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PubMed1991

Quantifying intermediary metabolites in whole blood after a simple deproteinization step with sulfosalicylic acid.

We assessed the reproducibility, recovery, and stability of several circulating metabolites--glucose, pyruvate, lactate, alanine, glutamate, glutamine, 3-hydroxybutyrate, acetoacetate, and glycerol--in the presence of sulfosalicylic acid (SSA), which was used to deproteinize blood. The assays, which involved reactions linked to NADH/NAD+, were carried out at 37 degrees C and measured at 355 nm with a Cobas-Bio centrifugal analyzer. The intra- and interbatch CVs were less than 2.1%, except for the interbatch CV for 3-hydroxybutyrate at low concentration (15-30 mumol/L), which was 5.4%. Analytical recovery of metabolites added to blood ranged from 96.4% to 103.0%. Of the metabolites studied, all were stable at -20 degrees C for 90 days in the SSA-blood extract, except for glutamine and acetoacetate, which progressively decreased with time. We conclude that these nine circulating metabolites can be satisfactorily measured after a single deproteinizing step with SSA. This single-step procedure has several advantages over many of the currently used methods.

Amino Acids↗

PubMed1990

Amiodarone inhibits the mitochondrial beta-oxidation of fatty acids and produces microvesicular steatosis of the liver in mice.

Amiodarone has been shown to produce microvesicular steatosis of the liver in some recipients. We have determined the effects of amiodarone on the mitochondrial oxidation of fatty acids in mice. In vitro, the formation of 14C-acid-soluble beta-oxidation products from [U-14C]palmitic acid by mouse liver mitochondria was decreased by 92% in the presence of 125 microM amiodarone and by 94% in the presence of 125 microM N-desethylamiodarone. Inhibition due to 100 or 150 microM amiodarone persisted in the presence of 5 mM acetoacetate, whereas acetoacetate totally relieved inhibition due to 15 microM rotenone. In vivo, exhalation of [14C]CO2 from [U-14C]palmitic acid was decreased by 31, 40, 58 and 78%, respectively, in mice receiving 19, 25, 50 and 100 mg.kg-1 of amiodarone hydrochloride 1 hr before the administration of [U-14C]palmitic acid. One hour after 100 mg.kg-1, the exhalation of [14C]CO2 from [1-14C]palmitic acid, [1-14C]octanoic acid or [1-14C]butyric acid was decreased by 78, 72 and 53%, respectively. Exhalation of [14C]CO2 from [1-14C]palmitic acid was normal between 6 and 9 hr after administration of 100 mg.kg-1 of amiodarone hydrochloride, but was still inhibited by 71 and 37%, 24 and 48 hr after 600 mg.kg-1. Twenty four hours after the latter dose of amiodarone, hepatic triglycerides were increased by 150%, and there was microvesicular steatosis of the liver. We conclude that amiodarone inhibits the mitochondrial beta-oxidation of fatty acids and produces microvesicular steatosis of the liver in mice.

Amiodarone↗

PubMed1990

Unmeasured anion during severe sepsis with metabolic acidosis.

It is assumed that the development of metabolic acidosis during sepsis is secondary to lactic acidosis. We assessed the composition of the anion gap during severe sepsis induced by cecal perforation in rats. In the first experiment, cardiac output, arterial blood gases, and arterial lactate were measured over a 6 hr interval in five septic rats and in five rats serving as sham-operated controls. The cardiac output decreased from 331 +/- 32 to 172 +/- 9 ml/kg/min (P less than 0.01) in the septic rats. Although the arterial lactate was increased to 2.1 +/- 0.2 mEq/L in septic rats compared to 0.8 +/- 0.1 mEq/L in sham rats (P less than 0.01), the HCO3- was decreased to 16.5 +/- 0.6 mEq/L in septic rats versus 23.8 +/- 1.10 mEq/L in sham rats (P less than 0.01). We further investigated this bicarbonate deficit in a second study in which arterial blood was sampled at 6 hr for blood gases, and plasma Na+, K+, Cl-, HCO3-, lactate, pyruvate, beta-hydroxybutyrate, acetoacetate, citrate, creatinine, albumin, and amino acids in five septic and five sham rats. The serum anion gap was calculated as [(Na(+) + K+) - (Cl(-) + HCO3-)]. The anion gap was 21.6 +/- 1.6 mEq/L in the septic animals as compared to 13.2 +/- 0.5 mEq/L in the sham animals (P less than 0.01). There were no differences in the concentration of pyruvate, beta-hydroxybutyrate, acetoacetate, citrate, creatinine, albumin, or amino acids.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗

PubMed1979

Lipid accumulation in the rat liver: a histological and biochemical study.

