Search PubMed⌕ Search

Biomedical subjects

G A Bray

Publications and source records attributed to G A Bray.

At least 235 records · Page 13Linked to original sources
PubMed1990

Effect of corticotropin releasing hormone and neuropeptide Y on electrophysiological activity of sympathetic nerves to interscapular brown adipose tissue.

It has been proposed that there is a reciprocal relationship between food intake and sympathetic activity. To test this hypothesis corticotropin releasing hormone, which suppresses feeding behavior, and neuropeptide Y, which stimulates it, were injected intracerebroventricularly and sympathetic nerve activity to interscapular brown adipose tissue measured in anesthetized rats. Multi-unit discharges of sympathetic nerves to interscapular brown adipose tissue were recorded electrophysiologically. The intracerebroventricular injection of corticotropin releasing hormone (250 and 500 pmol) increased sympathetic nerve activity and the intracerebroventricular injection of neuropeptide Y (250-500 pmol) suppressed sympathetic nerve activity in a dose-dependent manner. The intracerebroventricular injection of vehicle did not affect sympathetic nerve activity. The result is consistent with the hypothesis that these brain peptides are neuromodulators of the sympathetic nervous system which may control energy expenditure in interscapular brown adipose tissue. The effects of these two brain peptides on sympathetic nerve activity are opposite to their effects on feeding behavior suggesting that sympathetic activity and food intake may be reciprocally related.

Action Potentials↗
PubMed1990

Skinfold thickness measurements in obese subjects.

To determine the accuracy of skinfold thickness measurements in body composition assessment, skinfold thicknesses, bioelectrical impedance, body density by underwater weighing, and total body water by deuterium dilution were determined in 105 healthy adults who varied widely in body fatness. Body fat ranged from 2.9% to 61.2% of body weight and a substantial number of obese subjects was included. The correlation between body fat calculated from skinfold equations and body fat measured by underwater weighing was in the same range as that between body fat estimated from impedance and underwater weighing. However, body fat calculated both from skinfold equations and bioelectrical impedance tended to be underestimated compared with body fat calculated from underwater weighing and total body water in the most obese subjects. In obese subjects it was not possible to measure significant numbers of skinfold thicknesses because of the inadequate size of the calipers.

Adult↗
PubMed1990

Effects of glucose, 2-deoxyglucose, phlorizin, and insulin on food intake of lean and fatty rats.

Glucose, 2-deoxyglucose, phlorizin, and insulin were injected into the third ventricle of lean and fatty rats, and food intake recorded hourly for the next 6 h. In the lean rats, there was a significant but unimpressive decrease in food intake after the intraventricular injection of glucose, but there was no effect of glucose in the fatty rat. Phlorizin in the lowest dose (10 micrograms) increased the food intake in lean animals at 1 and 2 h, and all three doses increased it significantly at 6 h after intraventricular injection. The fatty rat, in contrast, showed no response to phlorizin. 2-Deoxyglucose showed a dose-related stimulation of food intake in the lean rats at 1, 2, 3, and 6 h after injection. In the fatty rat, there was no significant effect on food intake at any dose. The intraventricular injection of insulin had no effect on food intake in either the lean or fatty rats. These studies indicate that glucose-responding systems in the region of the third ventricle are defective in the fatty rat to signals that normally increase or decrease food intake in lean animals.

Animals↗
PubMed1990

Preoptic area injection of corticotropin-releasing hormone stimulates sympathetic activity.

To investigate the sites of action of corticotropin-releasing hormone (CRH) on sympathetic nerve activity to interscapular brown adipose tissue (IBAT), we injected CRH into the third cerebroventricle, medial preoptic area (MPOA), and other hypothalamic areas in anesthetized rats. The multiunit discharges of sympathetic nerves to IBAT were recorded electrophysiologically. The intracerebroventricular injection of CRH increased sympathetic nerve activity in a dose-dependent manner over the range 250-1,000 pmol. The microinjection of CRH (200 pmol) into the unilateral MPOA increased the sympathetic nerve activity to IBAT by +150.6 +/- 25.9% at 30 min after injection. However, the injection of saline (0.15 M NaCl) and glucagon (200 pmol) into the MPOA did not increase sympathetic nerve activity. The microinjection of CRH (200 pmol) into the anterior hypothalamic area, paraventricular hypothalamic nucleus, ventromedial hypothalamic nucleus, and lateral hypothalamic area had no significant effect on nerve activity. We conclude that central administration of CRH increases the sympathetic nerve activity to IBAT and that the MPOA is one of the sites for this action. The result is consistent with the hypothesis that CRH is a neurochemical stimulator of the sympathetic nervous system, which may be involved in control of energy expenditure in rodents.

