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PubMed1984

Odd-carbon fatty acid metabolism in hepatocytes from starved rats.

The metabolism of odd-chain fatty acids was investigated in hepatocytes from 24 h-starved rats. Rates of glucose and 14CO2 production from [1-14C]propionate, [1-14C]valerate and [1-14C]nonanoate were maximal at 0.1 mM. Glucose production was greater with propionate as substrate than with valerate or nonanoate. Ketone body, lactate and pyruvate release were not affected by addition of the odd carbon fatty acids. It is concluded that hepatic odd-chain fatty acid metabolism in starvation is partly oxidative and partly gluconeogenic. Vasopressin and angiotensin II stimulated 14CO2 production from [1-14C] valerate and [1-14C]nonanoate but not from [1-14C]propionate and [1-14C]oleate in hepatocytes from starved rats. Nonanoate and valerate generate acetyl-CoA and propionyl-CoA, whereas oleate or propionate produce acetyl CoA and propionyl-CoA respectively. Given this stoichiometry, it is inferred that in hepatocytes from starved rats there must be an input of a tricarboxylic acid cycle intermediate to permit expression of the hormonal sensitivity.

Angiotensin II↗
PubMedDate not supplied

Intravenous glycerol infusions: effect on free fatty acid metabolism.

The plasma-free fatty acid response to intravenous glycerol infused at 250 and 500 mumol/min was determined in five normal volunteers in the postabsorptive state. There was a drop in free fatty acid concentration in all five subjects (one-way ANOVA, p less than 0.01) after the glycerol infusion with no change in insulin concentration compared to the post-absorptive state. These results suggest that intravenous glycerol infusions decrease free fatty acid concentrations in the post-absorptive state by an insulin-independent mechanism. When pharmacologic nonisotopic glycerol infusions are used to determined lipolytic rate, simultaneous measurement of free fatty acid concentrations should be interpreted with caution.

Adult↗
PubMed1990

Abnormal essential fatty acid metabolism in Darier's disease.

Fatty acid levels in plasma and erythrocyte cell membranes were determined in 13 Danish patients with Darier's disease and 21 Danish controls. Concentrations of the main dietary essential fatty acids, linoleic acid (18:2n-6) and alpha-linolenic acid (18:3n-3), were consistently modestly above normal; concentrations of the delta 6-desaturase metabolites of both linoleic and alpha-linolenic acids, however, were consistently and often significantly below normal. These results suggest that the capacity of the enzyme delta 6-desaturase activity is inadequate in patients with Darier's disease.

Adult↗
PubMed1993

Fatty acid metabolism studies of human epidermal cell cultures.

Adult human epidermal keratinocytes grow rapidly in medium that is essential fatty acid (EFA)-deficient. In this medium they exhibit decreased amounts of the fatty acids, 18:2, 20:3, 20:4, and contain increased amounts of monounsaturated fatty acids. [14C]- and [3H]acetate and radiolabeled fatty acids, 16:0, 18:2, and 20:4 were used to study the fatty acid metabolism of these cells. Label from acetate appeared in 14- to 20-carbon fatty acids, both saturated and monounsaturated. No label was seen in the essential fatty acid 18:2, 18:3, and 20:4. Radiolabel from [9, 10-3H]palmitic acid (16:0) was detected in 16:0, 16:1, 18:0, and 18:1. [14C]linoleic acid (18:2) was converted to 18:3, 20:2, 20:3, and 20:4, demonstrating delta 6 and delta 5 desaturase activity in keratinocytes. Label from acetate, 16:0, or 18:2 was found mostly in the cellular phospholipids while only one third of the label from [14C]arachidonic was found in the phospholipids. [14C]acetate and [14C]18:2 time course data were used to construct a model of the metabolism of these reactants, using coupled, first-order differential equations. The data show that EFA-deficient keratinocytes metabolize fatty acids using pathways previously found in liver; they suggest the positioning of 18:2 desaturase and 18:3 elongase near the plasma membrane; they indicate that for the synthesis of nonessential fatty acids the formation of 18:0 from 16:0 is the rate-determining step; and they show that the conversion of 18:2 to 20:3 is rapid. These experiments demonstrate a method to study lipid enzyme kinetics in living cells.

