 ◽  
Vol 43 (9) ◽  
pp. 1575-1587 ◽  
Author(s):  
Hector F. DeLuca
Keyword(s):  
Fatty Acids ◽  
Vitamin D ◽  
Vitamin A ◽  
Tricarboxylic Acid Cycle ◽  
Essential Fatty Acids ◽  
Respiratory Control ◽  
Liver Mitochondria ◽  
Tricarboxylic Acid ◽  
Membrane Systems ◽  
Acid Cycle

The possible role of dietary lipids and lipid-soluble constituents in the tricarboxylic acid cycle, respiratory systems, and mitochondrial structure is discussed, with special emphasis on vitamin D, vitamin A, and essential fatty acids. Deficiency of any of these substances produces structural alterations in isolated kidney or liver mitochondria. In the case of vitamin D deficiency the structural alteration in kidney mitochondria is accompanied by an increased rate of citrate and isocitrate oxidation and a decreased transfer of calcium ions from inside to outside the mitochondria. Vitamin D added in vitro or given to the intact rat specifically decreases citrate oxidation and increases the translocation of calcium. Vitamin A deficiency increases the respiration of liver homogenates and mitochondria in the absence of phosphate acceptor, an effect which could readily be reversed within 48 hours after vitamin A administration. Increased ATPase and decreased respiratory control were also noted in liver mitochondria from vitamin A deficient rats. The structural change as well as the biochemical lesions could also be reversed within 48 hours after vitamin A administration. Similar experiments with essential fatty acid deficient mitochondria also revealed a high ATPase, low respiratory control, and marked structural damage. These changes could be reversed by the feeding of essential fatty acids to the deficient animals for 1–3 weeks. Despite many attempts, it was not possible to demonstrate structural changes in mitochondria in situ as a result of any of the deficiencies described. It is suggested that the respiratory and tricarboxylic acid cycle changes that have been attributed to the lipid constituents of the diet are secondary to alterations in subcellular membrane systems. The use of these membrane systems as tools or models in a study of the mechanism of action of the dietary lipid and lipid-soluble materials is discussed.

Effects of female sex hormones on mitochondria: possible role in acute fatty liver of pregnancy

1995 ◽  
Vol 268 (1) ◽  
pp. G107-G115 ◽  
Author(s):  
S. Grimbert ◽  
C. Fisch ◽  
D. Deschamps ◽  
A. Berson ◽  
B. Fromenty ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Fatty Liver ◽  
Palmitic Acid ◽  
Sex Hormones ◽  
Tricarboxylic Acid Cycle ◽  
Liver Mitochondria ◽  
Female Sex ◽  
Female Sex Hormones ◽  
Acute Fatty Liver

Acute fatty liver of pregnancy occurs in some women. As other cases of microvesicular steatosis are due to impaired mitochondrial oxidation of fatty acids, we investigated the effects of female sex hormones on liver mitochondria in female mice. Three hours after administration of both estradiol (36 mumol/kg) and progesterone (150 mumol/kg), the in vitro beta-oxidation of [U-14C]palmitic acid and the activity of the tricarboxylic acid cycle decreased 49 and 54%, whereas the in vivo oxidation of [U-14C]palmitic acid decreased 38%. One week of treatment with both sex hormones produced ultrastructural lesions of mitochondria, decreased the recovery of mitochondrial proteins by 34%, increased state 4 respiration by 54-77%, and decreased the activities per gram of liver of several enzymes involved in the activation, mitochondrial uptake, and oxidation of fatty acids by 34-54%. We conclude that female sex hormones have deleterious effects on liver mitochondria and suggest that these effects, together with other factors, may contribute to the development of acute fatty liver of pregnancy in some women.

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