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Biomedical subjects

E C Larkin

Publications and source records attributed to E C Larkin.

At least 37 records · Page 2Linked to original sources
PubMed1989

Reversal by glucose of pancreatic amylase insufficiency in chronic alcoholic rats.

Carbohydrate consumption regulates pancreatic amylase synthesis in rats. The Lieber-DeCarli 36% alcohol diet employed in chronic alcohol studies and the isocaloric control diet contain 11 and 47% of total calories from carbohydrates, respectively. Young rats fed ad libitum the 36% ethanol diet for 2 weeks obtained 1.2 g/day of carbohydrate, whereas those pair-fed with control diet received 5.8 g/day. Rats fed the 36% ethanol diet and given an intramuscular injection of a solution of 1.5 g of glucose daily for 2 weeks received twofold greater amounts of carbohydrate than saline-injected controls (2.7 versus 1.2 g). These changes in carbohydrate intake produced proportionate changes in pancreatic amylase levels. The secretory responses to cholecystokinin-octapeptide (CCK8) of acini from control and glucose-injected rats were significantly higher compared with those in the saline-injected or noninjected alcohol groups. The blood alcohol levels in glucose-injected rats were markedly reduced compared with other alcohol groups (71.7 versus 274.9 mg/dl) despite similar amounts of ethanol ingestion daily (2.4 g) in the three groups. In vitro experiments with acini from rats fed a nutritionally optimal diet revealed that high pharmacologic concentrations of ethanol, while inducing basal secretion, inhibited CCK8-stimulated amylase secretion. These results indicate that: (a) the amount of alcohol consumption does not correlate with either the levels of blood alcohol or of pancreatic amylase; (b) the carbohydrate availability in rats regulates pancreatic amylase levels despite significant levels of alcohol in blood; (c) blood alcohol levels observed in vivo may not affect synthetic and secretory processes of amylase in pancreatic acini.

Alcoholism↗
PubMed1989

Regulation of pancreatic amylase by dietary carbohydrate in chronic alcoholic rats.

The nutritional adequacy of dietary ingredients is essential for optimal food consumption and growth of animals. Dietary carbohydrate levels regulate pancreatic amylase synthesis. Ethanol diets with 36% of total calories from ethanol and 11% from carbohydrate are nutritionally inadequate, whereas a 26% ethanol diet made isocaloric to the 36% alcohol diet by the addition of maltose-dextrins provides all nutrients in amounts recommended for normal growth. Young rats fed the modified ethanol diet for 3 months consume 101.4 ml of diet daily compared to 66.5 ml by those on the 36% ethanol diet. Increased food consumption results in (a) similar amounts of alcohol consumption (3.6 vs. 3.3 g/day), (b) a threefold enhancement in carbohydrate intake (5.1 vs. 1.7 g/day), and (c) a normal growth rate (6.7 vs. 3.1 g/day). Both the acinar content of amylase (20.2 +/- 0.3 micrograms/mg of protein) and the acinar response to cholecystokinin-octapeptide in 36% ethanol diet-fed rats are significantly reduced compared to those of 26% ethanol diet-fed rats (34.1 +/- 5.6 micrograms/mg of protein). These results confirm (a) the nutritional adequacy of the 26% ethanol diet compared to the 36% ethanol diet, and (b) that carbohydrate inadequacy, and not ethanol consumption per se, is the primary cause of pancreatic amylase insufficiency in chronic alcoholic rats.

Alcoholism↗
PubMed1988

Is malnutrition necessary for the development of alcoholic fatty liver in the rat?

Ingestion of various liquid diets containing 36% calories as ethanol and 35% calories as fat does not provide adequate nutrition to young growing rats. Studies conducted with the aforementioned diets have the effects of malnutrition confounded with those of alcohol administration. Feeding a 26% alcohol liquid diet, which results in adequate nutrient intake with the same level of alcohol ingestion as the 36% alcohol diet, does not result in fatty liver development in the rat. The concept that prevailed for 25 years that fatty liver is caused despite adequate nutrition and hence is due to alcohol alone is therefore erroneous.

