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Biomedical subjects

H J Fallon

Publications and source records attributed to H J Fallon.

At least 37 records · Page 2Linked to original sources
PubMed1978

Hepatic lipid metabolism. Age-related changes in triglyceride metabolism.

Age-related changes in hepatic triglyceride formation have been described in developing rats. Triglyceride formation was measured in vitro in the presence of [14C]glycerol-3-phosphate, palmitate, ATP, CoA, and Mg2+ by using liver homogenates and microsomal fractions derived from various age groups of animals. Triglyceride formation was most active in one-day-old rats and then decrease with age. The increase in triglyceride formation following birth was prevented by the administration of puromycin or by denying suckling. In addition, changes in plasma and hepatic triglyceride concentrations, were also determined as functions of age. These studies suggest that the age of the animal significantly influences triglyceride metabolism.

Aging↗
PubMed1978

Treatment of alcoholic hepatitis with encephalopathy. Comparison of prednisolone with caloric supplements.

A previous report from this institution demonstrated significant improvement of caloric intake and survival in patients with alcoholic hepatitis and hepatic encephalopathy given prednisolone when compared with placebo. The purpose of this study was to compare the effects of prednisolone with a regimen of 1600 calories per day without prednisolone. Fourteen patients with alcoholic hepatitis and encephalopathy were studied. All 7 on caloric supplementation and 2 of 7 given prednisolone died (p less than 0.01). These results suggest that prednisolone therapy reduces the mortality of those patients with alcoholic hepatitis and hepatic encephalopathy. This effect does not appear to be related to total caloric intake.

Adult↗
PubMed1976

Triacylglycerol biosynthesis in the adipose tissue of the obese-hyperglycaemic mouse.

Obesity in obese-hyperglycaemic mouse is associated with an increase in number and size of adipocytes. Adipocytes from the obese mouse showed increased incorporation of [14C]acetate and[14C]glucose into triacylglycerol. This increased capacity of triacylglycerol formation was correlated with increased activities of various triacylglycerol-forming enzymes measured in the microsomal fraction of adipose tissue from obese mice. Microsomal fractions from lean and obese mice contained sn-glycerol 3-phosphate acyltransferase, phosphatidate phosphohydrolase and diacylglycerol acyltransferase. Phosphatidate phosphohydrolase was also detected in the soluble fraction. In the presence of Mg2+, the phosphatidate phsophohydrolase from the soluble and the microsomal fractions was active towards membrane-bound phosphatidate. Among the three enzymes studied here, the increase in Mg2+-dependent phosphatidate phosphohydrolase was most prominent in adipose tissue of obese mice.

Acetates↗
PubMed1976

Diphenylhydantoin-induced hepatic necrosis. A case study.

A patient with post-traumatic seizure disorder developed lymphadenopathy, exfoliative dermatitis, and hepatic failure while on diphenylhydantoin therapy and died in hepatic coma. Autopsy disclosed massive hepatic necrosis. The clinical and pathological pictures are similar to the six previously reported cases of diphenylhydantoin-induced hepatic necrosis, with the exception of the time of onset of hepatic failure, which is explained. The cause of such hepatotoxicity is unknown, although hypersensitivity is postulated. It appears that studies of liver function in patients receiving diphenylhydantion are indicated to assess the true indicence of hepatocellular injury.

Adult↗
PubMed1976

The effect of high sugar intake on the esterification of dihydroxyacetone phosphate by rat liver microsomes.

Rat liver microsomes were used as an enzyme source to study dietary-induced changes in the rate of dihydroxyacetone phosphate esterification. Rats were fed (1) 75% glucose or fructose diets for various time intervals, or (2) fed a fractose diet for six days and then a chow diet. Both the glucose and fructose diets produced a 2--3-fold increase in total and neutral glycerolipid formation from dihydroxyacetone phosphate measured in the presence of ATP, palmitate, CoA, and NADH. The increased rate of dihydroxyacetone phosphate esterification and a simultaneous rise in serum triglyceride level in rats fed fructose was rapidly reversed when chow was substituted for the fructose. The results indicate that an increased rate of dihyroxyacetone phosphate esterification may contribute to the acceleration of endogenous glycerolipid biosynthesis noted under these dietary conditions.

Animals↗
PubMed1975

Studies of rat liver microsomal diglyceride acyltransferase and cholinephosphotransferase using microsomal-bound substrate: effects of high fructose intake.

Radiolabeled phosphatidate and diglyceride were prepared bound to rat liver microsomes. These compounds were used as substrates in studies of diglyceride acyltransferase, cholinephosphotransferase, and CTP:phosphatidic acid cytidylyltransferase. Optimum incubation conditions for these reactions in microsomes from normal male rats are described. High fructose diets were fed to rats for 11 days; this resulted in an increased rate of neutral lipid formation from sn-glycerol-3-phosphate by liver microsomal preparations. This was attributed, in part, to a previously reported increase in liver phosphatidate phosphatase activity. The significance of this increase is supported by the finding of a fall in microsomal phosphatidate content and a doubling in microsomal diglyceride. In addition, diglyceride acyltransferase measured with microsomal-bound diglyceride was increased twofold with no equivalent change in cholinephosphotransferase activity. Such a change should result in preferential triglyceride formation from the increased microsomal diglyceride pool. CTP:phosphatidic acid cytidylytransferase activity was depressed by the high fructose diet. These combined alterations would lead to an accelerated hepatic triglyceride formation, a result found in vivo during high fructose feeding. The high fructose diet decreased slightly the total microsomal phospholipid content and markedly depressed phosphatidylethanolamine levels.

