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Biomedical subjects

V R Preedy

Publications and source records attributed to V R Preedy.

At least 19 recordsLinked to original sources
PubMed1992

Chronic effects of ethanol on muscle metabolism in the rat.

Chronic ethanol feeding in the rat is associated with a skeletal myopathy involving primarily type-II muscle fibres, which is recognised to be mediated via a specific impairment in protein turnover. This paper investigates whether the cause of this myopathy may be related to abnormalities in carbohydrate and lipid metabolism in different muscles. [U-14C]Glucose metabolism was examined in two muscles with different fibre compositions, the extensor digitorum longus (EDL) muscle, which contains predominantly type-II muscle fibres, and the soleus muscle, which is composed primarily of type-I muscle fibres. Feeding on the ethanol-supplemented Lieber-DeCarli liquid diet for 2 or 6 weeks was associated with profound disturbances in glucose metabolism in both EDL and soleus muscles, particularly in relation to rates of glycogen and alanine formation. We discuss the importance of these metabolic changes in relation to the genesis of chronic alcoholic skeletal myopathy.

Animals↗
PubMed1992

Protein synthesis in pulmonary, cardiac, and skeletal muscle in acute hypertension induced by aortic constriction in the rat.

OBJECTIVE: The aim was to investigate nucleic acid composition and rates of protein synthesis in cardiopulmonary tissues and skeletal muscle in response to hypertension induced by aortic constriction. METHODS: After five days of abdominal aortic constriction, protein, RNA, and DNA contents were measured in the lung, the left and right atria, the left and right ventricles, and gastrocnemius muscle from young male Wistar rats weighing 120-140 g. Rates of protein synthesis were also measured in these tissues with L[4-3H]phenylalanine. RESULTS: Aortic constriction significantly increased the right atrial weight and in contrast reduced the lung weight, compared to pair fed and sham operated controls. The wet weights of all other tissues were unaffected. The concentrations of right atrial proteins, RNA, and DNA were also significantly reduced though total protein, RNA, and DNA contents were unaltered. The left ventricular RNA concentration increased and there were variable alterations in protein and DNA composition. The protein, RNA, and DNA compositions of the other tissues showed patterned responses, which included reductions in lung and skeletal muscle DNA concentrations, reductions in the skeletal muscle RNA/DNA ratio, and a decrease in the lung protein/DNA ratio. In response to aortic constriction there were increases in the left ventricular fractional rate of protein synthesis in mixed, high salt (myofibrillar), and low salt (sarcoplasmic) fractions. Rates of protein synthesis in all other regions of the heart, lung and skeletal muscle were not significantly changed. CONCLUSIONS: We conclude that in abdominal aortic constriction, the left ventricles display early adaptive responses without any concomitant change in mass. Those regions of the rat cardiopulmonary system which are not directly exposed to the acute pressure overloading, ie, right atrium, lungs, and skeletal muscle, also show disturbances.

Acute Disease↗
PubMed1992

Studies of gut mucosal protein synthesis in a non-steroidal anti-inflammatory drug (NSAID) model of inflammatory bowel disease.

The extent to which defects in protein synthesis occurred in an experimental indomethacin induced rat model of nonsteroidal enteropathy has been examined. Male rats (nine) were fed indomethacin (8 mg/kg/day) for three days mixed with a powdered form of chow. The control group of rats (nine) were fed the same diet for three days without indomethacin. After the feeding period, both groups were fed a normal solid diet for four days. At the end of this period, the fractional rates of intestinal protein synthesis was determined by the 'flooding dose' technique. The mucosal protein, RNA and DNA contents in the proximal ileum of animals with enteropathy were not significantly different from controls (p greater than 0.05). Experimental enteropathy induced selective increases in the fractional rates of protein synthesis (26% increase, p less than 0.03) and RNA activities (23% increase, p less than 0.04). There were no significant changes in any of these variables in the duodenum (p greater than 0.05 in all instances). These changes may partly reflect the activity of those processes responsible for the pathogenic changes in NSAID enteropathy.

Animals↗
PubMed1992

Imidazole dipeptides in experimental alcohol-induced myopathy.