Adipose Tissue, Brown↗
PubMed1990

Endocrine disturbances and reduced sympathetic activity in the development of obesity.

Obesity is associated with a number of changes in the endocrine system. Some of them occur as a result of the obesity, and some, such as changes in the secretion of adrenal steroids, may be causal. The importance of a reduction in the activity of the sympathetic nervous system in the control of obesity and nutrient regulation has been discussed. The influence of insulin and adrenal steroids on this system have been discussed in relation to changes in the activity of the sympathetic nervous system.

Endocrine Glands↗
PubMed1990

Obesity--a state of reduced sympathetic activity and normal or high adrenal activity (the autonomic and adrenal hypothesis revisited).

In this paper I have briefly reviewed the effect of nutrition on the sympathetic nervous system. I have also examined the changes in sympathetic activity in experimental models of obesity and leanness. Finally, I have tried to relate these two sets of information to the regulation of energy store by the autonomic nervous system in a nutrient balance model for regulation of food intake.

Adipose Tissue, Brown↗
PubMed1990

Ventromedial hypothalamic lesions attenuate responses of sympathetic nerves to carotid arterial infusions of glucose and insulin.

The effects of intracarotid injections of glucose and insulin on the sympathetic firing of nerves to brown adipose tissue were measured in rats. The injection of glucose into the carotid artery of anesthetized rats increased the firing of nerve filaments from the sympathetic nerves which innervate brown adipose tissue. Injection of kainic acid into the ventromedial nucleus 6-9 days prior to the measurement of nerve recordings reduced the stimulatory effect of glucose by 60 percent. In contrast to the stimulation by glucose, injection of insulin into the carotid artery reduced the sympathetic firing rate of nerves to brown adipose tissue. Kainic acid destruction of neurons in the ventromedial hypothalamus also attenuated this effect by 40 percent. These experiments are consistent with the hypothesis that changes in the arterial concentration of glucose and insulin may modulate the firing rate of sympathetic nerves to brown adipose tissue, and that this effect is mediated, in part, by the ventromedial hypothalamus.

Adipose Tissue, Brown↗
PubMed1990

Obesity: historical development of scientific and cultural ideas.

The concept that obesity is a risk to health was clearly identified in the works of Hippocrates and frequently over the ensuing centuries. Obesity was originally discussed as part of more general texts. Scholarly theses on this subject began to appear in the late 16th century with the first monographs published in the 18th century. The value of dietary restriction, increasing exercise and reducing the amount of sleep were identified early in medical history dating at least from the time of Hippocrates. These concepts were often framed in a manner which implied a 'moral' weakness on the part of the overweight individual. The most spectacular dietary success was published by a layman in 1863 and was the forerunner to many subsequent diet books. Cases of massive obesity were identified in stone age carvings and have been described frequently since the time of Galen and the Roman Empire. More specific types of obesity began to be identified in the 19th century. Following the identification of the cell as the basic building block of animals and plants, fat cells were described and the possibility that obesity was due to too many fat cells was suggested. After the introduction of the calorimeter by Lavoisier, the suggestion that obesity might represent a metabolic derangement has been suggested and tested. Standards for measuring body weight appeared in the 19th century. The possibility that familial factors might also be involved was clearly identified in the 18th and 19th century. In conclusion, most of the concepts which are currently the basis for research in the field of obesity had their origin in the 19th century and often earlier.

Cross-Cultural Comparison↗
PubMed1990

Pennington Biomedical Research Center. Philanthropy refocuses nutrition thinking.