The sequential pattern of lipid accumulation and associated biochemical changes were studied in two commonly used experimental models of nutritional fatty liver in rats. Female rats were maintained for 8 weeks on high fat, low protein diets containing adequate methionine and choline, and drinking water ad libitum (Diet 1), or deficient in methionine and choline and containing 20% ethanol as a substitute for drinking water (Diet 2). Histologically, there was a progressive increase in liver lipids, mainly in the periportal areas. Occasional foci of liver cell necrosis with lipogranuloma formation occurred in areas of severe fatty change. These changes appeared earlier and were more marked in rats maintained on Diet 2. Electron micrographs revealed large lipid droplets in the liver cells, which sometimes contained myelin figures. The mitochondria were enlarged, distorted and appeared as amorphous structures with disorientated cristae in rats on Diet 1, whereas they had a condensed conformation in rats maintained on Diet 2. Rough endoplasmic reticulum was fragmented and degranulated particularly in rats on Diet 1, and smooth endoplasmic reticulum showed hyperplasia and vesiculation in rats on Diet 2. There was a progressive increase in the total liver lipids and triglycerides in both the groups of rats. This fatty change was accompanied by a significant increase in hepatic 3-hydroxybutyrate, acetoacetate, malate, 2-oxoglutarate, citrate, lactate, ammonia, glutamate, alanine and aspartate, and a significant decrease in oxaloacetate, urea and glucose concentrations. The mass action ratios for alanine aminotransferase, aspartate amino transferase, and glutamate dehydrogenase, generally moved in a parallel direction. Hepatic ATP content was considerably reduced accompanied by a decrease in [ATP]/[ADP] ratios and a significant increased in [lactate]/[pyruvate] and [3-hydroxybutyrate]/[acetoacetate] ratios. There was a corresponding decrease in the [NAD+]/[NADH] ratios both in the cytoplasmic and mitochondrial compartments. These biochemical changes were particularly severe in rats maintained on Diet 1 and Diet 2 for 8 weeks. There was a very good relationship between impaired mitochondrial and endoplasmic reticulum functions, redox and phosphorylation states, and the relevance of their changes to the fate of fatty liver cells.

Adenosine Triphosphate↗

PubMed1990

[The effect of glucose loading on changes in ketone and glucose metabolism during gastrectomy].

Plasma glucose, insulin, glucagon, free fatty acid, ketone body, lactate and pyruvate were measured in 14 patients undergoing gastrectomy under general anesthesia with nitrous oxide and oxygen. Lactated ringer solution with glucose load (10 g.hr-1) was administered in seven patients [glucose loading group: Glucose (+)] and the other seven patients received only lactated ringer solution [glucose free group: Glucose (-)]. Blood glucose increased significantly in both groups, but a significant difference appeared between Glucose (+) and Glucose (-). Plasma insulin activity and IRI/BS ratio increased in Glucose (+) and a significant difference was found between the two groups. No remarkable change in plasma glucagon level was found in both groups. Free fatty acid and ketone bodies (acetoacetate, beta-hydroxybutyrate) decreased significantly in Glucose (+), but they increased significantly in Glucose (-) and significant differences were found between the two groups. The rate of changes of beta-hydroxybutyrate was consistently higher than that of acetoacetate. Lactate and pyruvate increased significantly in both groups. These results suggest that continuous glucose loading may facilitate insulin release from the pancreas and suppress the hyperketonemia and hyperlipidemia during partial gastrectomy.

Blood Glucose↗

PubMed1987

Glucagon-stimulated calcium efflux in the isolated perfused rat liver is dependent on cellular redox potential.

