Fructose-induced Hypertriglyceridemia Research Articles

Masoprocol decreases serum triglyceride concentrations in rats with fructose-induced hypertriglyceridemia

Historically, extracts of the creosote bush have been used by native healers of the Southwest region of North America to treat symptoms of type 2 diabetes. More recently, we have shown that masoprocol (nordihydroguaiaretic acid), a pure compound isolated from the creosote bush (Larrea tridentata), decreases serum glucose and triglyceride (TG) levels when administered orally in rodent models of type 2 diabetes. The present studies were undertaken to determine if masoprocol also decreases TG concentrations in rats with fructose-induced hypertriglyceridemia (HTG), a nondiabetic model of HTG associated with insulin resistance and hyperinsulinemia. Serum TG levels, which were significantly higher after rats ate a fructose-enriched (60% by weight) diet for 14 days as compared with chow-fed controls (411 v 155 mg/dL, P <.01), decreased in a stepwise fashion in fructose-fed rats treated orally with masoprocol for 4 to 8 days over a dose range of 10 to 80 mg/kg twice daily. Using the nonionic detergent Triton WR 1339 to compare TG secretion rates in masoprocol- and vehicle-treated rats, masoprocol at a dose of 40 or 80 mg/kg twice daily, significantly reduced hepatic TG secretion (P<.01) and liver TG content (P<.001), whereas lower doses of masoprocol decreased serum TG without an apparent reduction in hepatic TG secretion. Administration of Intralipid (a fat emulsion) showed that the half-time for removal of TG from serum was also shorter in masoprocol-treated rats versus vehicle-treated controls (31 v 64 minutes, P<.05). In addition adipose tissue lipoprotein lipase (LPL) activity was increased in masoprocol-treated rats and adipose tissue hormone-sensitive lipase (HSL) activity was decreased. We conclude that masoprocol administration to rats with fructose-induced HTG results in lower serum TG levels associated with reduced hepatic TG secretion and increased peripheral TG clearance.

Masoprocol decreases rat lipolytic activity by decreasing the phosphorylation of HSL.

Masoprocol (nordihydroguaiaretic acid), a lipoxygenase inhibitor isolated from the creosote bush, has been shown to decrease adipose tissue lipolytic activity both in vivo and in vitro. The present study was initiated to test the hypothesis that the decrease in lipolytic activity by masoprocol resulted from modulation of adipose tissue hormone-sensitive lipase (HSL) activity. The results indicate that oral administration of masoprocol to rats with fructose-induced hypertriglyceridemia significantly decreased their serum free fatty acid (FFA; P < 0.05), triglyceride (TG; P < 0.001), and insulin (P < 0.05) concentrations. In addition, isoproterenol-induced lipolytic rate and HSL activity were significantly lower (P < 0.001) in adipocytes isolated from masoprocol compared with vehicle-treated rats and was associated with a decrease in HSL protein. Incubation of masoprocol with adipocytes from chow-fed rats significantly inhibited isoproterenol-induced lipolytic activity and HSL activity, associated with a decrease in the ability of isoproterenol to phosphorylate HSL. Masoprocol had no apparent effect on adipose tissue phosphatidylinositol 3-kinase activity, but okadaic acid, a serine/threonine phosphatase inhibitor, blocked the antilipolytic effect of masoprocol. The results of these in vitro and in vivo experiments suggest that the antilipolytic activity of masoprocol is secondary to its ability to inhibit HSL phosphorylation, possibly by increasing phosphatase activity. As a consequence, masoprocol administration results in lower serum FFA and TG concentrations in hypertriglyceridemic rodents.

Hypolipidaemic and Antioxidant Activity of Diallyl Disulphide in Rats

The efficacy of diallyl disulphide (DADS), a constituent of garlic oil, as a hypolipidaemic and antioxidant agent was evaluated in rats. In normolipidaemic rats DADS, at doses ranging from 10 to 50 mg kg−1, decreased plasma triglyceride without affecting cholesterolaemia and fast-or noradrenaline-induced lipolysis. DADS proved effective in reducing fructose-induced hypertriglyceridaemia and dietary hypercholesterolaemia in rats, in the latter model DADS significantly raised both the HDL cholesterol and the HDL/VLDL + LDL cholesterol ratio. DADS proved ineffective on triton induced hyperlipidaemia. To gain insight into the antioxidant effect of DADS, hepatic and cardiac antioxidant enzyme activity and glutathione content were studied in rats fed on a high diet and DADS. The antioxidant enzyme activity was significantly enhanced whereas glutathione content was markedly restored in rats fed on a high fat diet simultaneously with DADS. Thus, it appears that DADS exert antioxidant protection by activating the associated antioxidant enzymes.