Acetates↗
PubMed1986

[Correction of fatty acid metabolism in stomach surgery patients by the infusion of a fatty emulsion].

The method of gas-liquid chromatography was used for studying the content of high molecular weight fatty acids in blood serum of 48 patients after operations on the stomach. It was established that in the early postoperative period the level of high molecular weight fatty acids including essential ones was considerably lower which deteriorated the course of the postoperative period and caused complications. The inclusion of fat emulsions in the programme of parenteral feeding in the early postoperative period is an effective measure of correction of the disturbed fatty acid metabolism resulting in the improvement of immediate results of the operation and less amount of postoperative complications.

Chromatography, Gas↗
PubMed2005

Despite transient ketosis, the classic high-fat ketogenic diet induces marked changes in fatty acid metabolism in rats.

In contrast to humans, rats on a high-fat ketogenic diet seem incapable of maintaining plasma beta-hydroxybutyrate above 1 mmol/L for more than a week. Our goal was to determine whether fatty acid metabolism in rats changes despite the absence of sustained ketosis induced by the ketogenic diet. Fatty acid metabolism was assessed as changes in tissue fatty acid profiles and change in 13C-alpha-linolenic acid incorporation into plasma, liver, adipose tissue, and brain lipids. Despite loss of ketosis, the ketogenic diet reduced some polyunsaturated fatty acids in adipose tissue (up to 44%) and plasma (up to 90%) but raised polyunsaturates in liver triglycerides by up to 25-fold and raised arachidonic and docosahexaenoic acids in the brain by 15%. Lower tissue incorporation of 13C-alpha-linolenic acid but higher unlabeled and 13C-labeled docosahexaenoic acid in brain supports the view that the principal changes in fatty acid composition resulted from enhanced mobilization of polyunsaturates from adipose tissue to liver and brain. In the absence of sustained ketosis, changes in fatty acid metabolism resulting in an increase in brain polyunsaturates, particularly docosahexaenoic acid may, nevertheless, contribute to the seizure protection by the ketogenic diet.

Adipose Tissue↗
PubMed2003

Myocardial fatty acid metabolism: independent predictor of left ventricular mass in hypertensive heart disease.

The expression of myocardial fatty acid beta-oxidation enzymes is downregulated at the gene transcriptional level in animal models of left ventricular hypertrophy and of heart failure. Humans with idiopathic dilated cardiomyopathy have decreased myocardial fatty acid oxidation. The extent to which molecular mechanisms, such as a reduction in myocardial fatty acid oxidation, regulate the cardiac hypertrophic response in humans in vivo is unknown. Positron emission tomography was used to measure myocardial blood flow, oxygen consumption, fatty acid utilization, and oxidation in two groups of patients: (1) hypertensive left ventricular hypertrophy (n=19; left ventricular mass, 211+/-39 g; left ventricular ejection fraction, 67+/-4%) and (2) left ventricular dysfunction (n=9; left ventricular mass, 210+/-36 g; left ventricular ejection fraction, 31+/-10%); these were compared with a normal control group (n=36; left ventricular mass, 139+/-25 g; left ventricular ejection fraction, 66+/-6%). Left ventricular mass showed significant correlation with gender, diastolic and systolic blood pressure, myocardial fatty acid uptake, utilization and oxidation, myocardial blood flow, body mass index, and left ventricular ejection fraction (all P<0.02). Independent predictors of increased left ventricular mass were male gender (r=0.38, P<0.001), myocardial fatty acid oxidation (r=-0.24, P<0.018), systolic blood pressure (r=0.41, P<0.001), and left ventricular ejection fraction (r=-0.29, P=0.005). Thus, myocardial fatty acid metabolism is an independent predictor of left ventricular mass in hypertension and in left ventricular dysfunction. The extent to which reduced myocardial fatty acid metabolism affects cardiovascular morbidity and mortality and whether pharmacologic modulation results in improved outcomes remains to be determined.

Adult↗
PubMed1984

Effects of glucose-insulin-potassium solution on free fatty acid metabolism in ischemic myocardium.