Acyltransferases↗
PubMed1973

The effect of high-carbohydrate diets on liver triglyceride formation in the rat.

The effect of feeding diets containing 75% glucose or fructose on liver triglyceride formation in the rat was studied by both in vivo and in vitro techniques. The results were compared with those from control rats fed laboratory chow. Both high-sugar diets increased the capacity for triglyceride formation from sn-glycerol-3-P by rat liver homogenates and correspondingly increased incorporation of [1,3-(14)C]glycerol into hepatic triglyceride by the intact animal. These independent measures of hepatic triglyceride production changed with a similar time-course characteristic for each diet. The 75% fructose diet produced a greater increase in both determinations, reaching a maximum after 11 days.Despite the increase in hepatic triglyceride formation by both high-sugar diets, only the 75% fructose diet resulted in a consistent and sustained increase in serum triglyceride. This results most probably from differences in the fractional rate of serum triglyceride removal between the two groups.When serum triglyceride removal was inhibited by administration of Triton WR-1339, both high-sugar diets increased incorporation of [1,3-(14)C]glycerol in serum triglyceride in vivo and increased serum triglyceride level above that in control rats.

Animals↗
PubMed1973

Glycerolipid synthesis in rat adipose tissue. II. Properties and distribution of phosphatidate phosphatase.

The properties and subcellular distribution of phosphatidate phosphatase (EC 3.1.3.4) from adipose tissue have been investigated. The enzyme was assayed using both aqueous phosphatidate and membrane-bound phosphatidate as substrates. When measured with aqueous substrate, activity was detected in the mitochondria, the microsomes, and the soluble fraction. Mg(2+) at low concentration stimulated the phosphatidate phosphatase from soluble and microsomal fractions but had no effect on the mitochondrial phosphatidate phosphatase. At higher concentration Mg(2+) was inhibitory. In the presence of Mg(2+), the phosphatidate phosphatase from soluble and microsomal fractions was active against membrane-bound phosphatidate. No activity was demonstrated with membrane-bound substrate in the absence of Mg(2+). Mitochondria did not contain activity toward the membrane-bound substrate. The rate of utilization of aqueous phosphatidate was always higher than that of membrane-bound substrate. These results indicate that there are at least two different phosphatidate phosphatases in adipose tissue.

Adipose Tissue↗
PubMed1973

Glycerolipid biosynthesis in rat adipose tissue. I. Properties and distribution of glycerophosphate acyltransferase and effect of divalent cations on neutral lipid formation.

A sensitive radioactive assay of acyl CoA:sn-glycerol-3-phosphate-O-acyltransferase (EC 2.3.1.15) was developed to study the properties and subcellular distribution of this enzyme in rat epididymal adipose tissue. The esterification of sn-glycerol-3-phosphate was measured in the presence of palmitoyl CoA or palmitate, ATP, CoA, and Mg(2+) at pH 7.5. The presence of glycerophosphate acyltransferase was detected in both mitochondria and microsomes. The product of this reaction was identified as phosphatidate by thin-layer chromatography and dual isotope incorporation studies. Several divalent cations reduced the activity of this enzyme. Although Mg(2+) was not required for the activity of glycerophosphate acyltransferase, its addition to the incubation mixture resulted in an increased formation of neutral lipids at the expense of phosphatidate. This result is explained by an activation of microsomal phosphatidate phosphatase (EC 3.1.3.4). The effect of Mg(2+) was completely abolished by Ni(2+), Co(2+), Mn(2+), and Zn(2+). These studies suggest that the balance between Mg(2+) and several other divalent ions may be important in the regulation of neutral lipid synthesis in adipose tissue.

Acyltransferases↗
PubMed1973

Inhibition of palmitoyl CoA deacylase by chlorophenoxyisobutyrate and betabenzalbutyrate.

Palmitoyl CoA deacylase activity was measured in preparations of rat liver microsomes. Two hypolipidemic agents, chlorophenoxyisobutyrate and betabenzalbutyrate caused inhibition of palmitoyl CoA deacylase in vitro. The I(50) values for chlorophenoxyisobutyrate and betabenzalbutyrate were 5.0 and 7.5 mm, respectively. The inhibition by both agents was reversible, and both drugs lowered the palmitoyl CoA-binding capacity of microsomes. The deacylase reaction rate was maximum when the binding of palmitoyl CoA to soluble or microsomal protein was low. Addition of albumin to the reaction mixture resulted in greater binding of palmitoyl CoA to protein and a lower reaction rate. Inhibition of the deacylase by chlorophenoxyisobutyrate and betabenzalbutyrate also was greater when palmitoyl CoA was not protein bound. The inhibition of palmitoyl CoA deacylase by these hypolipidemic agents may contribute to their effects on lipid metabolism.

Albumins↗