scholarly journals Fatty Liver and Kidney Syndrome in Chicks I. Effect of Biotin in Diet

1976 ◽  
Vol 29 (6) ◽  
pp. 419 ◽  
Author(s):  
Judith A Pearson ◽  
AR Johnson ◽  
RL Hood ◽  
AC Fogerty
Keyword(s):  
Fatty Acids ◽  
Fatty Liver ◽  
Palmitic Acid ◽  
Palmitoleic Acid ◽  
Saturated Fatty Acids ◽  
Liver Lipids ◽  
Glucose Levels ◽  
Blood Glucose Levels ◽  
Young Parent ◽  
Liver And Kidney

Fatty liver and kidney syndrome, a disorder of young chicks, was studied under laboratory conditions. Affected chicks had enlarged livers (hepatomegaly), an increased content of lipid in the liver, and an increased level of palmitoleic acid in the liver lipids. The disorder was observed mainly in chicks from young parent flocks, and was associated either with commercial diets which were subsequently found to be low in biotin, or with specially formulated low-biotin diets. A third factor, imposition of stress, was required to initiate the disorder. There was evidence of increased lipogenesis causing an increase of triacylglycerols in the liver lipids and an increased production of saturated fatty acids, particularly palmitic acid. Increased levels of palmitoleic acid resulted from an increased desaturation of palmitic acid. Under stress, affected chicks had low blood glucose levels, suggesting that gluconeogenesis was impaired. Since biotin-dependent enzymes are involved in both gluconeogenesis and lipogenesis, it would appear that the relevant enzymes respond differently to a deficiency of biotin.

scholarly journals Fatty Liver and Kidney Syndrome in Chicks II. Biochemical Role of Biotin

1976 ◽  
Vol 29 (6) ◽  
pp. 429 ◽  
Author(s):  
RL Hood ◽  
A RJohnson ◽  
AC Fogerty ◽  
Judith A Pearson
Keyword(s):  
Fatty Liver ◽  
Pyruvate Carboxylase ◽  
Acetyl Coa Carboxylase ◽  
Defence Mechanisms ◽  
Acetyl Coa ◽  
Liver Size ◽  
Glucose Levels ◽  
Blood Glucose Levels ◽  
Liver And Kidney

The role of biotin-dependent enzymes in the fatty liver and kidney syndrome of young chicks was studied. Under conditions of a marginal deficiency of dietary biotin, the level of biotin in the liver has differing effects on the activities of two biotin-dependent enzymes, pyruvate carboxylase and acetyl-CoA carboxylase. The activity of acetyl-CoA carboxylase is increased, but when the dietary deficiency of biotin produces biotin levels which are below o� 8 p,g/g of liver, the activity of pyruvate carboxylase may be insufficient to completely metabolize pyruvate via gluconeogenesis. There is an increase in liver size and in the activities of enzymes involved in alternate pathways for the removal of pyruvate. Blood lactate accumulates and there is increased synthesis of fatty acids, and an accumulation of palmitoleic acid; these steps are accomplished by increased activities of at least the following enzymes: acetyl-CoA carboxylase, malate dehydrogenase (decarboxylating) (NADP+) and the desaturase enzyme. When the biotin level is below 0�35 p,g/g of liver and the chick is subjected to a stress, physiological defence mechanisms of the chick may be inadequate to maintain homeostasis and they finally collapse, resulting in accumulation of triacylglycerol in the liver and blood; the chick is unable to maintain blood glucose levels and death occurs, often only a few hours after the imposition of the stress.

scholarly journals Palmitic acid promotes resistin-induced insulin resistance and inflammation in SH-SY5Y human neuroblastoma

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Hamza Amine ◽  
Yacir Benomar ◽  
Mohammed Taouis
Keyword(s):  
Insulin Resistance ◽  
Fatty Acids ◽  
Palmitic Acid ◽  
Lipid Rafts ◽  
Acid Treatment ◽  
Protective Action ◽  
Saturated Fatty Acids ◽  
Membrane Lipid ◽  
Human Neuroblastoma ◽  
Peripheral Tissues