Pennington Biomedical Research Center (PBRC) is a $26 million facility constructed as the initial component of a generous gift from Baton Rouge oilman and philanthropist Claude B. "Doc" Pennington. The US Department of Agriculture provided a $9.4 million grant for equipment for the center. The Louisiana Public Facilities Authority provided $4.1 million for initial operating capital, and the center received a $3.5 million grant from the US Army for military nutrition research. The Pennington Center Foundation, a non-profit support organization, has so far raised $4.6 million from individuals, corporations, and private foundations. Traditional academic funding sources such as the National Institute of Health are also providing funding for research.

Financial Management↗
PubMed1989

Modulation by corticotropin-releasing factor of monoamine metabolism in the lateral hypothalamus.

Corticotropin-releasing factor (CRF) was injected into the lateral hypothalamus of conscious unrestrained rats and the local concentration of monoamines in the vicinity of the microinjection monitored by microdialysis. The concentration of norepinephrine and MHPG in the dialysis fluid from the lateral hypothalamic areas of rats fasted for 24 h was nearly 4 times higher than in fed rats. Following the injection of 2 micrograms of CRF into the lateral hypothalamus of fasted rats there was a rapid decline in levels of both norepinephrine and 3-methoxy-4-hydroxyphenylglycol (MHPG) to the level in fed rats after 60-90 min. The changes in MHPG and norepinephrine in the fed rats were not significant There was no difference in serotonin concentration between fasted and fed animals, although the mean value for 5-hydroxyindoleacetic acid (5-HIAA) was slightly increased. Following the injection of CRF, there was a fall in serotonin in the fed rats but not in the fasted animals. There was a fall in the concentration of 5-HIAA in both the fasted and fed rats so that at 30, 60 and 90 min their concentrations were not significantly different. The concentration of DOPAC in the lateral hypothalamus was twice as high in the fasted as in the fed rats. Following injection of CRF there was a rapid decline in DOPAC concentrations in the fasted rats and a small decline in the fed rats. By the end of 30 min after the injection of CRF, concentrations of DOPAC were similar in fed and fasted rats.(ABSTRACT TRUNCATED AT 250 WORDS)

3,4-Dihydroxyphenylacetic Acid↗
PubMed1989

Effect of norepinephrine, serotonin and tryptophan on the firing rate of sympathetic nerves.

The firing rate of sympathetic nerves innervating interscapular brown adipose tissue (IBAT) has been recorded following microinjection of monoamines into the ventromedial (VMN) and paraventricular nuclei (PVN). Microinjection of norepinephrine (10 nmol) into the paraventricular nucleus produced a biphasic pattern in the firing rate of the sympathetic efferent nerves to IBAT. There was an initial dose-related 20% inhibition of firing rate followed 2 min later by 10% increase above control. When 10 times as much norepinephrine was injected into the ventromedial hypothalamus, there was a small 5% decrease in firing rate and a later significant dose-related increase in firing rate. These effects of norepinephrine were blocked by phentolamine, an alpha-adrenergic blocking drug, but not by propranolol, a beta-adrenergic blocking drug. Injection of serotonin into the paraventricular nucleus produced a short-lived but significant increase in firing rate of sympathetic nerves to brown adipose tissue. Comparable amounts of serotonin injected into the ventromedial nucleus produced a similar magnitude of increase in firing rate which lasted longer. There was a clear dose-response effect of serotonin injected into the PVN, but a much less impressive response when serotonin was injected into the VMN. The response to injections of tryptophan in both the VMN and PVN was similar to those seen with serotonin. When serotonin or tryptophan were injected into the PVN and VMN simultaneously, there was a synergistic increase in sympathetic firing rate. These data are consistent with the hypothesis that both norepinephrine and serotonin can modulate sympathetic firing rate through interaction with neurons in either the VMN or PVN.

Action Potentials↗
PubMed1989

Obesity: basic considerations and clinical approaches.