Acetaminophen-Induced Hepatorenal Toxicity in High Fructose Diet-Fed Rats Is Sex-Dependent.

Male rats with fructose-induced hypertriglyceridemia become resistant to hepatotoxicity and more susceptible to nephrotoxicity of acetaminophen (APAP) as compared with normal male rats. To determine whether changes in APAP toxicity by fructose-treatment were sex-dependent, male and female rats were fed standard diet (non-pretreated rats) or high fructose diet (fructose-pretreated rats) for 3 weeks and then given a single ip dose of APAP at 800 mg/kg. At 24 hours after APAP dosing, they were sacrificed and examined histopathologically. Non-pretreated males showed severe hepatic lesions characterized by centrilobular hepatocyte necrosis and slight renal lesions characterized by single cell necrosis in the proximal straight tubules, while females showed no hepatic lesions and milder renal lesions than males. APAP-induced hepatotoxicity was prevented and APAP-induced nephrotoxicity was potentiated in fructose-pretreated males. In contrast, no apparent changes on APAP-induced toxicity were seen in fructose-pretreated females. Castration partially prevented such enhancement of APAP-induced nephrotoxicity in fructose-pretreated males. Furthermore, castration and estradiol treatment had greater protective effect against the enhancement of APAP-induced nephrotoxicity in fructose-pretreated males as compared with castration alone. Ovariectomy potentiated the enhancement of APAP-induced nephrotoxicity in females. These results indicate that the changes in APAP-induced hepatorenal toxicity by fructose-pretreatment are sex-dependent.

Effects of fructose-induced hypertriglyceridemia on hepatorenal toxicity of acetaminophen in rats: Role of pharmacokinetics and metabolism of acetaminophen

Fructose-induced hypertriglyceridemic rats become resistant to hepatotoxicity and susceptible to nephrotoxicity of acetaminophen (APAP), as compared with normal ones. The present study was designed to test the hypothesis that alterations in the distribution of APAP and in the intrinsic susceptibility to toxicants are responsible for the alteration in hepatorenal toxicity of APAP in fructose-induced hypertriglyceridemic rats. Following APAP-administration (750 mg/kg, i.p.), fructose-pretreated rats (25% fructose in drinking water for 5 weeks) showed nephrotoxicity of APAP more promptly and more severely than normal ones. Renal APAP-concentrations at the early phase (15 and 30 min. after APAP-administration) were significantly greater in fructose-pretreated rats than those in normal ones. Plasma and hepatic APAP concentrations in fructose-pretreated rats were greater than those in normal ones only at the later phase (plasma; 6 hr, liver; 6 and 12 hr after APAP-administration). There were no significant differences in the APAP-induced depletion of hepatic and renal glutathione and in the basal hepatic and renal cytochrome P-450 contents between these rats. Fructose-pretreated rats were also more susceptible to p-aminophenol (PAP), a nephrotoxic metabolite of APAP, than normal rats. Therefore, enhanced susceptibility to APAP-nephrotoxicity in fructose-pretreated rats may be due, at least in part, to increased renal APAP concentration and increased intrinsic susceptibility to the metabolic nephrotoxicant.

Effects of fructose-induced hypertriglyceridemia on hepatorenal toxicity of acetaminophen in rats: II. Role of enhancement of fructose metabolism and overproduction of triglyceride in the liver and kidney on hepatorenal toxicity of acetaminophen

Fructose-induced hypertriglyceridemic rats are resistant to hepatoxicity and susceptible to nephrotoxicity of acetaminophen (APAP) as compared with normal ones. The present studied were designed to evaluate how fructose-treatment affects the developmental mode of hepatorenal toxicity of APAP. First, following fructose-pretreatment for various durations (1 day, 1 week or 3 weeks), 1-day-fructose-pretreatment induced hypertriglyceridemia and enhancement of APAP-nephrectoxicity simultaneously. However, it took at least 3 weeks for fructose-pretreatment to reduce APAP-hepatotoxicity. Second, following fructose, sucrose or glucose-pretreatment for 3 weeks, fructose-pretreated rats showed marked hypertriglyceridemia and modification of APAP-hepatorenal toxicity. Sucrose-pretreated rats showed less effects than fructose-pretreated rats. Glucose-pretreated rats showed no changes in plasma triglyceride and APAP-hepatorenal toxicity. Third, rats with hypertriglyceridemia induced by olive oil or Triton WR-1339 which did not produce enhanced metabolism and triglyceride-overproduction in the liver and kidney showed no modification of APAP-hepatorenal toxicity. Pretreatment of glycerol which was metabolized in liver and kidney and induced an overproduction of triglyceride resulted in an enhancement of APAP-nephrotoxicity. These results indicate that an enhancement of fructose metabolism and an overproduction of triglyceride in liver and kidney are responsible for the modification of APAP-hepatorenal toxicity in fructose-induced hypertriglyceridemic rats.