Animals↗
PubMed1986

Ozone and the peroxidation of polyunsaturated fatty acids in vivo.

Two experiments were carried out to determine whether ozone causes significant oxidation of pulmonary polyunsaturated fatty acids in vivo. These involved ad libitum and pair-feeding. In the first experiment, rats were fed fat-free diets and exposed to ozone for 0, 1, 2, and 4 weeks. Lung and liver fatty acids were analyzed to determine if the rats exposed to ozone lost essential fatty acids more rapidly than those exposed to filtered air. In the second experiment, rats were divided into four groups. Two of these groups were fed fat-free diets, and two were fed diets containing essential fatty acids. Rats from the two diet groups (one of each type) were exposed to ozone, while the remaining two groups were exposed to filtered air. In the second experiment, rats were pair-fed. The amounts of lung and liver fatty acids were relatively uninfluenced by breathing ozone. Results from these experiments demonstrate that in the lung, the polyunsaturated fatty acids, linoleic and arachidonic acids, appear to be oxidized by filtered air and ozone at essentially the same rate.

Animals↗
PubMed1986

Effect of prenatal iron deficiency on myelination in rat pups.

In this study, a histopathologic examination of the brain from iron-deficient or iron-supplemented rat pups was carried out. Pups were obtained from female rats, which were fed an iron-deficient or iron-supplemented diet during both pregnancy and lactation. Immediately after anesthesia and the collection of blood, pups were fixed by intracardiac infusion of 2% glutaraldehyde. Brain and cervical spinal cord were fixed, embedded in paraffin, and cut at 6-mu thickness. Myelin was identified using Luxol fast blue stain. As compared with controls (hematocrit, 30.8%), 11-day-old iron-deficient pups (hematocrit, 11.9%) showed reduced myelination in the spinal cord. Although myelination increased somewhat in the iron-deficient 17-day-old pups (hematocrit, 8.5%), the amount of myelin in the spinal cord and white matter of cerebellar folds was reduced as compared with that of the corresponding controls. These observations show the importance of prenatal iron adequacy in myelinogenesis.

Anemia, Hypochromic↗
PubMed1986

Biologic effects of chronic ethanol consumption related to a deficient intake of carbohydrates.

Our present understanding of the many effects of chronic ethanol consumption originated mostly from the use of an experimental model in which animals were maintained on a liquid diet that provided 36% of the total calories as alcohol. Since this diet was considered to be nutritionally adequate, a concept developed that the observed effects were due to the toxicity of alcohol and its metabolites rather than malnutrition. However, several biologic effects can be attributed to a reduced carbohydrate ingestion that accompanies chronic alcohol consumption.

Alcoholism↗
PubMed1985

Cholecystokinin-induced secretion and synthesis of amylase and cationic trypsinogen by pancreatic acini isolated from rats given an ethanol diet.

Effects of chronic alcohol intake on secretion and synthesis of amylase and cationic trypsinogen (CT) were studied with pancreatic acini isolated from male Sprague-Dawley rats fed a Lieber-DeCarli ethanol or control diet for 30 days. Pancreatic acini were incubated in a media containing increasing concentrations of cholecystokinin octapeptide (CCK-8: 0-1000pM) followed by addition of [3H]leucine. Amylase and CT secreted in the media and those labeled in acini were quantitated. Basal and CCK-stimulated secretion of CT was not different in alcoholic and control groups. On the other hand, a dose-response curve of CCK-stimulated amylase secretion from alcoholic acini was markedly reduced with both basal and maximal secretion decreased to only 40% of controls. Basal incorporation of [3H]leucine into amylase was reduced by 70% in alcoholic acini compared to controls while that into CT was not different in the two groups. CCK-8 exhibited a biphasic effect on [3H]leucine incorporation into both enzymes in alcoholic acini: low concentrations of CCK-8 (less than 100pM) increased the incorporation whereas high concentrations (greater than 100pM) decreased it. However, in control acini, CCK-8 induced progressive suppression of the incorporation into these enzymes, the pattern of which was similar to that previously observed in fasted rats (Am. J. Physiol. 241:G116-G112, 1981). This difference in the response pattern resulted in significantly higher rates of CCK-8 induced incorporation into CT in alcoholic acini. These results suggest that the differences observed may possibly be attributable not only to alcohol intake but also to the differences in carbohydrate intake and in temporal patterns of diet consumption.

