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Biomedical subjects

G A Bray

Publications and source records attributed to G A Bray.

At least 109 records · Page 6Linked to original sources
PubMed1997

Effects of experimentally induced mild hyperthyroidism on growth hormone and insulin secretion and sex steroid levels in healthy young men.

Although triiodothyronine (T3) exerts major regulatory actions in both animals and humans, most clinical studies of T3 administration have been relatively short-term. The present study examined the effects of more than 2 months (63 days) of low-dose T3 treatment on overnight pulsatile growth hormone (GH) secretion, short-term insulin secretion, and of sex steroid levels in seven healthy, lean men studied at an inpatient metabolic unit. At baseline, there were strong correlations between sex hormone-binding globulin (SHBG) and several measures of GH production, including total GH production (r = .99), GH interburst interval (r = -.75), and GH mass (r = .82). SHBG was also inversely correlated with basal insulin secretion (r = -.74). There was a 42% increase in serum levels of total testosterone (18.5 +/- 1.3 to 26.3 +/- 1.8 nmol/L, P = .005) and a 150% increase in SHBG (18.0 +/- 2.2 to 44.9 +/- 7.0 nmol/L, P = .008) following T3 treatment. Estradiol and free testosterone levels were unchanged by treatment, although free testosterone decreased from 142.8 +/- 18.4 to 137.3 +/- 19.5 pmol/L. T3 treatment significantly reduced the GH interburst interval (P < .05) and produced slight increases in the measures of GH secretion. There were no statistically significant effects of T3 treatment on insulin secretion, although insulin peak amplitude, mass secreted per burst, and total production all decreased. We conclude that experimentally induced T3 excess in healthy men produces significant and sustained changes in sex hormone levels and GH secretion. Furthermore, there are strong associations between SHBG and both GH and insulin secretion independent of thyroid hormone excess that require additional study.

Adult↗
PubMed1997

Relationship between resting metabolic rate and the composition of the fat-free mass.

Although a low resting metabolic rate (RMR) has been shown to be a risk factor for future weight gain, little is known about the mechanisms determining its level. We tested the hypothesis that the composition of the fat-free mass (FFM) is a main determinant of RMR. If this hypothesis is true, a regression model including internal organ masses as independent variables should explain a larger fraction of the variance in RMR than is explained using only FFM as a predictor. We measured fat mass by hydrodensitometry, liver and kidney volumes by computed tomography (CT), heart mass by echocardiography, muscle mass by dual-energy x-ray absorptiometry (DEXA), and RMR by calorimetry in 40 subjects. FFM and fat mass explained 83% of the variability in RMR (standard error of the estimate [SEE], 420 kJ/d) in a multiple regression analysis. Combinations of organ and muscle masses performed as well as but not better than stepwise multiple regression models. The fact that the composition of the lean mass could not improve the prediction of RMR in comparison to the traditional FFM-fat mass model suggests that the weight of internal organs is not a main determinant of RMR. This may indicate that the variability in RMR is associated with variation in energy expenditure per kilogram of tissue of the individual organs.

Adipose Tissue↗
PubMed1997

Differential effects of baseline macronutrient preferences on macronutrient selection after galanin, NPY, and an overnight fast.

Rats display individual patterns of fat and carbohydrate intakes when allowed to self-select among individual macronutrient diets. We investigated whether these individual preferences in macronutrient selection could be modified by an overnight fast or by two orexigenic peptides, galanin and neuropeptide Y (NPY), which may selectively stimulate fat and carbohydrate intake. Rats were grouped by preference based on the ratio of average baseline fat:carbohydrate intake. In counterbalanced tests conducted on separate days, saline, galanin, or NPY was infused into the paraventricular nucleus of the hypothalamus and 60-min food intake was measured. When the macronutrient intakes were expressed as percent of total caloric intake, galanin administered into the PVN did not increase fat consumption compared to saline injection in either preference group. NPY slightly enhanced the proportion of carbohydrate intake, but only in carbohydrate-preferring rats. When all three feeding stimuli were compared to baseline preferences, the only condition that significantly altered macronutrient selection was an overnight fast, which augmented fat intake. These data demonstrate that baseline preferences for fat or carbohydrate are not significantly modified by galanin or NPY but that an overnight fast increases fat preference.