Dietary oligofructose modifies the impact of fructose on hepatic triacylglycerol metabolism

The aim was to investigate if chronic feeding with oligofructose (OFS), a nondigestible fructan that decreases triacylglycerol-very-low-density lipoproteins (TAG-VLDLs) in the serum of rats by reducing hepatic de novo lipogenesis, could counteract the impact of fructose on TAG metabolism. Male Wistar rats fed a standard diet supplemented or not with 10% OFS for 30 days received either tap water or a 10% fructose drinking solution for 48 hours. TAG, phospholipids (PLs), cholesterol, and free fatty acids were assayed both in serum and in liver. Fatty acid de novo synthesis, esterification, and β-oxidation were assessed in the liver by measuring the activity of key enzymes: fatty acid synthase (FAS), phosphatidate phosphohydrolase (PAP), glycerol-3-phosphate acyltransferase (GPAT), and carnitine palmitoyltransferase-I (CPT-I), respectively. The acute load of fructose increased (1) both liver and serum TAG without affecting other lipids, and (2) de novo fatty acid synthesis and esterification, through induction of FAS and PAP without affecting CPT-I. Long-term feeding with OFS protected rats against liver TAG accumulation induced by fructose. The lower lipogenic capacity of the liver could be the key event in this protection, since even after the fructose load FAS activity remained significantly lower in OFS-fed rats. However, despite its protective effect on the liver, OFS was not able to prevent fructose-induced hypertriglyceridemia, suggesting that OFS feeding could not counteract the fructose-induced defect in TAG-VLDL clearance.

Partial characterization of the fructose-induced defect in very-low-density lipoprotein triglyceride metabolism

Very-low-density lipoprotein triglyceride (VLDL-TG) catabolism was studied in rats receiving either fructose or glucose as a 10% drinking solution. Consumption of either of the hexoses for 16 hours significantly elevated postheparin plasma (PHP) lipoprotein lipase (LPL) activity compared with normal control animals. Prolonged feeding of the carbohydrates for 14 days abolished the higher LPL activities, which were similar to control levels. PHP hepatic lipase (HL) activity was significantly reduced in carbohydrate-fed rats compared with control animals despite the duration of feeding. The kinetic parameters K m and V max cannot be obtained with lipoproteins and so the first-order rate constant ( k1) of triglyceride hydrolysis was used to asses the effectiveness of VLDL-TG as substrates for endothelial lipases. VLDL-TG from fructose and VLDL-TG from glucose donors was lipolyzed with PHP LPL and HL from normal rats. The k1 (fraction of VLDL-TG lipolyzed) of VLDL-TG was found to be lower when donors had been fed fructose compared with VLDL that had come from glucose-fed donors. Rates of VLDL-TG removal from fructose and glucose donors were determined simultaneously in perfused livers of normal control, fructose-fed, and glucose-fed animals. Livers of fructose-fed animals cleared VLDL-TG at a slower rate than livers from glucose-fed or control rats. VLDL-TG from fructose-fed rats was cleared less effectively than VLDL-TG from glucose-fed rats in livers of both control and glucose-fed animals. We conclude that an impairment in the ability of fructose-fed rats to hydrolyze VLDL-TG, and of their livers to remove VLDL-TG, may in part explain fructose-induced hypertriglyceridemia.

Interaction of dietary carbohydrate and fat in the regulation of hepatic and extrahepatic lipogenesis in the rat.