The accumulation of intermediates subsequent to impaired oxidation of free fatty acids has been suggested as a cause of cellular damage in ischemic myocardium. Many reviews have supported the theory that glucose-insulin-potassium (GIK) solution has a beneficial effect on the ischemic myocardium. We evaluated the effects of GIK solution on intermediates of free fatty acid metabolism in ischemic myocardium. The left coronary artery was occluded for 40 minutes in twelve dogs. In six dogs, 10 minutes before coronary artery occlusion, GIK solution (50 percent of glucose, 50 units/liter of regular insulin, 50 mEq/liter of potassium) was given at the rate of 0.1 ml/kg per minute until the time of excision of the heart. In the ischemic area, adenosine triphosphate (ATP) level in the GIK group (3.80 +/- 1.34 mumole/g) was significantly higher than that in the control group (2.04 +/- 0.68, p less than 0.05). The free carnitine level was significantly increased was GIK in both ischemic and nonischemic areas (p less than 0.05). In the control group, the long chain acyl coenzyme A (CoA) level in the ischemic area (23.0 +/- 7.0 nmole/g) was significantly higher than that in the nonischemic area (17.1 +/- 3.5, p, less than 0.05). On the other hand, GIK prevented the increase in the long chain acyl CoA in the ischemic area (17.8 +/- 5.6). This study suggests that GIK has a protective effect on ischemic myocardium, probably by preventing the accumulation of long chain acyl CoA by improving free fatty acid metabolism.

Acyl Coenzyme A↗
PubMed1992

Interrelationship between lactate and cardiac fatty acid metabolism.

This overview is presented, in the main, to summarize the following aspects of lactate and cardiac fatty acid metabolism: 1. The utilization of exogenous carbohydrates and fatty acids by the heart. 2. The competition between lactate and fatty acids in cardiac energy metabolism. 3. The effect of lactate on endogenous triacylglycerol homeostasis. 4. Lactate-induced impairment of functional recovery of the post-ischemic heart. 5. The effect of lactate on lipid metabolism in the ischemic and post-ischemic heart. 6. The consequences of hyperlactaemia for cardiac imaging.

Animals↗
PubMedDate not supplied

Lipoxygenase products of polyunsaturated fatty acid metabolism in the central nervous system: biosynthesis and putative functions.

Twenty-five years ago prostaglandin (PG) F2 alpha was identified as the first cyclooxygenase-derived metabolite of polyunsaturated fatty acid metabolism in the bovine central nervous system (CNS). On the other hand, 12-hydroxyeicosatetraenoic acid (12-HETE) was the first lipoxygenase product of polyunsaturated fatty acid metabolism to be identified in rat and gerbil brain. For various cyclooxygenase products of arachidonic acid metabolism a substantial body of evidence suggests a mediator role in CNS functions such as in the regulation of local blood flow, in the induction of fever and in the prevention or limitation of seizure activity. By contrast, rather limited information is available on the possible roles of lipoxygenase products of polyunsaturated fatty acid metabolism in the CNS. This review is intended to give a survey on biosynthesis, regional distribution and possible functional importance of HETEs and leukotrienes (LT) in the CNS.

Animals↗
PubMed1985

Impaired essential fatty acid metabolism in latent tetany.

Because of the biochemical role of magnesium in the metabolism of polyunsaturated fatty acids, we measured the levels of polyunsaturated fatty acids in the plasma phospholipids of 40 patients with latent tetany (LT). The level of linoleic acid (18:2 n-6) was 25% higher in patients than in controls (p less than 0.001). In contrast, dihomogamma linoleic acid (20:3 n-6) was 34% lower, arachidonic acid (20:4 n-6) was 14% lower than in controls (p less than 0.01) and the ultrapolyunsaturates, 22:4 n-6 and 22:5 n-6, were reduced by 27 and 53%, respectively (p less than 0.001). Linolenic acid (18:3 n-3) was not significantly different from control levels, but its metabolite, eicosapentaenoic acid (20:5 n-3) was reduced by 43% (p less than 0.05). Since the levels of plasma phospholipid fatty acids are a reflection of hepatic metabolism, these findings suggest that patients with LT have impaired desaturation of 18:2 n-6 and possibly 18:3 n-3. The desaturase enzyme is Mg dependent, and impaired desaturation has been demonstrated in animals rendered Mg deficient. Possible consequences of this impairment in essential fatty acid (EFA) metabolism are an increase in membrane viscosity and a distortion in the availability of fatty acid precursors for prostaglandin synthesis. Either of these abnormalities may contribute to the pathogenesis of illness associated with LT.