Rats were chronically fed a nutritionally complete liquid diet containing 35% of total calories as either ethanol, or (for the controls) an isocaloric amount of glucose. After 6 weeks of treatment, the feeding regime induced skeletal muscle myopathy as characterised by reductions in muscle weight and RNA content. Ethanol preferentially affected the metabolically glycolytic plantaris (Type II fibre-predominant) muscle of the rat, compared with the metabolically oxidative soleus (Type I fibre-predominant). The changes in the plantaris were associated with increases in the concentration (mumol per g wet weight) of anserine (18%) and carnosine (50%). No significant changes were seen for the concentrations of either anserine or carnosine in the soleus muscle. The total contents (mumol per muscle) of carnosine and anserine in the plantaris were not significantly altered by ethanol treatment, though a significant decrease in anserine content (30%) occurred in the soleus. It is concluded that reductions in imidazole dipeptide content, considered to be antioxidants and/or intracellular buffering agents, are not mediating factors in the development of chronic experimental myopathy.

Animals↗
PubMed1992

The acute effects of ethanol and acetaldehyde on rates of protein synthesis in type I and type II fibre-rich skeletal muscles of the rat.

Young rats were injected with either ethanol (75 mmol/kg), acetaldehyde (2.8 mmol/kg) or isovolumetric amounts of NaCl (0.15 mol/l, i.e. controls) with or without inhibitors of alcohol dehydrogenase (4-methylpyrazole) or aldehyde dehydrogenase (cyanamide). After 2.5 hr, fractional rates of protein synthesis (i.e. ks) in the soleus (Type I fibre-rich) and plantaris (Type II fibre-rich) muscles were measured. Ethanol alone reduced ks in both soleus and plantaris muscles, by approx. 25%. Pretreatment of ethanol-dosed rats with 4-methylpyrazole raised plasma ethanol levels and reduced ks in the soleus and plantaris by approx. 35%. Pretreatment of ethanol-dosed rats with cyanamide also increased plasma ethanol and further potentiated the effects of ethanol by reducing ks in the soleus and plantaris by approx. 65%. Acetaldehyde alone reduced ks by approx. 15%, and this effect was not significantly altered by 4-methylpyrazole pretreatment. In some instances, the plantaris was slightly more sensitive to ethanol and acetaldehyde than the soleus. Similar conclusions were derived when data were expressed relative to either RNA or DNA. The data thus suggest that the ethanol-induced inhibition of skeletal muscle protein synthesis may possibly be independently mediated by both ethanol and acetaldehyde.

Acetaldehyde↗
PubMed1992

Ethanol-induced chronic myopathy in the young rat: a light and electron microscopic study in type I or type II fibre-rich skeletal muscles.

An investigation was made into the characteristics of an experimental chronic alcoholic myopathy in the young rat. Male Wistar rats were fed a diet for 6 weeks in which ethanol comprised 36% of total energy. Controls were pair-fed the same diet except ethanol was substituted by isoenergic glucose. Soleus (type I fibre-rich) and plantaris (type II fibre-rich) muscles were examined by light microscopy, histochemistry and electron microscopy. Muscles from ethanol-fed rats showed a low-grade myopathy and the diameters of individual type II fibres were reduced. Infrequent atrophic fibres were necrotic and undergoing phagocytosis. Ultrastructurally, there were no observable differences in the subcellular organelles of the alcohol-fed and control rats. It was concluded that alcohol causes a specific myopathic process in the rat, selectively affecting type II fibres. These changes correlate well with the abnormalities seen in human chronic alcoholic myopathy.

Alcoholism↗
PubMed1992

Non-invasive laser-Doppler assessment of cutaneous blood-flow in alcohol studies: effects of chronic ethanol consumption on peripheral blood-flow in unanaesthetised rats.

We investigated the use of a microprocessor-controlled laser-Doppler monitor to measure blood-flow in unanaesthetised animals. The apparatus permitted real-time assessment of cutaneous blood-flow, identified artifactual changes due to limb and body movements and was able to calculate rapidly the average value for blood-flux between two selected time points. The practical applicability of the apparatus was appraised by determining the effects of chronic ethanol toxicity. Male Wistar rats were fed nutritionally adequate liquid diets containing 35% of dietary calories as ethanol, or pair-fed identical amounts of the same diet in which ethanol was replaced isocalorically by glucose. After 2 weeks of treatment, peripheral cutaneous flux was reduced in all ethanol-fed rats by 25%, from a mean of 322 arbitrary units (control rats) to 243 arbitrary units (ethanol-fed rats; P less than 0.05); the laser-Doppler studies also indicated that there was no alteration in blood cellular contents.

Alcohol Drinking↗
PubMed1992

Effects of chronic ethanol consumption and pair feeding on rates of protein synthesis and nucleic acid composition in rat tibia.

