Dietary Fatty Acids and the Control of Glucose-6-Phosphate Dehydrogenase and Malic Enzyme in the Starved-Refed Rat

Nace, C. S.; Szepesi, B.

doi:10.1093/jn/106.2.285

Cited by 25 publications

(9 citation statements)

References 14 publications

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“…No change in enzyme activities was observed, unlike earlier studies (Nace et al, 1976;Kochan et al, 1997). This could be due to the experimental animal conditions that are employed herein, and those that were reported by others.…”

Section: Resultscontrasting

confidence: 55%

“…This physiological alteration may have some advantages for survival by directing the newly-synthesized fatty acids to form triglycerides as a high-energy source; this increases weight and lipid accumulation in the liver and adipose tissues (Nace et al, 1976;Baltzell et al, 1985). Belury et al observed that CLA can modulate hepatic lipid composition in rats.…”

Section: Introductionmentioning

confidence: 99%

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Short-term Administration of Conjugated Linoleic Acid Reduces Liver Triglyceride Concentration and Phosphatidate Phosphohydrolase Activity in OLETF Rats

Rahman¹,

Huda²,

Uddin³

et al. 2002

BMB Reports

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The present study explored the short-term effects of dietary conjugated-linoleic acid (CLA) on liver lipid metabolism in starved/refed Otsuka Long Evans Tokushima Fatty (OLETF) rats. Male OLETF rats (12 weeks old) were starved for 24 hours, then refed for 48 hours with either a CLA diet [7.5% CLA and 7.5% Safflower oil (SAF)] or a SAF control diet (15% SAF). The results demonstrated a 30% reduction of hepatic triglyceride (TG) concentration in the CLA group when compared to the control group. Liver cholesterol concentration was also 26% lower in the CLA fed rats. The activity of mitochondrial carnitine palmitoyltransferase, the rate-limiting enzyme of fatty acid oxidation, was moderately elevated by 1.2-fold in the livers of the CLA group when compared to the control. In contrast, phosphatidate phosphohydrolase, the ratelimiting enzyme for TG synthesis, was found to be 20% lower in the livers of the CLA-fed rats. Therefore, dietary CLA evidently lowers liver lipid concentrations through a reduced TG synthesis and enhanced fatty acid oxidation in starved/refed OLETF rats.

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Section: Resultscontrasting

confidence: 55%

Section: Introductionmentioning

confidence: 99%

Short-term Administration of Conjugated Linoleic Acid Reduces Liver Triglyceride Concentration and Phosphatidate Phosphohydrolase Activity in OLETF Rats

Rahman¹,

Huda²,

Uddin³

et al. 2002

BMB Reports

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“…Indeed, our findings suggest there are as yet unidentified factors in serum that act to inhibit the ME response to carbohydrate induction. This finding is not surprising since serum contains factors such as glucagon, known to inhibit the induction of ME in vitro (17), and lipids that inhibit ME induction in vivo (18).…”

Section: Resultsmentioning

confidence: 92%

Glucose and triiodothyronine both induce malic enzyme in the rat hepatocyte culture: evidence that triiodothyronine multiplies a primary glucose-generated signal.

Mariash¹,

McSwigan²,

Towle³

et al. 1981

J. Clin. Invest.

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A B S T R A C T We have simulated in a cultured hepatocyte system the synergistic interaction between triiodothyronine (T3) and dietary carbohydrate in the induction of malic enzyme (ME). Kinetic studies revealed that isolated hepatocytes equilibrate with media T3 within 5 min; nuclei equilibrate with media T3 by 45 min; and the half-time of T3 metabolism was 10 h in 10% serum. We demonstrated nuclear T3 receptors in isolated hepatocytes and the induction of ME by T3 in physiological concentrations. However, in the complete absence of T3 glucose could still induce ME. At all concentrations of glucose (100-1,000 mg/dl), T3 (0.3 nM free T3) resulted in a relatively constant (1.4-to 1.7-fold) increase in ME response. The augmentation in ME activity was paralleled by an enhanced rate of enzyme synthesis as determined by [3H]leucine incorporation into immunoprecipitable ME. Cells cultured in serum free media also demonstrated a glucose-dependent increase in ME. Insulin greatly stimulated the glucose induction of ME, whereas dexamethasone had very little influence on ME induction. These studies demonstrate the usefulness of an adult hepatocyte tissue culture model for the study of the effects of T3 on gene expression in cells that are not derived from tumor. They clearly demonstrate that well established effects of T3 can be simulated in such a system at levels of free hormone that approximate those in extracellular body fluids. Our results indicate that an increased concentration of glucose per se can induce the formation of ME in the absence of alterations in extrahepatic hormones or factors. Moreover, our findings confirm inferences from in vivo studies that T3 acts as a multiplier of a glucoseinduced signal.