In the absence of any exogenous substrates, glucagon (1 X 10(-9) M) stimulated 45Ca2+ efflux from perfused livers derived from fed rats but not in livers of 24-h-fasted animals. In livers of 24-h-fasted animals perfused under conditions which would decrease cellular NAD(P)H/NAD(P)+ ratio (pyruvate (2.0 mM) or acetoacetate (10.0 mM], glucagon (1 X 10(-9) M) did not stimulate 45Ca2+ efflux. Similarly, in livers of 24-h-fasted animals perfused with substrates which increase cellular NAD(P)H content (lactate (2.0 mM) or beta-hydroxybutyrate (10.0 mM], glucagon (1 X 10(-9) M) did not increase 45Ca2+ efflux. Glucagon (1 X 10(-9) M) elicited an increase in 45Ca2+ efflux from livers of 24-h-fasted animals, only when the livers were perfused with [lactate]/[pyruvate] and [beta-hydroxybutyrate]/[acetoacetate] ratios similar to those reported for livers of fed rats. Stimulation of 45Ca2+ efflux elicited by either 8-CPT-cAMP, a cAMP analog, or high glucagon concentrations (1 X 10(-8) M) was not affected whether livers were perfused with pyruvate (2.0 mM) or lactate (2.0 mM). Administration of isobutylmethylxanthine (50 microM) alone, or glucagon (1 X 10(-9) M) in the presence of isobutylmethylxanthine (50 microM) stimulated 45Ca2+ efflux from livers of 24-h-fasted animals perfused with pyruvate (2.0 mM) but not from livers perfused with lactate (2.0 mM). The ability of glucagon (1 X 10(-9) M) to elevate tissue cAMP levels was also regulated by the oxidation-reduction state of the livers. The data indicate that glucagon-stimulated 45Ca2+ efflux from perfused livers is mediated via cAMP and is dependent on the oxidation-reduction state of the livers.

1-Methyl-3-isobutylxanthine↗

PubMed1989

Variations in parameters of liver function and plasma progesterone related to underfeeding and ketosis in a dairy herd.

Twenty-eight Norwegian Red Cattle dairy cows were fed silage ad libitum and restricted amounts of concentrates. Blood samples were collected before morning feeding, once or twice weekly, from 2 weeks before to 12 weeks after calving. Parameters of liver function, carbohydrate status and fertility were recorded in order to assess their interrelationships. Eight cows were treated for clinical ketosis. Four of these had to be treated 2 or 3 times. Aspartate aminotransferase and bilirubin showed the highest within-animal coefficients of correlation with acetoacetate. Analysis of variance revealed a significant effect of carbohydrate status (indicated by plasma acetoacetate levels) on the levels of aspartate aminotransferase, glutamate dehydrogenase and sorbitol dehydrogenase, though only a small part of the total variation was explained by this factor. The estimated volume density of liver fat in the 4th week of lactation averaged 6.0 +/- 6.4% (+/- SD) ranging from 0.1-25.1%. Liver fat content at this stage of lactation was not significantly correlated with other indicators of liver function or carbohydrate status. Cows treated for clinical ketosis had significantly lower plasma progesterone values at the time of first ketosis treatment than untreated multiparous cows. The frequency of high progesterone values (greater than 3 ng/ml) being significantly lower in treated than in untreated cows during the period from 3-5 weeks post partum, though not at later stages. In conclusion, the results revealed a significant relationship between carbohydrate status and liver function, and also between clinical ketosis and luteal function.

Acidosis↗

PubMedDate not supplied

[Effect of nonselective and cardioselective beta-adrenergic blockade on fatty acid metabolism in the myocardium].

Effects of beta-adrenoblocker obsidan and selective beta-adrenoblocker cordanum on metabolism of fatty acids in the rat myocardium were studied. Obsidan increased the concentration of triglycerides and decreased that of nonesterified fatty acids in the myocardial tissue, reduced the amounts of ketone bodies, beta-oxybutyrate and acetoacetate, accelerated oxidation of fatty acids by myocardial mitochondria. Cordanum produced no changes in beta-oxybutyrate concentration, decreased the concentrations of acetoacetate, induced accumulation of triglycerides. The drug reduced respiration control at the expense of an increase in controlled respiration rate. Thus, in contrast to total beta-adrenergic blockade induced by obsidan, cardioselective beta-adrenergic blockade by cordanum results in a decrease of myocardial oxygen consumption and a reduction of respiration controlled respiration rate.

Adenosine Triphosphate↗

PubMed1988

Glucose uptake, lactate release, ketone body turnover, metabolic micromilieu, and pH distributions in human breast cancer xenografts in nude rats.