AbstractSaturated fatty acids such as palmitic acid promote inflammation and insulin resistance in peripheral tissues, contrasting with the protective action of polyunsaturated fatty acids such docosahexaenoic acid. Palmitic acid effects have been in part attributed to its potential action through Toll-like receptor 4. Beside, resistin, an adipokine, also promotes inflammation and insulin resistance via TLR4. In the brain, palmitic acid and resistin trigger neuroinflammation and insulin resistance, but their link at the neuronal level is unknown. Using human SH-SY5Yneuroblastoma cell line we show that palmitic acid treatment impaired insulin-dependent Akt and Erk phosphorylation whereas DHA preserved insulin action. Palmitic acid up-regulated TLR4 as well as pro-inflammatory cytokines IL6 and TNFα contrasting with DHA effect. Similarly to palmitic acid, resistin treatment induced the up-regulation of IL6 and TNFα as well as NFκB activation. Importantly, palmitic acid potentiated the resistin-dependent NFkB activation whereas DHA abolished it. The recruitment of TLR4 to membrane lipid rafts was increased by palmitic acid treatment; this is concomitant with the augmentation of resistin-induced TLR4/MYD88/TIRAP complex formation mandatory for TLR4 signaling. In conclusion, palmitic acid increased TLR4 expression promoting resistin signaling through TLR4 up-regulation and its recruitment to membrane lipid rafts.

Abstract MP014: Very Long Chain Saturated Fatty Acids and Diabetes Risk: Meta-Analysis of Cohort Studies in the FORCE Consortium

Circulation ◽  
2017 ◽  
Vol 135 (suppl_1) ◽  
Author(s):  
Amanda Fretts ◽  
Fumiaki Imamura ◽  
Chaoyu Yu ◽  
Alexis C Frazier-Wood ◽  
Maria Lankinen ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Palmitic Acid ◽  
Lower Risk ◽  
Fixed Effects ◽  
Meta Analysis ◽  
Arachidic Acid ◽  
Saturated Fatty Acids ◽  
Diabetes Risk ◽  
Incident Diabetes ◽  
Long Chain

Background: Circulating saturated fatty acids are biomarkers of diet and metabolism that may influence the pathogenesis of diabetes. Unlike palmitic acid (16:0), which has been extensively studied, little is known of the relationship of very long-chain saturated fatty acids (VLSFAs), with 20 carbons or more, to diabetes risk. Objective: To investigate the associations of circulating levels of VLSFA with incident diabetes. Methods: A meta-analysis was conducted within a consortium of prospective (cohort or nested case-control) studies having circulating measures of one or more VLSFAs, including arachidic acid (20:0), behenic acid (22:0) and lignoceric acid (24:0). Standardized analysis was conducted in each study using pre-specified models, exposures, outcomes, and covariates. Study-specific estimates were pooled using fixed effects meta-analysis. Results: Current findings were based on 9 participating studies, including 46,549 total participants and 13,750 incident diabetes. In multivariable-adjusted analyses, higher levels of all 3 VLSFAs were associated with lower risk of incident diabetes. Pooled RRs (95% CI) per interquintile range were 0.80 (0.71-0.90) for 20:0; 0.83 (0.76-0.91) for 22:0; and 0.70 (0.63-0.79) for 24:0, after adjustment for demographics, lifestyle factors and clinical conditions. Additional adjustments for circulating palmitic acid and triglyceride levels moved the RRs toward the null (illustrated for 24:0, in model 3 of the Figure ). Conclusions: Based on meta-analysis of results from several studies around the world, biomarker levels of VLSFA are associated with lower risk of incident diabetes, potentially mediated by effects on circulating triglycerides and 16:0.

scholarly journals Antagonism Between Saturated and Unsaturated Fatty Acids in ROS Mediated Lipotoxicity in Rat Insulin-Producing Cells

2015 ◽  
Vol 36 (3) ◽  
pp. 852-865 ◽  
Author(s):  
Wiebke Gehrmann ◽  
Wiebke Würdemann ◽  
Thomas Plötz ◽  
Anne Jörns ◽  
Sigurd Lenzen ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Oleic Acid ◽  
Palmitic Acid ◽  
Unsaturated Fatty Acids ◽  
Saturated Fatty Acids ◽  
H2o2 Production ◽  
Β Cell ◽  
Specific Expression ◽  
Insulin Producing Cells ◽  
H2o2 Formation