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“…Carbohydrate deprivation reduced T3 formation by a reduction in the hepatic content of endogenous cytosolic thiol compounds (principally GSH) (20,23), restoration of which can improve the rate of conversion in vitro (4,15). During starvation, lack of glucose substrate and decreased activity of G6PD and malate dehydrogenase result in a decrease in cytosol NADPH (1, 25,28,32). NADPH is an essential cofactor of GSH formation, which is primarily generated by HMS.…”

Section: Discussionmentioning

confidence: 99%

Correlation of Hepatic Thyroxine 5′-Monodeiodination with Hexose Monophosphate Shunt in Young Rats

Sato

Maruyama

et al. 1982

Pediatr Res

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Summarydeiodinating system through NADPH-GSH cycle. In the present study, we attempted to elucidate the changes in the two pathways The role of NADPH and glutathione (GSH) in hepatic thyroxine during maturation, and the role of NADPH and GSH in the (~4 ) 5'deiodination and possible metabolic linkage between T4 hepatic conversion of T4 to T3, by sequential determination of converting system and hexose monophosphate shunt were studied the activity of glucose-6-phosphate dehydrogenase (G6PD) (EC in young rats during maturation. activity of T4 s'd-deiodinase 1.1.1.49), glutathione reductase (GSSG-R) (EC 1.6.4.2), T4 5'-in young rats was enhanced 2-Qfold with the addition of 1 mM deiodinase and the content of GSH and glycogen in liver.NADPH and GSH in vitro, the effect of which was more prominent with NADPH than with GSH. The highest enhancement was observed at 2-3 wk of age, whereas basal T4 5'-deiodinase activity MATERIALS AND METHODS was gradually increased until 5-6 wk of age, decreasing to adult level thereafter. hi^ change was associated with a rise in csH Pregnant Wistar rats were provided with commercial rat chow and glycogen content in the liver and significantly correlated to and water ad libitum. On the 21-22nd day of pregnancy, '-I3 the changes in glutathione reductase activity (,. = 0.622, < pups were delivered from each rats. Five to eight rats from 0.00~). In contrast, glucos~phosphate dehydrogenase (G6pD) different litters were used as the source of liver at weekly intervals activity remained depressed until 5 wk of age and rose sharply up to 7 wk of age. Maternal rats served as control. Under ether thereafter. B~~~~~ T4 5,deiodinase and G6PD activities after 6 anesthesia, the liver was removed, weighed and homogenized in wk of age, an inverse correlation was noted (r = -0.749, P < 0.01).ice phosphate buffer (pH 7.0) A doseresponse relationship between triiodothyronine (T3) pro-5 mM EDTA with Teflon homogenizer. After centrifugation at duction and NADPH in vitro showed similar agerelated changes, 3000 vm for min at 40C, the supernatant was whereas dosedependency of T3 formation on GSH was decreasing used for the assays except for protein and glycogen with age, especially under the presence of 1 mM NADPH.analysis. NADP, NADPH, GSH, GSSG, glycogen, G6P, T4 and These results indicate that: (1) NADPH and GSH are important T3 were purchased from Sigma Co. cofactors of T4 conversion to T3; (2) NADPH appears to be more T4 assay. The was determined the ratelimiting in the maturational process of the system; and (3) method of C h o p (10) under the presence or the absence of I hexose monophosphate shunt plays a significant role in the regu-mM NADPH7 mM GSH and a combination of both in each lation of T4 9-monodeiodination through NADPH and GSH sample. On each assay, duplicated samples of liver homogenate formation.from an adult female rat or those from maternal rat after weaning (3 wk postpartum) were settled as control. One ml of assay mixture contained 400 pl of 20% liver homogenate, 100 p1 of T4 (10 p...

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Dietary Fatty Acids and the Control of Glucose-6-Phosphate Dehydrogenase and Malic Enzyme in the Starved-Refed Rat

Cited by 25 publications

References 14 publications

Short-term Administration of Conjugated Linoleic Acid Reduces Liver Triglyceride Concentration and Phosphatidate Phosphohydrolase Activity in OLETF Rats

Short-term Administration of Conjugated Linoleic Acid Reduces Liver Triglyceride Concentration and Phosphatidate Phosphohydrolase Activity in OLETF Rats

Glucose and triiodothyronine both induce malic enzyme in the rat hepatocyte culture: evidence that triiodothyronine multiplies a primary glucose-generated signal.

Correlation of Hepatic Thyroxine 5′-Monodeiodination with Hexose Monophosphate Shunt in Young Rats

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