Analysis of Variance↗
PubMed1997

Effect of enterostatin and kappa-opioids on macronutrient selection and consumption.

Enterostatin, the activation peptide of pancreatic procolipase, suppresses consumption of high-fat diets and selectively suppresses fat consumption over carbohydrate consumption. Kappa-opioid subtype agonists stimulate feeding whereas antagonists suppress feeding. We investigated the effects of enterostatin, the kappa-opioid agonist U50488, and the kappa-opioid antagonist nor-binaltorphimine (nor-BNI) on macronutrient selection and food consumption in rats adapted to choose between a high-fat (HF) diet or a low-fat-high-carbohydrate (LF) diet. In fasted rats, lateral cerebro-ventricular injection (LV) of enterostatin selectively suppressed consumption of the HF diet, with no effect on LF diet consumption. Nor-BNI also selectively suppressed consumption of the HF diet without affecting LF diet consumption. Additionally, U50488 prevented the suppression of consumption of the HF diet in response to enterostatin. In food-sated rates, U50488 preferentially increased consumption of the HF diet and had no effect on consumption of the LF diet. Combined infusions of subthreshold doses of enterostatin and nor-BNI also inhibited consumption of the HF but not the LF diet, whereas combined infusions of maximal doses of enterostatin and nor-BNI had no additive effects. Collectively, these data suggest that a kappa-opioid pathway modulates selection and consumption of diets high in fat and that enterostatin modulates consumption of dietary fat by interacting with this pathway.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1997

Does vegetable oil attenuate the beneficial effects of fish oil in reducing risk factors for cardiovascular disease?

Contradictory reports on the protective effect of fish consumption on cardiovascular disease (CVD) risk could be due to variations in the intake of n-3 and n-6 polyunsaturated fatty acids (PUFAs). Metabolic competition between n-3 and n-6 PUFAs suggests that n-6 PUFAs in vegetable oils could attenuate the efficacy of n-3 PUFAs in fish oil to favorably alter endpoints relevant to CVD risk. We determined the effects of varying dietary amounts of fish oil on lipid and thrombotic endpoints relevant to risk factors for CVD and whether these effects were attenuated by vegetable oils. Two randomized, double-blind, placebo-controlled, parallel studies were conducted in human subjects fed varying amounts of n-3 and n-6 PUFAs; n-3 PUFA intake was varied by using fish or placebo oil capsules, and n-6 PUFA intake was modified by incorporating varying amounts of safflower oil into the diet. Endpoints included changes in membrane fatty acid composition, blood lipids, and thrombotic profile. The results indicated that absolute amounts of fish oil, and not the relative amounts of fish and vegetable oil (ratios of n-3 to n-6 PUFAs), determined the magnitude of the reduction of arachidonic acid and increase in eicosapentaenoic acid in phospholipids of plasma and platelets. The suppression of plasma triacylglycerols by fish oil was not affected by varying amounts of dietary n-6 PUFAs. Fibrinogen concentrations decreased with 15 g but not with 9 g fish oil/d fed at the same ratio of n-3 to n-6 PUFAs. The efficacy of fish oil in favorably modifying certain risk factors for CVD was not attenuated by vegetable oil.

Adolescent↗
PubMed1997

Effect of an acute reduction in carbohydrate intake on subsequent food intake in healthy men.