An investigation was made into the chronic effects of ethanol feeding on bone (represented by the tibia). Treated rats were fed a liquid diet containing ethanol as 36% of total calories, and controls were pair-fed identical amounts of the same diet in which ethanol was substituted by isocaloric glucose. Bone DNA and RNA contents in ethanol-fed rats were not significantly different from glucose-fed controls at days 3, 7, 14, 28 and 42 of treatment. Fractional rates of bone protein synthesis were measured with [43H]-phenylalanine. At 3, 7, 14, 28 and 42 days, ethanol feeding had no effect on free and protein-bound specific radioactivities, nor on fractional or absolute rates of protein synthesis. Synthesis rates relative to RNA (RNA activities) and DNA (cellular efficiencies) were also not significantly altered by ethanol feeding at these time points. Comparisons were made between rats fed a standard solid laboratory diet ad libitum (i.e. normal rats), and those fed restricted amounts of glucose-containing liquid diet (i.e. dietary-restricted rats) for 42 days. In normal rats, there was an increase in tibial mass and accretion of total collagen content, but in dietary-restricted rats, this accretion was markedly impaired. Furthermore, whilst RNA and DNA contents were increased in tibia of normal rats, the contents of these nucleic acids were reduced in bones of dietary restricted rats. Fractional rates of bone protein synthesis in normal rats were unaltered after 42 days, but reduced by feeding the control liquid diet in restricted amounts.(ABSTRACT TRUNCATED AT 250 WORDS)

Alcoholism↗
PubMed1991

A comparative study of the effects of the diamine oxidase inhibitor aminoguanidine, with or without dietary restriction, on the nucleic acid and protein composition of cardiac and type I and type II skeletal muscles of the rat.

It has been proposed that the diamine oxidase inhibitor aminoguanidine may be a potential therapeutically important anabolic agent. An investigation was therefore made into the effects of aminoguanidine treatment with or without nutritional restriction, on cardiac and skeletal muscles containing mainly of either Type I (i.e. soleus) or Type II fibres (i.e. plantaris) or a mixture of Type I and II fibres (i.e. gastrocnemius). After 3 weeks, dietary restrictions reduced cardiac weight, protein, RNA and DNA contents by between 31 per cent and 36 per cent. Similar, but smaller, reductions were observed in the soleus (18-31 per cent), plantaris (22-34 per cent) and gastrocnemius (22-34 per cent). Aminoguanidine had no effect on the heart of the rats fed ad libitum, nor did it alter the response to dietary restriction. Treatment with aminoguanidine had no overt anabolic effect on skeletal muscle, but a reduction in DNA content was observed. It was concluded that cardiac protein and nucleic acid contents are more sensitive to dietary deprivation than either anaerobic or aerobic skeletal muscles. Furthermore, aminoguanidine does not appear to promote growth or reduce catabolism as previous studies have suggested.

Amine Oxidase (Copper-Containing)↗
PubMed1991

Urinary excretion of nitrogenous and non-nitrogenous compounds in the chronic ethanol-fed rat.

1. The metabolic consequences of chronic ethanol feeding was investigated by assay of urinary metabolites. Male Wistar rats were fed a liquid diet containing 35% of total energy as ethanol or isovolumetric, isocaloric and isonitrogenous amounts of the same diet in which ethanol was substituted by isocaloric glucose (controls). 2. At 6 weeks the entire skeletal muscle mass was reduced by approximately 20%. The urinary excretion of nitrogen, urea and uric acid increased by between 23 and 128%. Urinary creatinine excretion was not significantly altered. 3. Urinary excretion of magnesium was significantly increased by 43%. Urinary excretion of sodium, potassium, calcium and phosphate was increased slightly (i.e. 5-22%), but this change was not statistically significant. 4. Proton n.m.r. spectroscopic analysis showed that ethanol feeding reduced the urinary excretion of citrate and 2-oxoglutarate (by approximately 50%), suggesting decreased citric acid cycle activity. There was an increased excretion of alanine (44%), but excretion of succinate and acetate was not significantly altered. Ethanol in the urine of ethanol-fed rats comprised approximately 2% of total ethanol intake and less than 1% of total energy intake. 5. Lactose was detectable in urine of ethanol-fed rats, but not in control rats, reflecting the reported decreased intestinal lactase activity and increased gut permeability in alcoholics. Urinary galactose excretion decreased by 41%, but relatively large increases in lactate excretion (50%) did not achieve statistical significance. 6. It was concluded that chronic ethanol feeding causes disturbances in whole-body nitrogen homoeostasis and alterations in intermediary metabolism.

Alanine↗