Glucose uptake, lactate release, ketone body utilization, spatial distribution of glucose, lactate, and ATP concentrations as well as tissue pH distributions were systematically investigated in s.c. and/or "tissue-isolated" human breast cancer xenografts in T-cell-deficient rnu/rnu rats. Large variations in all parameters were detected within and between tumors indicating a very nonuniform substrate turnover. Glucose was taken up by all xenografts. Glucose consumption rates increased with increasing glucose availabilities, implying that the glucose uptake is mainly determined by the efficiency of nutritive tumor blood flow. The average glucose uptake was 0.37 mumol/g/min in medullary and 0.26 mumol/g/min in squamous cell carcinomas of the breast. At wet weights below 5 g, medullary breast cancers consumed more glucose than squamous cell carcinomas (2P less than 0.05). Most tumors (97%) released lactate in an amount linearly related to glucose consumption. The lactate production of medullary (0.33 mumol/g/min) and squamous cell (0.31 mumol/g/min) breast cancers was similar. In general, the xenografts utilized ketone bodies. beta-Hydroxybutyrate was consumed by 82% and acetoacetate by 73% of the tumors, the uptake rates being linearly related to the respective availabilities. The mean uptake of beta-hydroxybutyrate was 3.48 nmol/g/min and that of acetoacetate 2.56 nmol/g/min. No significant differences were seen between medullary and squamous cell breast cancers. The beta-hydroxybutyrate/acetoacetate ratio in the tumor-venous blood rose with decreasing tumor blood flow indicating the development of hypoxia at advanced growth stages. Glucose, lactate, and ATP levels were all very heterogeneously distributed in medullary and squamous cell tumors as compared with normal tissue. No relationship was evident between the spatial distribution of concentrations of these three substrates. The xenografts were acidotic compared with pH values in normal subcutis. The mean tissue pH in medullary breast cancers was 6.81 +/- 0.25 (SD). Compared with these values, the tissue pH distribution in squamous cell breast cancers was shifted to significantly higher values. The mean pH of the latter tumors was 7.04 +/- 0.19 (2P less than 0.001). From the experimental data presented there is clear indication that the metabolism of the xenografts investigated was mainly determined by the efficiency of nutritive blood flow, i.e., by substrate availability, and not by the metabolic demand of the cancer cells.

Animals↗

PubMed1988

Effects of ethanol on fetal fuels and brain growth in rats.

The mechanism of fetal brain growth retardation caused by maternal alcoholism is unclear. In this study we examined fuel concentrations in brain and blood samples and their relationship to brain growth in term fetuses of rats fed ethanol during pregnancy. The offspring of ethanol-fed (EF) rats showed a significant decrease in body and brain weights compared with those of pair-fed (PF) control rats and control rats given free access to food (ad libitum fed) (AF). The EF and PF rats consumed nearly 20% less food than the AF rats, and both groups showed a slight but significant reduction of the maternal blood glucose level. In PF rats, beta-hydroxybutyrate concentration was increased in maternal as well as in fetal blood and brain samples, but no adverse effect of this magnitude of maternal undernutrition was observed on fetal body or brain weights. In EF fetuses, plasma glucose and pyruvate levels were decreased and lactate levels were increased, resulting in a nearly twofold increase in the lactate-to-pyruvate ratio when compared with levels in control fetuses. The beta-hydroxybutyrate--to-acetoacetate ratio was increased because of low plasma acetoacetate concentration. In EF fetuses, brain glucose and pyruvate levels were decreased. Fetal brain weight showed a positive correlation with brain glucose concentration and a negative correlation with the brain concentrations of lactate or ketones. It is surmised that an aberrant fetal fuel mixture may play a role in the fetal growth retardation associated with maternal alcoholism.

Animals↗

PubMed1986

Hereditary tyrosinemia type I--an overview.

