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Biomedical subjects

G A Bray

Publications and source records attributed to G A Bray.

At least 361 records · Page 20Linked to original sources
PubMed1979

Obesity.

Explore the source record for details and available documents.

Adipose Tissue↗
PubMed1979

Metabolic and behavioral differences between dieting and intestinal bypass.

The present studies were designed to compare physiological and behavioral changes produced by weight loss induced with dieting and the weight loss which follows intestinal bypass. A group of 7 grossly obese individuals were hospitalized in a metabolic unit and studied at their initial weight after 4 weeks on a hypocaloric diet and again following a comparable weight loss after intestinal bypass surgery. The score indicating depression increased after dieting, but returned to initial levels after bypass. A number of other behavioral changes were recorded including a reduction in the time spent thinking about food, the time when the individual felt hungry and a greater percentage of time when they felt "full". After bypass, the patients also selected and ate smaller quantities of food. There were no metabolic differences following the period of dieting. Among the metabolic changes after bypass were an increase in glycerol and a decrease in insulin. The possible relationships between the metabolic and behavioral changes have been reviewed.

Blood Glucose↗
PubMed1979

Synthesis of fatty acids and cholesterol by liver, adipose tissue and intestinal mucosa from obese and control patients.

Biopsies of adipose tissue, liver and small bowel mucosa obtained from grossly obese and control subjects were used to study absolute rates of fatty acid, cholesterol, and other nonsaponifiable lipid synthesis using glucose as substrate and 3H2O as the isotopic marker. Fatty acid synthesis in subcutaneous adipose tissue expressed on a cell basis was greater in obese than control subjects and was stimulated by a high concentration of insulin (1000 micro U/ml), but not by a lower amount (100 micro U/ml). Fatty acid synthesis in omental adipose tissue exceeded by 3-fold that of subcutaneous fat. Fatty acid synthesis in obese liver was twice that of control liver and 20 times greater than obese adipose tissue. In terms of total organ activity fatty acid synthesis in fat tissue equalled or exceeded that of liver in both obese and control subjects. The cholesterol content of obese adipose tissue 1.86 +/- 0.11 mg/g exceeded that of controls 1.47 +/- 0.07 mg/g. All tissues examined synthesized cholesterol and nonsaponifiable lipids, liver greater than adipose tissue greater than small bowel mucosa. Nonsaponifiable lipid synthesis per gram of adipose tissue or liver was similar in obese and control tissue. The synthesis of total nonsaponifiable lipids including sterols, hydrocarbons and squalene was appreciable in adipose tissue and was approximately 15% of that of liver. However, cholesterol synthesis in the liver exporessed in terms of total organ activity was 50 times that in adipose tissue. The study demonstrates by direct comparison that liver is the dominant cholesterogenic organ in man and also shows that adipose tissue is a significant site of formation of fatty acids and nonsaponifiable lipids.

Adipose Tissue↗
PubMed1979

Human obesity and some of its experimental counterparts.

Human obesity is a manifestation of a positive energy balance. A variety of different factors influence this balance. The varieties of human obesity may be classified as follows: 1. Childhood onset with or without an increased number of adipocytes; 2. The syndromes of neuroendocrine dysfunction including hypothalamic obesity, Cushing's disease, and hyperinsulinism; 3. Dietary obesity; 4. Obesity due to physical inactivity; and 5. Genetic forms of obesity. Among the genetic form of obesity are the Laurence-Moon-Bardet-Biedl syndrome. Alstrom's syndrome, and possibly the Prader-Willi syndrome. Studies in experimental animals have increased our understanding of two of these forms of human obesity. These are: 1. Hypothalamic obesity associated with decreased sympathetic activity, hyperphagia and an increased secretion of insulin. Subdiaphragmatic vagotomy can reverse this syndrome; 2. Genetic forms of obesity inherited as recessive or dominant traits.

Adipose Tissue↗
PubMed1979

Nutrition in the Humphrey tradition.

This is only a partial overview of some of the activities within DHEW related to nutrition, with a particular focus on the Nutrition Coordinating Committee. Although the activities are already broad, they will expand as we identify additional problems and decide on appropriate solutions. Let me call on the members of The American Dietetic Association to assist us in our efforts to assign priorities to our activity. My discussion began with nutrition education, because this is a priority for both The American Dietetic Association and DHEW. We would welcome your help now and in the future as we attempt to make our programs in nutrition education and information more effective, more available, and more responsive to the needs of the American people. Nutrition in the Humphrey tradition is alive and well in DHEW.

Food Labeling↗
PubMed1978

Secondary amenorrhea in obesity: etiologic role of weight-related androgen excess.

A massively obese, amenorrheic young woman had elevated levels of plasma androgens which could be reduced either acutely by dexamethasone administration or chronically by weight loss. Normalization of plasma androgen levels in both instances led to resumption of ovulation, suggesting that weight-related hyperandrogenism is a cause of amenorrhea in obesity.

Adult↗
PubMed1978

An enzymatic defect in the obese (ob/ob) mouse: loss of thyroid-induced sodium- and potassium-dependent adenosinetriphosphatase.

Genetically obese (ob/ob) mice, mice that became obese after treatment with gold thioglucose, and lean animals were studied in the euthyroid state, after induction of hypothyroidism, and after treatment with triiodothyronine. The activity of glycerol 3-phosphate dehydrogenase (sn-glycerol-3-phosphate:(acceptor) oxidoreductase; EC 1.1.99.5] was reduced in the livers from hypothyroid animals and was increased by treatment with triiodothyronine in all groups. The activity of the ouabain-suppressible sodium- and potassium-dependent ATPase (ATP phosphohydrolase; EC 3.6.1.3) was increased by triiodothyronine and reduced by hypothyroidism in the lean and gold thioglucose-treated obese animals. In the obese (ob/ob) mice, on the other hand, treatment with triiodothyronine did not increase the activity of this enzyme, which remained at the level found in hypothyroid animals. This enzymatic activity was reduced in both liver and kidney. Adenylate cyclase [ATP pyrophosphate-lyase (cyclizing); EC 4.6.1.1] activity in liver membranes, however, was similar in all three groups of mice. This enzyme complex was activated by glucagon and was unaffected by treatment with thyroid hormones. The lack of a thyroid-dependent ouabain-suppressible (Na(+) + K(+))-ATPase in the tissues of the obese (ob/ob) mouse could explain most, if not all, of the abnormalities that have been described in this animal.

Adenosine Triphosphatases↗