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Biomedical subjects

W E Lands

Publications and source records attributed to W E Lands.

161 records · Page 9Linked to original sources

Control of lecithin biosynthesis in erythrocyte membranes.

The detailed relationship between the relative composition of the potential precursor acids, the esterification rates of their CoA thiol ester derivatives, and the relative composition of the fatty acids in the product, lecithin, which was isolated from normal erythrocytes, suggests that in humans the stromal acyltransferases could be the significant enzymatic factor controlling the fatty acid composition at the 2-position of lecithin in erythrocytes.

Acyltransferases↗

Specificity of acyl-CoA:phospholipid acyltransferases: solvent and temperature effects.

Acyltransfer from CoA thiol esters to either the 1- or 2-position of monoacylglycerophosphoryl choline, which is catalyzed by a microsomal preparation from rat liver, had a temperature optimum of 30-35 degrees C. No significant alteration was observed in the ability of the acyltransferases to distinguish among the various thiol esters tested in the range of 15-40 degrees C. Acyl-CoA:1-acylglycerophosphoryl choline acyltransferase activity is inhibited by urea, N-alkyl ureas, and short-chain alcohols. The effect is not equal for all acyl derivatives, and ethylene glycol has much less inhibitory effect on the transfer of acids with an n - 6 (omega6) double bond. On the other hand, this inhibition of acyltransfer was relatively insensitive to the configuration of the Delta(9)-double bond of octadecadienoates. The specificity of the enzyme-catalyzed transfer of different acids to the 2-position can be correlated in part with the dissociation constants for the urea clathrate complexes. Added glycol does not appreciably alter the specificity of enzyme-catalyzed transfer to the 1-position, but it inhibits the transfer of all acids in a similar fashion.

Acyltransferases↗

Insulin and glucagon secretion in essential fatty acid deficient rats.

Insulin and glucagon secretion in response to common secretagogues were ascertained in the perfused pancreas isolated from essential fatty acid deficient rats. The pattern of insulin secretory response to glucose (16.7 mmol/L) by isolated rat pancreas perfused for 30 min was biphasic in EFA-deficient and control rat pancreas. The amplitude of glucose-stimulated acute secretion (phase I) was significantly greater (p less than 0.01) in magnitude and amplitude in EFA-deficient rats than in the control rats. There was no significant difference in the second phase of glucose-stimulated insulin secretion in the two groups. Glucagon secretion in EFA-deficient and control rats was inhibited by glucose (16.7 mmol/l). Glucagon secretion induced by L-arginine (10 mmol/l) was not significantly different in EFA-deficient and in control rat pancreata (p greater than 0.05). However, arginine (10 mmol/l)-stimulated insulin release was significantly higher in EFA-deficient than in control rats. Growth hormone (100 mumol/l)-induced glucagon and insulin secretion was variable in the two groups but significantly higher than basal secretion. The level of L-leucine (10 mmol/l)-stimulated glucagon and insulin secretion in EFA-deficient rats was minimal but significant. Our results show that isolated pancreata of rats devoid of precursors for endogenous prostaglandin synthesis secreted insulin and glucagon in response to common secretagogues. On the basis of our data, it is concluded that endogenous prostaglandins are probably not obligatory for normal secretory functions of islets of Langerhans.

Animals↗

A role for behavioral sensitization in uncontrolled ethanol intake.

The processes that underlie the transition from controlled to uncontrolled consumption of ethanol are unknown. Behavioral sensitization is proposed as one of these processes and occurs with repeated administration of psychomotor stimulants whereby both behavioral and neurochemical responses to the drugs are progressively enhanced. Because ethanol shares some actions in common with these drugs, chronic exposure to ethanol may intensify its reinforcing properties. The effect of ethanol on several behavioral models suggests that behavioral sensitization may develop especially in the presence of environmental cues. Thus, a research opportunity exists to study factors that contribute to an increasing probability of progressively higher ethanol consumption. Knowledge of these factors will lead to a better understanding of why some people drink uncontrollably.

Alcohol Drinking↗

Alcohol and calories: a matter of balance.