Hereditary tyrosinemia type I is a metabolic disorder of autosomal recessive inheritance. The disorder is characterized by progressive liver disease and renal tubular defects with accompanying hypophosphatemic rickets. It occurs in an acute and a chronic form. Hepatocellular carcinoma is frequently encountered in the chronic form of the disorder. The primary enzyme defect is a deficiency of fumarylacetoacetase (FAH) (EC 3.7.1.2), the last enzyme in the degradation of tyrosine. The enzyme defect results in accumulation of fumaryl- and maleyl-acetoacetate which are thought to cause the cellular damage in tyrosinemia. Fumaryl- and maleyl-acetoacetate are reactive compounds and have not been identified in tyrosinemia patients. Succinylacetone, however, presumably derived from these metabolites by reduction and decarboxylation, is elevated in serum and urine from the patients. The diagnosis of tyrosinemia can be established by determination of succinylacetone in urine or serum and by assay of FAH in lymphocytes and fibroblasts. Heterozygotes for FAH can be identified by fumarylacetoacetase analysis in lymphocytes and fibroblasts. Prenatal diagnosis of tyrosinemia is possible by analysis of succinylacetone in amniotic fluid supernatant and by assay of FAH in cultured amniotic fluid cells or chorionic villus material. Genetic variants of FAH may interfere in the prenatal diagnosis of tyrosinemia by the FAH assay and in the detection of the carrier state. Immunoblotting technique has shown absence of immunoreactive protein in liver tissue from tyrosinemia patients. Liver transplantation is as yet the only definite treatment of the disorder.

4-Hydroxyphenylpyruvate Dioxygenase↗

PubMed1987

Production of acetone and conversion of acetone to acetate in the perfused rat liver.

The utilization of millimolar concentrations of [2-14C]acetone and the production of acetone from acetoacetate were studied in perfused livers from 48-h starved rats. We devised a procedure for determining, in a perfused liver system, the first-order rate constant for the decarboxylation of acetoacetate (0.29 +/- 0.09 h-1, S.E., n = 8). After perfusion of livers with [2-14C]acetone, labeled acetate was isolated from the perfusion medium and characterized as [1-14C]acetate. No radioactivity was found in lactate or 3-hydroxybutyrate. After 90 min of perfusion with [2-14C]acetone, the specific activity of acetate was 30 +/- 4% (n = 13) of the initial specific activity of acetone. We conclude that, in perfused livers from 2-day starved rats, acetone metabolism occurs for the most part via free acetate.

Acetates↗

PubMed1986

Factors affecting determination of delta-aminolevulinate by use of Ehrlich's reagent.

We investigated the formation of delta-aminolevulinic acid (ALA)-pyrrole and subsequent color development used in determining ALA in urine. Of three condensation reagents examined--acetylacetone, ethyl acetoacetate, and methyl acetoacetate--the last was the best. When the ALA-pyrrole is reacted with Ehrlich's reagent in ethyl acetate according to one procedure, the optimum concentration of perchloric acid in the reagent is 0.5 to 1.0 mol/L. Its optimum concentration is 1.0 to 2.3 mol/L when the reaction takes place in water.

Aminolevulinic Acid↗

PubMed1966

The oxidation of fatty acids combined with albumin by isolated rat liver mitochondria.

Long chain fatty acids at concentrations inhibiting mitochondrial respiration were, in the presence of serum albumin, found to produce almost as high a rate of oxygen uptake as alpha-ketoglutarate, succinate, or acetate. This oxidation was characterized in terms of its coupling to phosphorylation, need for cofactors, and production of different metabolites during the reactions. Fatty acids were oxidized to carbon dioxide, acetoacetate, beta-hydroxybutyrate, and other water-soluble metabolites, tentatively identified as intermediates of the citric acid cycle. An agent to spark the citric acid cycle and adenosine tri- or monophosphate were necessary for optimal oxidation rate, as described for other fatty acid oxidation systems. Balance experiments with different amounts of malate were performed with incubations lasting as long as oxygen uptake took place. In the presence of 1 mumole of malate, practically all added palmitic acid was used up and found to be converted primarily to carbon dioxide, acetoacetate, and other water-soluble metabolites of which the major part was tentatively identified as succinate. A significant portion was found in mitochondrial phospholipids. With 10 mumoles of malate some palmitic acid remained in the system, while a comparatively small amount was converted to carbon dioxide, and a major part was found as succinate. Here also incorporation into phospholipids occurred. With no malate added, fatty acid oxidation was much smaller than with malate, although significant conversion to carbon dioxide took place. Only a little succinate and phospholipid were found. Oxygen uptake was greater than a theoretical value calculated from radioactive balance experiments. It was concluded that albumin contains oxidizable material even after extraction and dialysis. Albumin at high concentrations inhibited both fatty acid and alpha-ketoglutarate oxidation. The oxidation of long chain fatty acids in high concentrations in the form of albumin-fatty acid complex was coupled to phosphorylation. Thus P:O ratios above 2 were found as well as evidence for respiratory control. It was concluded that oxidation of long chain fatty acids by isolated mitochondria occurs from their albumin complex. This process can also be studied at high concentrations of fatty acids, where high rates of oxygen uptake are obtained from oxidation which is coupled to phosphorylation.