Background/Aims: Elevated levels of non-esterified fatty acids (NEFAs) are under suspicion to mediate β-cell dysfunction and β-cell loss in type 2 diabetes, a phenomenon known as lipotoxicity. Whereas saturated fatty acids show a strong cytotoxic effect upon insulin-producing cells, unsaturated fatty acids are not toxic and can even prevent toxicity. Experimental evidence suggests that oxidative stress mediates lipotoxicity and there is evidence that the subcellular site of ROS formation is the peroxisome. However, the interaction between unsaturated and saturated NEFAs in this process is unclear. Methods: Toxicity of rat insulin-producing cells after NEFA incubation was measured by MTT and caspase assays. NEFA induced H2O2 formation was quantified by organelle specific expression of the H2O2 specific fluorescence sensor protein HyPer. Results: The saturated NEFA palmitic acid had a significant toxic effect on the viability of rat insulin-producing cells. Unsaturated NEFAs with carbon chain lengths >14 showed, irrespective of the number of double bonds, a pronounced protection against palmitic acid induced toxicity. Palmitic acid induced H2O2 formation in the peroxisomes of insulin-producing cells. Oleic acid incubation led to lipid droplet formation, but in contrast to palmitic acid induced neither an ER stress response nor peroxisomal H2O2 generation. Furthermore, oleic acid prevented palmitic acid induced H2O2 production in the peroxisomes. Conclusion: Thus unsaturated NEFAs prevent deleterious hydrogen peroxide generation during peroxisomal β-oxidation of long-chain saturated NEFAs in rat insulin-producing cells.

scholarly journals Plasma Ceramides and Sphingomyelins in Relation to Atrial Fibrillation Risk: The Cardiovascular Health Study

2020 ◽  
Vol 9 (4) ◽  
Author(s):  
Paul N. Jensen ◽  
Amanda M. Fretts ◽  
Andrew N. Hoofnagle ◽  
Colleen M. Sitlani ◽  
Barbara McKnight ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Fatty Acids ◽  
Palmitic Acid ◽  
Cardiovascular Health ◽  
Saturated Fatty Acids ◽  
Behenic Acid ◽  
Hazard Ratio ◽  
Health Study ◽  
Cardiovascular Health Study ◽  
Long Chain

Background Ceramides exhibit multiple biological activities that may influence the pathophysiological characteristics of atrial fibrillation (AF). Whether the length of the saturated fatty acid carried by the ceramide or their sphingomyelin precursors are associated with AF risk is not known. Methods and Results Among 4206 CHS (Cardiovascular Health Study) participants (mean age, 76 years; 40% men) who were free of prevalent AF at baseline, we identified 1198 incident AF cases over a median 8.7 years of follow‐up. We examined 8 sphingolipid species: ceramide and sphingomyelin species with palmitic acid and species with very‐long‐chain saturated fatty acids: arachidic; behenic; and lignoceric. In adjusted Cox regression analyses, ceramides and sphingomyelins with very‐long‐chain saturated fatty acids were associated with reduced AF risk (ie, per 2‐fold higher ceramide with behenic acid hazard ratio, 0.71; 95% CI, 0.59–0.86; sphingomyelin with behenic acid hazard ratio, 0.60; 95% CI, 0.46–0.77). In contrast, ceramides and sphingomyelins with palmitic acid were associated with increased AF risk (ceramide with palmitic acid hazard ratio, 1.31; 95% CI, 1.03–1.66; sphingomyelin with palmitic acid hazard ratio, 1.73; 95% CI, 1.18–2.55). Associations were attenuated with adjustment for NT‐proBNP (N‐terminal pro‐B‐type natriuretic peptide), but did not differ significantly by age, sex, race, body mass index, or history of coronary heart disease. Conclusions Our findings suggest that several ceramide and sphingomyelin species are associated with incident AF, and that these associations differ on the basis of the fatty acid. Ceramides and sphingomyelins with palmitic acid were associated with increased AF risk, whereas ceramides and sphingomyelins with very‐long‐chain saturated fatty acids were associated with reduced AF risk.