Adolescent↗
PubMedDate not supplied

Current progress in the fatty acid metabolism in Cryptosporidium parvum.

Cryptosporidium parvum is one of the apicomplexans that can cause severe diarrhea in humans and animals. The slow development of anti-cryptosporidiosis chemotherapy is primarily due to the poor understanding on the basic metabolic pathways in this parasite. Many well-defined or promising drug targets found in other apicomplexans are either absent or highly divergent in C. parvum. The recently discovered apicoplast and its associated Type II fatty acid synthetic enzymes in Plasmodium, Toxoplasma, and Eimeria apicomplexans are absent in C. parvum, suggesting this parasite is unable to synthesize fatty acids de novo. However, C. parvum possesses a giant Type I fatty acid synthase (CpFAS1) that makes very long chain fatty acids using mediate or long chain fatty acids as precursors. Cryptosporidium also contains a Type I polyketide synthase (CpPKS1) that is probably involved in the production of unknown polyketide(s) from a fatty acid precursor. In addition to CpFAS1 and CpPKS1, a number of other enzymes involved in fatty acid metabolism have also been identified. These include a long chain fatty acyl elongase (LCE), a cytosolic acetyl-CoA carboxylase (ACCase), three acyl-CoA synthases (ACS), and an unusual "long-type" acyl-CoA binding protein (ACBP), which allows us to hypothetically reconstruct the highly streamlined fatty acid metabolism in this parasite. However, C. parvum lacks enzymes for the oxidation of fatty acids, indicating that fatty acids are not an energy source for this parasite. Since fatty acids are essential components of all biomembranes, molecular and functional studies on these critical enzymes would not only deepen our understanding on the basic metabolism in the parasites, but also point new directions for the drug discovery against C. parvum and other apicomplexan-based diseases.

Acetyl-CoA Carboxylase↗
PubMed1997

Essential fatty acid metabolism in cardiomyocytes grown in media enriched with different N-6/N-3 fatty acid combinations.

We have evaluated the effects of three different 18:3n-6, 20:5n-3 and 22:6n-3 fatty acid combinations on essential fatty acid (EFA) metabolism in rat cultured cardiomyocytes. The desaturating/elongating activities for linoleic (LA) and alpha-linolenic acid (ALA) were evaluated by radiolabeling the cells with 1-[14C]LA or 1-[14C]ALA and the fatty acid pattern of cardiomyocytes was assessed by gas chromatography. LA and ALA conversion to more unsaturated metabolites was reduced by increasing respectively n-3 and n-6 fatty acid concentration in the media. The all three combinations used reduced the saturated and increased the polyunsaturated fatty acid content of cardiomyocytes. The n-6/n-3 fatty acid ratio did not change compared to control cells in cardiomyocytes receiving the highest amount of 18:3n-6 and the lowest amounts of n-3 fatty acids. This combination may be suitable for modifying EFA desaturating/elongating activities without altering the physicochemical parameters which are related to the correct balance between n-6 and n-3 fatty acid content.

Animals↗
PubMed2001

Depressed myocardial fatty acid metabolism in patients with muscular dystrophy.

