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Biomedical subjects

G L DUFF

Publications and source records attributed to G L DUFF.

At least 19 recordsLinked to original sources
PubMed1954

The effect of alloxan diabetes on experimental cholesterol atherosclerosis in the rabbit. IV. The effect of insulin therapy on the inhibition of atherosclerosis in the alloxan-diabetic rabbit.

Experiments were undertaken to ascertain whether the previously demonstrated inhibition of the development of experimental aortic atherosclerosis in alloxan-diabetic rabbits fed cholesterol was due to the injection of alloxan per se or to the existence of the diabetic state produced by alloxan. It was established that, by treating the diabetic state with insulin, the diabetic state could be ameliorated and the inhibitory effect obviated. It was therefore concluded that the inhibitory phenomenon was not due to the injection of alloxan per se but that it was associated with one or more factors that characterize the alloxan diabetic state in the rabbit and that are reversible by insulin therapy. In the course of the experiment it was demonstrated that the inhibitory effect was apparent in cholesterol-fed diabetic rabbits whether or not their diet was supplemented with vegetable oil. The previously reported metabolic abnormalities of the diabetic animals were confirmed. It was established that suitable treatment of the cholesterol-fed diabetic animals with insulin would bring all the metabolic aberrations, including those of the serum lipids, into reasonably close correspondence with those observed in non-diabetic rabbits fed cholesterol.

Alloxan↗
PubMed1954

The effect of cortisone on the serum lipids and on the development of experimental cholesterol atherosclerosis in the rabbit.

An experiment was performed to determine the effect of cortisone on the serum lipids and on the development of experimental cholesterol atherosclerosis in the rabbit. Litter mate rabbits of the same sex were employed; both sexes were represented in the experiment. The report is based upon four experimental groups comprising (1) 12 rabbits fed cholesterol and treated with cortisone vehicle; (2) 12 rabbits fed cholesterol and treated daily with cortisone; (3) 11 rabbits treated with cortisone; and (4) 7 rabbits that received cortisone vehicle. It was observed that: (1) There was less aortic atherosclerosis in the cholesterol-fed cortisone-treated rabbits as judged by both morphological and chemical means than in the rabbits fed cholesterol without cortisone treatment. (2) Cortisone depressed appreciably the hypercholesterolemia resulting from the feeding of cholesterol to rabbits. (3) Cortisone treatment caused a moderate hypercholesterolemia in normal rabbits. (4) Cortisone caused a moderate increase in serum lipid phosphorus equal to that produced by cholesterol feeding alone. (5) The combination of cholesterol feeding and cortisone did not result in a higher phospholipidemia than either one of these agents alone. (6) Cortisone caused a great increase in serum-neutral fat; it was not apparent whether cholesterol feeding affected the neutral fat lipemia due to cortisone treatment alone. (7) The total cholesterol to lipid phosphorus ratio was about normal in the rabbits that received cortisone only. It was doubled in the animals receiving both cholesterol and cortisone, and it was increased about four times in those that received only cholesterol. The significance of the alterations in the serum lipids induced by cortisone is discussed in relation to the inhibition of the development of aortic atherosclerosis that occurred in the cholesterol-fed rabbits treated with cortisone.

Animals↗
PubMed1954

The effect of undernutrition on cholesterol atherosclerosis in the rabbit.

Experiments were done to determine whether undernutrition with consequent loss of weight or failure to gain weight inhibited the development or promoted the regression of the aortic lesions of experimental cholesterol atherosclerosis in the rabbit. The experiments were conducted in such a way as to determine whether undernourished and adequately nourished rabbits fed the same daily doses of cholesterol would manifest different degrees of atherosclerosis at the end of an experiment. Different experiments tested the effect of undernutrition in young, growing animals that failed to gain weight normally (Experiments 1 and 2); in young rabbits subjected to marked undernutrition both before and during cholesterol feeding (Experiment 3); in fully grown, mature rabbits that lost weight during undernutrition (Experiment 4); and in rabbits that had completed a period of cholesterol feeding before caloric restriction was begun (Experiment 5). In every experiment it was observed that, if two groups of rabbits were fed cholesterol, one group being subjected to caloric restriction while the other received an adequate diet, no difference in aortic atherosclerosis was observed between the two groups at the termination of the experiment. Furthermore, no obvious effect of undernutrition on the regression of atherosclerotic lesions was observed in the rabbit. At the same time, undernutrition was found to promote hypercholesterolemia in the rabbit fed cholesterol. The possible significance of this result was discussed.

Animals↗
PubMed1950

The effect of alloxan diabetes on experimental cholesterol atherosclerosis in the rabbit. III. The mechanism of the inhibition of experimental cholesterol atherosclerosis in alloxan-diabetic rabbits.

A study of the serum lipids in normal and alloxan-diabetic rabbits during the course of cholesterol feeding is presented, particular attention being paid to the factors considered to be responsible for the stability of the serum lipids; namely, (1) their interrelations and (2) their association with the serum proteins. As far as the interrelations of the lipids were concerned a definite correlation was found between the development of atherosclerosis and an increase of serum cholesterol that was out of all proportion to the increase of serum lipid phosphorus and neutral fat. When these last two lipid constituents rose almost parallel with the serum cholesterol (as they did in some alloxan-diabetic rabbits), then the development of atherosclerosis was inhibited. This correlation was independent of the diabetic state, per se. It appeared likely that the marked elevation of serum neutral fat and lipid phosphorus in the diabetic animals was due to mobilization of body fat because of the disturbed carbohydrate metabolism. Because of their hydrophilic and emulsifying properties, it was thought probable that the elevation of the phospholipids was the important factor responsible for the stability of serum cholesterol. That neutral fat played a role, however, could not be denied. In normal rabbit sera, as we have previously shown, only small proportions of the lipid phosphorus and cholesterol are "readily extractable" (i.e., unattached or only loosely attached to protein). On the other hand, in every case in which the serum lipids were elevated, the greater proportion of the lipid phosphorus and cholesterol was "readily extractable," irrespective of whether atherosclerosis developed or was inhibited. Analysis of the lipid content of the aorta of rabbits not fed cholesterol, whether diabetic or non-diabetic, and from alloxan-diabetic rabbits fed cholesterol but protected from the development of atherosclerosis, showed that there was no significant difference in lipid content or composition among the animals of these groups. When atherosclerosis developed following cholesterol feeding, the lipid composition of the aortas was essentially the same in both control and diabetic animals. The deposited lipid consisted predominantly of cholesterol with small and fairly constant proportions of other lipids that did not vary significantly regardless of the quantities of these other lipids present in the circulating blood. In the less severe lesions the proportion of ester cholesterol was greater than that of free cholesterol, but in advanced lesions the reverse was true. The following conclusions are drawn concerning the pathogenesis of experimental cholesterol atherosclerosis in the rabbit: 1. Instability of cholesterol in the blood rather than hypercholesterolemia, per se, is the general condition responsible for the deposition of this substance in the arterial walls. 2. Of the two factors considered to be responsible for the stability of the lipids in the blood, the interrelations of the lipids appear to be more important than their relation to the serum proteins, at least in so far as the development of experimental cholesterol atherosclerosis is concerned. The importance of these conclusions in relation to the pathogenesis of human atherosclerosis is discussed.

Alloxan↗