Animals↗

PubMed1966

Effect of ketone bodies on lipolysis in adipose tissue in vitro.

Norepinephrine-sensitive lipase activity was measured in rat epididymal fat pads by determining release either of free fatty acids or of glycerol. Stimulation of the lipase activity by norepinephrine in vitro could not be duplicated by injecting norepinephrine into the rats before sacrifice. A reliable method for assay of lipase deactivation rate was developed in which the tissue is incubated for 80 min, norepinephrine is added for a further incubation of 10 min, and the decay of lipase activity is measured during the next 10 min in the absence of hormone. Of the ketone bodies tested, -hydroxybutyrate and probably acetoacetate inhibited the activation of lipase by norepinephrine but had no effect on lipase deactivation rate, whereas acetone increased lipase activity stimulated by norepinephrine when tested at the concentration at which acetoacetate gave an inhibition. Substances other than -hydroxybutyrate that produce reduced nucleotides-alpha-glycerophosphate, malate, and ethanol-had no effect on lipase activity as tested in the present system.

Adipose Tissue↗

PubMed1981

Effects of pyruvate and other metabolites on cyclic GMP levels in incubations of rat hepatocytes and kidney cortex.

Pyruvate increased cyclic GMP levels in rat hepatocytes. The effects were observed without or with 1-methyl-3-isobutylxanthine. Lactate, acetate, oxaloacetate, alpha-ketoglutarate, succinate, acetoacetate and beta-hydroxybutyrate also increased cyclic GMP levels. Some compounds increased cyclic GMP in kidney cortex slices. The effects were dependent upon Ca2+ in the medium. Cyclic AMP was increased 30-50% by some of these substances with 2.6 mM Ca2+. Rotenone, oligomycin, antimycin, dinitrophenol, KCN, and arsenate decreased GTP and ATP, basal cyclic GMP and the pyruvate effect, but did not alter cyclic AMP. Although fluoroacetate alone had no effect on cyclic nucleotides, GTP, or ATP, it potentiated the pyruvate effect on cyclic GMP. Adenosine and guanosine increased cyclic GMP and GTP to a similar extent of 30-50%. Aminooxyacetate, cycloserine, pentenoic acid and mepacrine decreased the pyruvate effect while cycloserine or mepacrine alone increased cyclic GMP. Citrate and mepacrine inhibited soluble and particulate guanylate cyclase from rat liver while cycloserine and acetoacetate increased guanylate cyclase activity. None of the other compounds altered guanylate cyclase activity. These results indicate that various metabolites and inhibitors can alter cyclic GMP accumulation in hepatocytes and renal cortex slices. Several mechanisms may be involved in these effects.

1-Methyl-3-isobutylxanthine↗

PubMedDate not supplied

The effect of two glucocorticoids on plasma glucose and milk production in healthy cows and the therapeutic effect in ketosis.

In a cross-over study of six clinically healthy cows in early lactation, injection of 10 mg dexamethasone isonicotinate caused significantly increased plasma glucose for six days and significantly decreased milk yield for one day. The corresponding effects of 10 mg dexamethasone phosphate + 20 mg dexamethasone phenylpropionate lasted for at least nine and seven days, respectively. The therapeutic effect in bovine ketosis of the two preparations was measured by means of analysis of acetone plus acetoacetate in milk sampled daily during eight days post treatment. Acetone plus acetoacetate in milk from cows given dexamethasone phosphate + dexamethasone phenylpropionate (n = 11) decreased to normal levels and from the fourth day after treatment was significantly lower than in cows given dexamethasone isonicotinate (n = 12).

Animals↗

PubMed1978

Stimulation of ketogénesis after glycogen depletion by nicotinic acid in perfused rat liver.

Treatment with nicotinic acid produced an enhancement of ketone bodies production from endogenous, substrates, either oleate or octanotate. The enhancement was accounted for by an increase of acetoacetate synthesis. These results suggest that the increase of acetoacetate production may be due to the enhancement of extramitochondrial ketogenesis as a consequence of the inhibition of lipogenesis.

Animals↗