Obesity, defined as an excess of body fat, can be measured with a variety of techniques, but in most epidemiologic studies it is estimated from height and weight or from skinfold thickness. The "gold standard" for body fat is the body density from which fat and fat-free body mass can be calculated. The new technique of bioelectric impedance analysis may substantially improve the estimation of total body fat. For estimating regional fat distribution, either waist to hip circumference ratio or subscapular skinfold have been most useful. Using the body mass index, defined as weight in kilograms divided by the square of the height in meters (kilogram per square meter), the National Health and Nutrition Examination Survey estimated that 26%, or 34 million, adult Americans aged 20 to 75 were overweight. The prevalence of severe overweight (a body mass index above 30 kg/m2) is higher in the United States and Canada than in Great Britain, the Netherlands, or Australia. Obesity results from an increase in energy intake relative to expenditure. Total daily energy expenditure includes energy used during resting metabolism, energy associated with the ingestion of food, and energy needed for physical activity. The obese are often observed to be less active, but since carrying a heavier load requires more energy, their total energy expenditure may not be low. A low resting metabolic rate has been suggested as a predictor of future risk of becoming obese. Adipose tissue is the major site for fat storage and may contain more than 90% of total energy stores. The increase in body mass index or degree of body weight is associated with an increased risk of heart disease, hypertension, gall bladder disease, and diabetes mellitus. When fat is centrally located in either males or females, the risk for these diseases is also increased, and may be a more important risk factor than total overweight itself. Genetic factors form the background from which obesity develops. The best estimates suggest that these genetic factors may be of less importance than environmental events in determination of total body fat and its distribution. Obesity can be classified on the basis of the total number of fat cells and regional fat distribution by using the etiological factors which caused the obesity or by determining the age at which the obesity began. Regardless of the cause, treatment for obesity should be based on an evaluation of the individual's risk from obesity as compared with the risk of the treatment under consideration. (ABSTRACT TRUNCATED AT 400 WORDS)

Female↗
PubMed1989

Effects of MSH on food intake, body weight and coat color of the yellow obese mouse.

Viable yellow obese mice (Avy/a) were treated for 10 days with 5, 15, 50 or 150 micrograms/d of either alpha-MSH or desacetyl-MSH. The half-maximal effect on weight gain occurred with a dose of 5 micrograms/d for desacetyl-MSH and at a 30 fold higher level of 150 micrograms/d for alpha-MSH. In contrast, the half-maximal stimulation of eumelanin production by alpha-MSH occurred at 15 micrograms/d and with desacetyl-MSH at 150 micrograms/d, a 10-fold increase. Desacetyl-MSH produced a dose-related increase in the weight of muscle, as well as white and brown adipose tissue. Desacetyl-MSH and alpha-MSH both increased plasma corticosterone concentrations, but desacetyl-MSH was more potent. In a 2 x 2 factorial designed study, body weight was significantly increased in viable yellow mice only by treatment with desacetyl-MSH but in the lean animals, both alpha-MSH and desacetyl-MSH increased body weight. Food intake was significantly different between genotypes, and was stimulated by desacetyl-MSH. These studies demonstrate potent differences in biological actions on food intake, body weight, and a variety of organ weights between acetylated and desacetylated forms of MSH.

Animals↗
PubMed1989

Effect of carbohydrate refeeding on free fatty acids after a fast in obese diabetic and obese non-diabetic females.

The metabolic effects of refeeding with oral or intravenous carbohydrate were studied in obese women after ten or 14 days of fasting. Seven patients were refed with protein-free fruit juice for a total of 250 g of carbohydrate (1,000 kcal) over ten hours. The juice was sipped continuously throughout this time, causing a drop in free fatty acids (FFA) from 1.07 +/- 0.08 to 0.61 +/- 0.05 mmol/L (P less than .01) over the first four hours. Over the next four hours, despite continuous ingestion of the carbohydrate and elevated plasma glucose (132 +/- 9 mg/dL) and insulin (2.81 +/- 0.86 ng/mL) (1 ng/mL = 25 microU/mL), FFA rose to 0.99 mmol/L (P less than .01). Similar results were obtained in five patients refed with similar amounts of oral glucose and four patients who received an equivalent amount of glucose intravenously (IV). Refeeding with carbohydrate of obese diabetic and non-diabetic women after a two-week fast caused an abrupt decrease in FFA that was followed after four hours by an increase in FFA and glycerol, despite continued ingestion of carbohydrate glucose and insulin.