Myocardial involvement is frequently associated with various types of muscular dystrophy and Thallium-201 scintigraphy can show regional myocardial perfusion abnormalities in patients with muscular dystrophy. Myocardial fatty acid metabolism can now be imaged using a radioiodinated branched fatty acid (123I-BMIPP). The present study evaluates myocardial fatty acid metabolism in muscular dystrophy. Twenty-eight patients underwent 123I-BMIPP(BMIPP) and Thallium dual single photon emission tomography. Regional uptake of both tracers was visually analyzed. We also assessed electrocardiography and echocardiography. The results showed that the BMIPP uptake compared to Thallium was smaller in 57% of all patients. BMIPP SPECT images revealed abnormalities in four of eight patients with a normal electrocardiogram. Abnormal BMIPP uptake with normal regional wall motion was evident in nine patients. The size of the region with defective BMIPP uptake was larger than that of asynergic areas detected by echocardiography in 11 patients. In conclusion, muscular dystrophy involves depressed myocardial fatty acid metabolism in larger extent of region than that in perfusion or mechanical abnormality.

Adolescent↗
PubMed1999

The liver carnitine pool reflects alterations in hepatic fatty acid metabolism in rats with bile duct ligation before and after biliodigestive anastomosis.

BACKGROUND/AIMS: Rats with long-term bile duct ligation (BDL rats) have impaired hepatic fatty acid metabolism and alterations in carnitine homeostasis. Analysis of the carnitine tissue and body fluid pools was used as a tool to study hepatic fatty acid metabolism in BDL rats and after reversal of bile duct ligation by Roux-en-Y anastomosis for 5 (RY5) or 14 days (RY14) METHODS: Control rats were pair-fed to treated rats, and all rats were studied after starvation for 24 h. Carnitine was analyzed by a radioenzymatic method and by high performance liquid chromatography. RESULTS: Both BDL and RY rats had decreased plasma beta-hydroxybutyrate concentrations, whereas free fatty acid plasma concentrations were not different from control rats. Free carnitine plasma concentrations were not different between BDL or RY and control rats, whereas acetylcarnitine concentrations were decreased in BDL and RY rats, and showed a positive correlation with the plasma beta-hydroxybutyrate concentrations. In comparison to control rats, the total hepatic carnitine content was increased in BDL and RY rats, both when expressed per g tissue and per total liver. This rise in the hepatic carnitine content was due to increases in both free and acylcarnitines, including acetylcarnitine. In comparison to control rats, the hepatic concentration of beta-hydroxybutyrate was decreased in BDL and RY rats, findings compatible with impaired formation of ketone bodies from acetyl-CoA. Urinary excretion of total carnitine was not different between treated and control rats. CONCLUSIONS: Hepatic metabolism of fatty acids is impaired in BDL rats and does not recover during the 14 days after Roux-en-Y anastomosis. The increased hepatic carnitine content in BDL and RY rats can best be explained by decreased export of carnitine from the hepatocytes. The alterations in the hepatic carnitine pool and impaired hepatic fatty acid metabolism in BDL and RY rats are compatible with impaired ketogenesis.

Anastomosis, Roux-en-Y↗
PubMed1987

Glucose and fatty acid metabolism in normal and diabetic rabbit cerebral microvessels.

Rabbit cerebral microvessels were used to study fatty acid metabolism and its utilization relative to glucose. Microvessels were incubated with either [6-14C]glucose or [1-14C]oleic acid and the incorporation of radioactivity into 14CO2, lactate, triglyceride, cholesterol ester, and phospholipid was determined. The inclusion of 5.5 mM glucose in the incubation mixture reduced oleate oxidation by 50% and increased esterification into both phospholipid and triglyceride. Glucose oxidation to CO2 was reduced by oleate addition, whereas lactate production was unaffected. 2'-Tetradecylglycidic acid, an inhibitor of carnitine acyltransferase I, blocked oleic acid oxidation in the presence and absence of glucose. It did not effect fatty acid esterification when glucose was absent and eliminated the inhibition of oleate on glucose oxidation. Glucose oxidation to 14CO2 was markedly suppressed in microvessels from alloxan-treated diabetic rabbits but lactate formation was unchanged. Fatty acid oxidation to CO2 and incorporation into triglyceride, phospholipid, and cholesterol ester remained unchanged in the diabetic state. The experiments show that both fatty acid and glucose can be used as a fuel source by the cerebral microvessels, and the interactions found between fatty acid and glucose metabolism are similar to the fatty acid-glucose cycle, described previously.

Alloxan↗