1. In order to examine the interaction of dietary fat and carbohydrate in the regulation of lipid metabolism, we have studied hepatic and extrahepatic lipogenesis, and adipose tissue lipoprotein lipase (EC 3.1.1.34) in rats fed on one of the following diets: a fructose-based diet containing 0 (F0) or 150 g maize oil (F15)/kg, or a glucose-based diet containing 0 (G0) or 150 g maize oil (G15)/kg. 2. The rats were meal-fed on the diets for 2 weeks after which the activities of a number of hepatic 'lipogenic' enzymes were measured and the activity of epididymal-fat-pad lipoprotein lipase. The activities of the lipogenic enzymes were: F0 greater than G0 greater than G15 greater than F15. Lipoprotein lipase activity was F0 = G0 = F15 = G15. The percentage of total body fatty acid synthesis which occurred in the liver was F0 greater than G0 greater than F15 greater than G15. 3. We conclude that fructose-induced hypertriglyceridaemia is primarily a result of the increased hepatic synthesis rather than decreased adipose-tissue lipoprotein lipase activity.

Reduction of fructose-induced hypertriglyceridemia and fatty liver in rats by 4-(4'-chlorobenzyloxy)benzyl nicotinate (KCD-232).

The effect of KCD-232, a new compound with a structure of 4-(4'-chlorobenzyloxy)benzyl nicotinate, on fructose-induced hypertriglyceridemia and fatty liver was studied in rats refed experimental diets for 3 days after having been starved for 2 days. In younger or older rats refed 7% corn oil-containing diets, both the serum and livertriglyceride (TG) levels were higher in the fructose (F) group than in the glucose (G) group, and those of the F group were higher in the older rats than the younger rats. KCD-232effectively inhibited fructose-induced hypertriglyceridemia and fatty liver in both the younger and older rats. In older rats refed 7% corn oil diets, an increase in hepatic fatty acid (FA) synthesis and decreases in the activities of hepatic TG lipase (HTGL) and adipose tissue lipoprotein lipase (LPL) were found in the F group, while the serum free FA level and hepatic FA oxidative activity of the F group were equal to those of the G group. KCD-232 strongly inhibited the fructose-enhanced FA synthesis, slightly repressed the fructose-suppressed HTGLactivity and had no effect on LPL activity and FA oxidation. These results suggest that fructose-induced hypertriglyceridemia and fatty liver are due to an enhanced hepatic FA synthesis and decreased hydrolytic activities required for TG clearance from the circulation system and that KCD-232 prevents them by inhibiting enhanced FA synthesis.

Experimental studies on the hypolipidemic activity of chloridarol

The efficacy of chloridarol (2-benzofuryl-p-chlorophenyl carbinol) as hypolipidemic agent was evaluated in rats and rabbits. In normolipidemic rats chloridarol, at doses ranging from 50 to 200 mg/kg/day, decreased plasma triglycerides without affecting cholesterolemia and fast- or norepinephrine-induced lipolysis. The drug proved effective in reducing fructose-induced hypertriglyceridemia and dietary hypercholesterolemia in rats; in the latter model chloridarol significantly raised both the HDL cholesterol and the HDL/VLDL + LDL cholesterol ratio. In hyperlipidemic rabbits the drug had no effect on plasma cholesterol, but it lowered triglyceridemia. The action of chloridarol on rat liver ultrastructure was also investigated. Treatment for one month induced peroxisome proliferation, less marked, however, than that elicited by clofibrate; after a prolonged chloridarol treatment (9 months), this effect had almost completely disappeared and the ultrastructure of the hepatocytes was close to that of controls.

Studies of the mechanism of fructose-induced hypertriglyceridemia in the rat

Carbohydrate-induced hypertriglyceridemia is easily produced in the rat, and fructose has been shown to be particularly potent in this regard. In this study we have compared the effects of feeding rats diets high (66% of total calories) in fructose or glucose on various aspects of carbohydrate and lipid metabolism. The results confirmed previous observations that fructose (456 ± 276 mg/dl) was more potent ( p < 0.001) in raising plasma TG concentration than was glucose (242 ± 13 mg/dl), and indicated that the difference in magnitude of hypertriglyceridemia produced by the two carbohydrates was closely related to the ability of the test diets to increase VLDL-TG secretion ( r = 0.85, p < 0.001). Both glucose and fructose feeding led to comparable degrees of hyperinsulinemia, and plasma TG concentrations increased before hyperinsulinemia evolved in fructose-fed rats. Therefore, it was concluded that fructose can act directly on the liver to increase VLDL-TG secretion, and that fructose-induced hypertriglyceridemia can occur in the absence of hyperinsulinemia. On the other hand, the rise in plasma TG concentration produced by fructose was reduced dramatically in exercise-trained rats, and this was associated with a decrease in plasma insulin concentration. Based upon these observations, we suggest that fructose feeding produces hypertriglyceridemia by directly stimulating hepatic VLDL-TG secretion, as well as by producing insulin resistance and hyperinsulinemia, and that it is the combined effect of these two separate actions which accounts for the magnitude of fructose-induced hypertriglyceridemia.