Studies on Carbohydrate Metabolism in Lizards

1972 ◽  
Vol 27 (12) ◽  
pp. 1531-1535 ◽  
Author(s):  
H. S. Ali Athar ◽  
S. Nazrul Hasnain ◽  
M. Zain-Ul-Abedin
Keyword(s):  
Blood Glucose ◽  
Carbohydrate Metabolism ◽  
Mammalian Species ◽  
Liver Homogenate ◽  
Titratable Acidity ◽  
Glucose Levels ◽  
Blood Glucose Levels ◽  
Concomitant Decrease ◽  
Liver And Kidney ◽  
Reducing Capacity

1. Initial glycogen levels in the liver were found to be significantly higher than in the kidneys of the two species studied. The glycogen levels in kidney were however considerably higher than in some mammalian species.2. Total reducing capacity, true glucose, saccharoid fraction and titratable acidity increase gradually with concomitant decrease in the glycogen levels when liver and kidney homogenates of uromastix and liver homogenate of varanus were incubated for a period of 4 hours.3. Total reducing capacity, true glucose and the titratable acidity increase gradually, while the glycogen and the saccharoid fraction remain unchanged when the kidney homogenates of varanus are incubated for 4 hours.4. Total reducing capacity, true glucose and saccharoid fraction in the blood of uromastix are higher than in varanus. The blood glucose levels in both the species are higher than found in the mammals

scholarly journals Metabolic fate of oleic acid, palmitic acid and stearic acid in cultured hamster hepatocytes

1996 ◽  
Vol 316 (3) ◽  
pp. 847-852 ◽  
Author(s):  
Jennifer S. BRUCE ◽  
Andrew M. SALTER
Keyword(s):  
Fatty Acids ◽  
Oleic Acid ◽  
Fatty Acid ◽  
Stearic Acid ◽  
Palmitic Acid ◽  
Ketone Bodies ◽  
Plasma Cholesterol ◽  
Saturated Fatty Acids ◽  
Metabolic Fate ◽  
Cellular Phospholipid

Unlike other saturated fatty acids, dietary stearic acid does not appear to raise plasma cholesterol. The reason for this remains to be established, although it appears that it must be related to inherent differences in the metabolism of the fatty acid. In the present study, we have looked at the metabolism of palmitic acid and stearic acid, in comparison with oleic acid, by cultured hamster hepatocytes. Stearic acid was taken up more slowly and was poorly incorporated into both cellular and secreted triacylglycerol. Despite this, stearic acid stimulated the synthesis and secretion of triacylglycerol to the same extent as the other fatty acids. Incorporation into cellular phospholipid was lower for oleic acid than for palmitic acid and stearic acid. Desaturation of stearic acid, to monounsaturated fatty acid, was found to be greater than that of palmitic acid. Oleic acid produced from stearic acid was incorporated into both triacylglycerol and phospholipid, representing 13% and 6% respectively of the total after a 4 h incubation. Significant proportions of all of the fatty acids were oxidized, primarily to form ketone bodies, but by 8 h more oleic acid had been oxidized compared with palmitic acid and stearic acid.

EFFECTS OF SATURATED FAT IN RATS FED RAPESEED OIL

1963 ◽  
Vol 41 (1) ◽  
pp. 605-612 ◽  
Author(s):  
Joyce L. Beare ◽  
J. A. Campbell ◽  
C. G. Youngs ◽  
B. M. Craig
Keyword(s):  
Fatty Acids ◽  
Erucic Acid ◽  
Palmitic Acid ◽  
Rapeseed Oil ◽  
Unsaturated Fatty Acids ◽  
Corn Oil ◽  
Methyl Esters ◽  
Saturated Fatty Acids ◽  
Weight Gains ◽  
Similar Content

The effects of increasing the saturated fatty acids in a dietary vegetable oil composed mostly of unsaturated fatty acids were studied in rats. A mixture of palm oil and Swedish rapeseed oil fed for 4 weeks as 20% of a purified diet promoted weight gains which exceeded those obtained with Polish rapeseed oil of a similar content of erucic acid, and altered the proportion of saturated fatty acids in the tissues to reflect that of the diet. When methyl esters of saturated fatty acids were added to Swedish rapeseed oil, similar effects on weight gain were not observed, but methyl esters of fatty acids from corn oil and rapeseed oil were shown to be of less nutritional value than the original glycerides. From fatty acids of olive oil, glycerides containing 3% palmitic acid were prepared, and produced weight gains which did not differ significantly from those of rats fed Polish rapeseed oil with a similar content of palmitic acid and 20% erucic acid. The characteristic effects of rapeseed oil are, therefore, attributed to its low content of saturated fatty acids as well as its high content of erucic acid.

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