Amylases↗
PubMed1985

Comparison of the thin layer chromatography/flame ionization detection system with other methods for the quantitative analysis of liver lipid contents in alcohol-fed rats and controls.

In this study, we have examined the feasibility of using the Thin Layer Chromatography/Flame Ionization Detection (TLC/FID) system to evaluate the lipid content of alcohol-induced fatty liver by comparing the results with those from other methods. Various amounts of standards (tripalmitin, phosphatidylcholine and cholesterol) were spotted on Chromarods and scanned either with or without development in a solvent system. The detector responses were significantly greater when the spots were not developed. From the results with developed rods, conversion factors (amount/area) were calculated. These were used for the quantitative analysis of the liver lipids from rats fed a Lieber-DeCarli ethanol diet or a control diet for four weeks. The triglyceride (TG), phospholipid (PL), cholesterol (CH) and cholesterol ester (CE) contents (65.9, 25.4, 2.9 and 6.8 mg/g, respectively) obtained by the TLC/FID system were similar to those observed by other methods (67.9, 27.6, 3.0 and 8.3 mg/g, respectively). The liver lipid content in control rats also was similar to that obtained by other methods (TG, 19.0 vs 20.6; PL, 24.2 vs 21.8, CH, 2.1 vs 2.1 and CE, 1.8 vs 2.6 mg/g). Thus, the magnitude of changes in liver lipid levels due to chronic alcohol ingestion obtained by alternate methods also was found with TLC/FID. The TLC/FID system provides a convenient method for rapid analysis of the extent of fatty liver in alcohol-fed animals.

Animals↗
PubMed1985

Changes in lipids of lung lavage in monkeys after chronic exposure to ambient levels of ozone.

A group of 8 sub-adult bonnet monkeys (Macaca radiata) was exposed to 0.3 ppm ozone (O3) and another group of 7 monkeys to 0.15 ppm O3 for 8 h/day for 90 days. A third group of 4 monkeys was exposed to 0.15 ppm O3 for 8 h/day for 21 days. The control group consisted of 7 monkeys which breathed filtered air for 90 days. Levels of linoleic and arachidonic acids in the total lipids from lung lavage increased about 2-fold in those exposed to O3 as compared to the levels in the controls. Furthermore, the relative level of cholesterol ester (CE) decreased and phosphatidylcholine (PC) increased markedly with chronic exposure of animals to O3. Enhanced polyunsaturated fatty acid (PUFA) composition in lung lavage and changes in the levels of CE and PC may be related to animals' adaptation to O3-exposure.

Air Pollutants↗
PubMed1984

Alcohol ingestion and levels of hepatic fatty acid synthetase and stearoyl-CoA desaturase activities in rats.

Male Sprague-Dawley rats were fed, ad libitum for 30 days, a fat-free (FF) liquid diet containing 34% of the calories as ethanol or a control FF diet in which alcohol was replaced by an isocaloric amount of dextrins. The cytosolic fatty acid synthetase and the microsomal stearoyl-CoA desaturase activities in the livers of rats fed the alcohol diet were about half of those observed in the livers of control rats. The conclusion is that chronic ethanol consumption depresses the activities of these lipogenic enzymes in the liver.

Animals↗