Hyperinsulinemia in fructose-induced hypertriglyceridemia in the rat

Rats were fed diets containing (as percent of calories) 66% glucose or fructose, 22% casein, and 12% lard, for 1 wk. The effects of these diets on plasma triglyceride, glucose, and insulin concentrations were compared to those of control rats eating regular rat chow. Plasma triglyceride levels increased from a mean (± SE) control level of 85 ± 7 to 142 ± 9 ( p < 0.001) and 380 ± 38 ( p < 0.001) mg/dl in dextrose- and fructose-fed rats, respectively. Plasma insulin concentrations demonstrated a similar increase, rising from a mean (± SE) control value of 29 ± 4 μU/ml to 55 ± 10 μU/ml in dextrose-fed rats and to 85 ± 12 μU/ml in rats eating the fructose diet. Plasma glucose concentrations of the three groups were comparable. These results indicate that fructose-induced hypertriglyceridemia is associated with significant hyperinsulinemia.

Effect of clofibrate and gemfibrozil on the activities of mitochondrial carnitine acyltransferases in rat liver dose-response relations

The effects of different doses of clofibrate and gemfibrozil on liver size, serum triglyceride concentration and the activities of hepatic mitochondrial α-glycerophosphate dehydrogenase (α-GPD) and carnitine acyltransferases were studied in male rats. Both clofibrate and gemfibrozil treatment effectively decreased the fructose-induced hypertriglyceridaemia and increased the liver to body weight ratio. Clofibrate treatment also induced an increase of many times in the activities of mitochondrial α-GPD and carnitine acyltransferases, the effect increasing with the dose used. The effect of gemfibrozil on the activities of the enzymes was significantly smaller. There was no correlation between the decrease in serum triglyceride concentration and the changes in the activities of the enzymes. Only clofibrate increased the rate of fatty acylcarnitine oxidation in isolated mitochondria. It is concluded that both drugs increased the size of the rat liver, but that only clofibrate influenced the mitochondrial enzyme activities studied. The data give indirect evidence that the increase in the activities of mitochondrial carnitine acyltransferases and the accelerated mitochondrial oxidation of fatty acids are not the mechanisms by which these drugs lower serum lipid levels.

Palmitate and glucose oxidation by diaphragm of rats with fructose-induced hypertriglyceridemia

Palmitate and glucose oxidation were investigated in isolated hemidiaphragm of rats in which hypertriglyceridemia was induced by dietary fructose. Palmitate oxidation was increased, and glucose oxidation was reduced, in fructose-fed rats, as compared with glucose-fed controls. Glucose incorporation into muscle glycogen was similar in both dietary groups.

Effect of Dietary Fructose on Free Fatty Acid Release from Adipose Tissue and Serum Free Fatty Acid Concentration in the Rat

The administration of a diet, containing 70 cal% of fructose, increases in rats, as compared with a diet containing 70 cal% of glucose, the release of free fatty acids (FFA) from adipose tissue in vitro. Since the glycerol release from adipose tissue is not increased by the high fructose diet, it may be concluded that the enhanced FFA release in the fructose group is due to a reduced re-esterification of FFA in adipose tissue rather than to an enhanced hpolysis. The serum concentrations of FFA are increased by fructose intake temporarily (for the first week of the diet administration), the increased FFA release from adipose tissue being present up to 1 month after starting the diet. The reduced re-esterification of FFA in fructose-fed rats is probably connected with the reduced glucose utilization in adipose tissue. None of the described effects of the fructose diet seems to result from insulin deficiency since no difference was found in the serum insulin concentrations between the groups on the fructose and glucose diet. It is speculated whether the enhanced FFA release from adipose tissue in rats fed the fructose diet may participate in the mechanism of fructose-induced hypertriglyceridaemia.

Effects of high-carbohydrate diets on lipid and carbohydrate metabolism in the rat.