3-Hydroxybutyric Acid↗
PubMed1989

Hypothalamic monoamines measured by microdialysis in rats treated with 2-deoxy-glucose or d-fenfluramine.

The effects on brain monoamines (norepinephrine, serotonin and the metabolite of dopamine) following administration of d-fenfluramine (10 mg/kg IP) and 2-deoxy-d-glucose (500 mg/kg IP) have been measured by microdialysis from the ventromedial hypothalamus, lateral hypothalamic area and dorsomedial hypothalamus of conscious, unrestrained rats. Following administration of d-fenfluramine there was a significant increase in the concentration of serotonin in the ventromedial hypothalamus and lateral hypothalamic area, but no significant increase in the DMH. 5-HIAA (5-hydroxy-3-indoleacetic acid), the metabolite of serotonin, was increased in the DMH, but not in the other two regions. DOPAC (3,4-dihydroxyphenylacetic acid) was increased following fenfluramine treatment in all three regions examined. An increase in norepinephrine was observed in the VMH, but not in the other two regions, while the concentration of the 3-methoxy-4-hydroxyphenylglycol (MHPG) was increased in both areas. Treatment with 2-deoxy-D-glucose (2DG) was associated with fewer changes. In the lateral hypothalamic area there was a decrease in 5-HIAA and an increase in DOPAC. In the VMH there was an increase in norepinephrine and a decrease in MHPG in the DMH, but otherwise no significant alterations were observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Interaction of adrenalectomy and fenfluramine treatment on body weight, food intake and brown adipose tissue.

Three experiments have examined the interaction of adrenalectomy and fenfluramine on food intake, body weight and the binding of guanosine-5'-diphosphate (GDP) to interscapular brown adipose tissue (IBAT). In the first experiment, GDP-binding by IBAT mitochondria from adrenalectomized or sham-operated animals was measured for 3 hr after one of 3 doses of fenfluramine. Fenfluramine stimulated GDP-binding at lower doses in the adrenalectomized animals than in the controls. In the first chronic experiment, adrenalectomy prevented the restoration of normal food intake observed 8-10 days after the beginning of fenfluramine treatment. Adrenalectomy also increased weight loss and enhanced GDP binding to mitochondria from IBAT in rats treated with fenfluramine. In the second chronic experiment, the combination of fenfluramine and adrenalectomy led to a progressive weight loss, continuing hypophagia and stimulation of GDP-binding by IBAT, whereas rats treated with fenfluramine alone showed a recovery of food intake at a stabilized but lower body weight. These data are consistent with the hypothesis that adrenalectomy and fenfluramine disable two separate components of the food intake system and that when combined, produce a profound and persisting disturbance in energy or nutrient balance.

Adipose Tissue, Brown↗
PubMed1989

Effects of corticotropin releasing factor on genetically obese (fatty) rats.

Corticotropin releasing factor (CRF) has been administered into the third ventricle of lean and genetically obese Zucker fatty rats in both acute and chronic experiments. Following a single injection of CRF (5 micrograms or approximately 1 nmole) there was an acute reduction of food intake in both the lean and obese animals, but the effect was greater in the obese. This effect persisted for the first three hours but was no longer detectable in either lean or genetically obese animals at 6 hours. Binding of GDP to mitochondria from interscapular brown adipose tissue in 21-hour deprived animals was lower in the fatty rats than in the lean controls. The injection of CRF significantly increased GDP binding in both the lean and fatty rats. During chronic infusion of CRF into the third ventricle of fatty rats, there was a significant decrease in food intake in the obese rats and fall of body weight in both groups. The basal levels of GDP binding were significantly lower in the saline-infused fatty rats than in the saline-infused lean controls. The chronic infusion of CRF increased GDP binding in the fatty rats but not in the lean animals. The CRF-treated values for GDP binding in fatty rats however, remained significantly below the baseline values in the control animals. Chronic CRF infusion also significantly lowered glucose levels in the fatty rat. These studies are consistent with the hypothesis that CRF may be involved in the decreased food intake and increased sympathetic activity observed in genetically obese fatty rats following adrenalectomy.

Adipose Tissue, Brown↗