Many epidemiological studies show that alcohol-derived calories added to food intake of men and women in amounts of 0-25% of total energy do not appreciably alter the average daily intake of other macronutrients (carbohydrate, fat, and protein). With such lack of evidence for caloric compensation, alcohol and its calories seem to make little contribution to metabolic energy, body weight, or body composition (as indicated by the body mass index, BMI). In fact, a major study by Colditz et al. (Am. J. Clin. Nutr. 54:49-55; 1991) reported a clear inverse relationship between alcohol intake and BMI for women! Research on alcohol metabolism has left unresolved some apparent contradictions regarding the effect of alcohol on caloric control, appetite and satiation, and body mass and composition. To resolve those apparent contradictions, the National Institute on Alcohol Abuse and Alcoholism cosponsored with the National Institute of Diabetes and Digestive and Kidney Diseases and the Beltsville Human Nutrition Research Center of the U.S. Department of Agriculture an all-day workshop titled "Alcohol and Calories: A Matter of Balance" on January 27, 1993. The workshop included sessions on calorimetry and body mass maintenance, alcohol metabolism, thermoregulation, and an overview of energy balance. This report provides summaries of the four discussion sessions at the workshop.

Alcohol Drinking↗

Alcohol, slow wave sleep, and the somatotropic axis.

When alcohol is a large proportion of daily nutrient energy, the network of signals for energy homeostasis appears to adapt with abnormal patterns of sleep and growth hormone (GH) release along with gradual acquisition of an addictive physical dependency on alcohol. Early relapse during treatment of alcoholism is associated with a lower GH response to challenge, perhaps reflecting an altered balance of somatostatin (SS) to somatropin releasing hormone (GHRH) that also affects slow wave sleep (SWS) in dependent patients. Normal patterns of sleep have progressively shorter SWS episodes and longer rapid eye movement (REM) episodes during the overall sleep period, but the early sleep cycles of alcoholics have truncated or non-existent SWS episodes, and the longer REM episodes occur in early cycles. During SWS delta wave activity, the hypothalamus releases GHRH, which causes the pituitary to release GH. Alcohol-dependent patients have lower levels of SWS power and GH release than normal subjects, and efforts to understand the molecular basis for this maladaptation and its relation to continued alcohol dependence merit encouragement. More needs to be learned about the possibility of decreasing alcohol dependency by increasing SWS or enhancing GHRH action.

Adult↗

Development of atherosclerosis in genetically hyperlipidemic rabbits during chronic fish-oil ingestion.

The evidence for a reduction in cardiovascular mortality from fish oil is based on epidemiologic observations. To test whether fish-oil supplementation influences the development of atherosclerosis, we treated Watanabe heritable hyperlipidemic rabbits (WHHL), an inbred strain that spontaneously develops atherosclerosis, with 2.5 ml of MaxEPA fish-oil concentrate daily and compared them to a control group fed unsupplemented rabbit chow. Serial cholesterol and triglyceride levels were monitored as were plasma lipid hydroperoxides. The animals were given fish oil from the time of weaning until 1 year of age, when they were sacrificed and their aortas were compared for the extent of atherosclerosis. No significant differences in the cholesterol or triglyceride levels were noted between the two groups. Fatty acid hydroperoxide levels were also similar and were noted to increase from weaning (1.0 +/- 0.7 microM) to the time of sacrifice (1.8 +/- 1.5 microM, p less than 0.01). Fish oil had no influence on the extent of aortic atherosclerosis (25% +/- 14% surface area for controls vs. 28% +/- 19% for treated, p = NS), plaque thickness, or plaque volume after 1 year. We conclude that fish oil does not reduce the levels of serum cholesterol, lipid hydroperoxides, or aortic atherosclerosis in WHHL rabbits. The hypothesis that fish oil protects against atherosclerosis was not supported by this study.

Animals↗

Alcohol's impact upon glycobiology.

This report reviews and illustrates ways in which some of the problems linked to excessive alcohol intake may develop from alcohol-induced alterations of eukaryotic cell surface molecules. Alcohol is the number one drug of abuse in the US, affecting at least 15 million Americans and causing annual losses of more than $80 billion and 100,000 lives. An estimated 20-40% of all persons admitted to general hospitals have alcohol-related problems and are often undiagnosed alcoholics being treated for the consequences of their drinking. Chronic alcohol-related cirrhosis of the liver is the ninth leading cause of death in the US, with over 28,000 deaths annually. Alcohol has harmful effects on almost every organ system in the body, producing cardiovascular disorders, liver disease, neuropathological illness and fetal injury. The etiologic mechanisms for these effects of alcohol is a research area of considerable importance to the National Institute for Alcohol Abuse and Alcoholism.

Alcoholism↗