ARTICLESEffects of high-carbohydrate diets on lipid and carbohydrate metabolism in the ratRP Eaton, and DM KipnisRP Eaton, and DM KipnisPublished Online:01 Oct 1969https://doi.org/10.1152/ajplegacy.1969.217.4.1160MoreSectionsPDF (2 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByMolecular aspects of fructose metabolism and metabolic diseaseCell Metabolism, Vol. 33, No. 12A 72-hour high fat diet increases transcript levels of the neuropeptide galanin in the dorsal hippocampus of the rat11 August 2015 | BMC Neuroscience, Vol. 16, No. 1Modulation of insulin secretion by feeding behavior and physical activity: Possible beneficial effects on obese and aged ratsNeuroscience & Biobehavioral Reviews, Vol. 20, No. 2Effect of troglitazone (CS-045) and bezafibrate on glucose tolerance, Liver Glycogen synthase activity, and β-oxidation in fructose-fed ratsMetabolism, Vol. 44, No. 12Effect of sucrose diet on expression of apolipoprotein genes A-I, C-III and A-IV in rat liverAtherosclerosis, Vol. 95, No. 2-3Insulin secretion to glucose stimulus in pancreatic islets isolated from rats fed unbalanced dietsPhysiology & Behavior, Vol. 50, No. 4Effect of Sucrose Diet on Apolipoprotein Biosynthesis in Rat LiverJournal of Biological Chemistry, Vol. 264, No. 2Health AspectsEffect of high sucrose diet on insulin secretion and insulin action: a study in the normal ratDiabetologia, Vol. 30, No. 4Effect of diet on glucose tolerance and insulin response in chemically diabetic ratsMetabolism, Vol. 31, No. 12Studies of the mechanism of fructose-induced hypertriglyceridemia in the ratMetabolism, Vol. 31, No. 11Hyperinsulinemia in fructose-induced hypertriglyceridemia in the ratMetabolism, Vol. 29, No. 4Characterization of a model of dietary-induced hypertriglyceridemia in young, nonobese rats.Journal of Lipid Research, Vol. 20, No. 3Influence of fructose feeding on individual enzymic reactions in the formation and metabolism of bile acids in rat liver homogenates10 January 2017 | British Journal of Nutrition, Vol. 36, No. 2Effect of qualitatively different carbohydrates on lipoprotein spectrum and composition of blood lipidsBulletin of Experimental Biology and Medicine, Vol. 81, No. 4Alterations in levels and interrelations of plasma apolipoproteins induced by dietMetabolism, Vol. 25, No. 3Mammalian Low Density LipoproteinsLipoproteins in AnimalsDrugs, lipids and atherosclerosisPharmacological Research Communications, Vol. 7, No. 2DECREASED GLUCAGON ACTIVITY: A MECHANISM FOR GENETIC AND ACQUIRED ENDOGENOUS HYPERLIP&#xC6;MIAThe Lancet, Vol. 304, No. 7896Kohlehydrat- und Palmitinsäurestoffwechsel am Myokard der Ratte bei HypoxieBasic Research in Cardiology, Vol. 68, No. 3Hypolipemic action of glucagon in experimental endogenous lipemia in the ratJournal of Lipid Research, Vol. 14, No. 3Plasma pre-α-lipoproteins in ethionine induced fatty liver in ratsExperientia, Vol. 29, No. 4Effects of high sucrose diets and 4-aminopyrazolopyrimidine on serum lipids and lipoproteins in the ratJournal of Lipid Research, Vol. 12, No. 5Utilization of exogenous free fatty acids for the production of very low density lipoprotein triglyceride by livers of carbohydrate-fed ratsJournal of Lipid Research, Vol. 12, No. 5The effect of prolonged fasting and of glucose refeeding on rat serum and liver lipid levelsLipids, Vol. 6, No. 5Intermediary Aspects and Tissue Interactions of Ruminant Fat MetabolismJournal of Dairy Science, Vol. 54, No. 4Co-induction of the hepatic amino acid transport system and tyrosine aminotransferase by theophylline, glucagon and dibutyryl-cyclic AMPLife Sciences, Vol. 9, No. 19Synthesis of Phospholipids and Triglycerides in Human Liver Slices8 July 2009 | Scandinavian Journal of Clinical and Laboratory Investigation, Vol. 26, No. 4 More from this issue > Volume 217Issue 4October 1969Pages 1160-1168 Copyright & PermissionsCopyright © 1969 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1969.217.4.1160PubMed5824318History Published online 1 October 1969 Published in print 1 October 1969 Metrics