We investigated the effect of a combined carbohydrate and energy deficit in the regulation of food intake during 1 d. Seven lean, male subjects were studied in a crossover design. After 7 d of consuming a baseline diet (40% of energy as fat, 45% as carbohydrate, and 15% as protein), subjects were deprived of carbohydrate for 24 h; baseline amounts of fat and protein were consumed but only one-third of the baseline amount of carbohydrate. On the following outcome day, subjects were free to select ad libitum from a selection of either high-carbohydrate or low-carbohydrate food. On the baseline diet subjects consumed on average 10.9 +/- 1.7 MJ/d (carbohydrate: 305 +/- 49 g/d; fat: 116 +/- 18 g/d) and there was no difference in baseline intake between the two phases of the crossover study. During the deficit day, intake was reduced to 7.7 +/- 1.2 MJ/d [carbohydrate: 110 +/- 25 g/d (66% reduction); fat: 116 +/- 18 g/d]. On the outcome day, energy intake from high-carbohydrate foods was on average 10.5 MJ/d (carbohydrate: 430 +/- 112 g/d; fat: 48 +/- 20 g/d) compared with 16.6 MJ/d from high-fat foods (carbohydrate: 312 +/- 84 g/d; fat: 258 +/- 78 g/d). We conclude that the restoration of an energy deficit is not the main factor determining acute food intake. Rather, the data support the hypothesis that, under the conditions of our experiment, the intake of carbohydrate required to maintain carbohydrate balance was a more important factor in the regulation of acute food intake than was the restoration of energy deficit is not.

Adult↗
PubMed1997

Obesity and reproduction.

Obesity produces a variety of alterations in the reproductive system and, similarly, manipulations of the hypothalamic-pituitary-gonadal axis produce changes in food intake, body weight and fat distribution. In men, the primary effects of obesity are a weight related reduction in testosterone and, with massive overweight, a reduction in free testosterone. In females, the weight-related development of menarche leads to earlier menarche in obese girls than in normal weight girls. One explanation for the relationship of fatness to menarche may be the ob protein (leptin) which is defective in the obese (ob/ob) mouse. Leptin is secreted by adipose tissue in proportion to the quantity of fat and may serve as a signal to the hypothalamus that fat stores are adequate to nourish a conceptus to term. In women, parity affects obesity and obesity in turn affects the regularity of the menstrual cycle. In many experimental animals with obesity, particularly the genetic forms of obesity, there is complete infertility in the females and marked impairment of reproductive function in the males. In animals with hypothalamic lesions, there is a gender effect on the magnitude of weight gain associated with the sexually dimorphic regions in the medial preoptic area. Castration with removal of oestrogen is followed by obesity in female animals and this can be prevented, as can most forms of obesity, by adrenalectomy. The inhibitory effects of oestrogen on food intake may result from suppression of neuropeptide-Y or galanin peptidergic systems in the arcuate nucleus or medial preoptic area.

Animals↗
PubMed1997

Progress in understanding the genetics of obesity.

Progress in understanding the genetics of obesity has moved rapidly in the past few years. The genes for all of the single gene defects that produce obesity in experimental animals have now been cloned. The new insights from these models are one spur for the examination of possible links to human obesity. In thinking about the biology of obesity produced by single gene defects, it must be kept in mind that adrenalectomy can prevent the phenotypic expression in all of the single gene models of obesity. Thus, nongenetic components can play a major role in regulating even single gene models of obesity. Transgenic mice have also expanded our understanding of obesity. Transgenic models that both increase and decrease body fat have been published. Of particular interest from the perspective of the physiological control of obesity is the destruction of the uncoupling protein in brown adipose tissue, which is followed by hyperphagia and obesity, suggesting that the sympathetic nervous system is involved in both modulation of food intake and energy storage. Gene mapping using quantitative trait loci and studies of candidate genes have been applied to experimental models of animals with differing susceptibilities to dietary fat and have been applied to the human genome in more detail.

Animals↗
PubMed1997

A paradigm of experimentally induced mild hyperthyroidism: effects on nitrogen balance, body composition, and energy expenditure in healthy young men.

Although T3 exerts major regulatory actions in both animals and humans, most clinical studies of T3 administration have been relatively short term. The present study examined the effects of more than 2 months (63 days) of low dose T3 treatment on nitrogen balance, body composition, 24-h energy expenditure (EE), and protein turnover in seven healthy men studied at an in-patient metabolic unit. Subjects were also randomly assigned to either high or low fat diets to determine the effects of diet composition. T3 treatment produced significant losses in both lean mass (1.5 +/- 0.3 kg) and fat mass (2.7 +/- 0.4 kg) by 6 weeks, with similar reductions in both at 9 weeks. The high fat diet somewhat attenuated the loss of body fat. Nitrogen balance was significantly negative for the first 3 weeks of T3 treatment, but tended to return to baseline thereafter. There were no significant effects of treatment on protein turnover at 9 weeks, although there was a slight increase in leucine oxidation (P = 0.07). Despite the apparent adaptation in nitrogen balance, total 24-h EE and sleeping EE were significantly increased at 9 weeks. We conclude that although healthy men are able to adapt to mild hyperthyroidism in terms of nitrogen balance, they exhibit significant and persistent changes in fat and fat-free mass as well as energy balance.

Adult↗
PubMed1996

Effect of galanin and enterostatin on sympathetic nerve activity to interscapular brown adipose tissue.

The effects of galanin and enterostatin on sympathetic activity have been examined in rats using electrophysiological techniques. Galanin, in doses of 25-300 pmol, and enterostatin, in doses of 0.5-10 nmol, were injected into the third ventricle of anesthetized male Sprague-Dawley rats in 1-microliter volumes. Galanin produced a dose-dependent suppression (ranging between 20 and 80%) of sympathetic firing rate of nerves innervating interscapular brown adipose tissue. In rats fed a chow diet, injection of enterostatin produced only a transient 10% rise in firing rate which returned to baseline within 10-15 min. In contrast, animals fed a high-fat diet showed a dose-dependent increase in firing rate lasting for 60 min. The results of this experiment are consistent with the hypothesis that food intake and sympathetic nervous system activity have a reciprocal relationship. The implications of this relationship are discussed.

Adipose Tissue, Brown↗
PubMed1996

Coherent, preventive and management strategies for obesity.

The increased risk of morbidity and mortality from obesity, central body fat and weight gain, and the benefits of weight reduction argue that the cost associated with obesity could be beneficially affected by prevention of weight gain or induction of weight loss. Genetic, metabolic and demographic predictors of weight gain have been identified that allow the selection of high risk individuals. Among the metabolic predictors are a low metabolic rate, insulin sensitivity and a high respiratory quotient. Demographic predictors include current smokers, certain dieting behaviours, lower socioeconomic class, a low level of education, use of contraceptives, status post-partum and rapid weight gain in childhood. Several studies suggest that weight gain can be prevented. Targets for such strategies might be high risk families, current smokers, those who are planning to stop smoking and those with a low metabolic rate. For those who fail primary prevention, treatment may be appropriate. The greater the degree of excess weight, the greater the risk and the more appropriate treatment becomes to reduce body weight.

Humans↗
PubMed1996

Autonomic activity assessed by heart rate spectral analysis varies with fat distribution in obese women.

Obesity in humans has been associated with altered autonomic nervous system activity. The objective of this study was to examine the relationship between autonomic function and body fat distribution in 16 obese, postmenopausal women using power spectrum analysis of heart rate variability. Using this technique, a low frequency peak (0.04-0.12 Hz) reflecting mixed sympathetic and parasympathetic activity, and a high frequency peak (0.22-0.28 Hz) reflecting parasympathetic activity, were identified from 5-minute consecutive heart rate data (both supine and standing). Autonomic activity in upper body (UBO) vs. lower body obesity (LBO)(by waist-to-hip ratio) and subcutaneous vs. visceral obesity (by CT scan) was evaluated. Power spectrum data were log transformed to normalize the data. The results showed that standing, low-frequency power (reflecting sympathetic activity) and supine, high-frequency power (reflecting parasympathetic activity) were significantly greater in UBO than in LBO, and in visceral compared to subcutaneous obesity. Women with combined UBO and visceral obesity had significantly higher cardiac sympathetic and parasympathetic activity than any other subgroup. We conclude that cardiac autonomic function as assessed by heart rate spectral analysis varies in women depending on their regional body fat distribution.

Adipose Tissue↗