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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twenty-four-hour energy expenditure (EE) and substrate oxidation rates were measured two times in eight postobese women and eight matched controls. On one occasion the subjects were exposed to a room temperature of 16 degrees C, on the other to 24 degrees C. Cold exposure elicited a 2% increment in 24-h EE (P < 0.05), with similar response in the two groups. The slight increase in EE was entirely covered by an enhanced carbohydrate oxidation rate. Fasting plasma norepinephrine (NE) increased from 0.74 +/- 0.08 to 1.29 +/- 0.21 nmol/l under cold exposure (P < 0.05), with no group difference. The cold-induced increase in 24-h EE was positively correlated to the increase in NE concentration (r2 = 0.41, P = 0.01). Sleeping EE was found to be 5% lower in the postobese women than in the controls (P = 0.04). The postobese group also had higher 24-h nonprotein respiratory quotient than the control group (P = 0.04), which was due to a 26% lower lipid-to-carbohydrate oxidation ratio. The study demonstrates that the thermogenic response to cold is normal in women susceptible to obesity, but it supports previous reports of a slightly lower basal EE and lower lipid-to-carbohydrate oxidation ratio in postobese subjects.
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PMID:Effect of moderate cold exposure on 24-h energy expenditure: similar response in postobese and nonobese women. 147 75

The existence of a link between obesity and hypertension is nowadays universally accepted; however, there are still some doubts about the fact that weight reduction induces a significant long-term decrease in blood pressure. This clinical trial aimed at evaluating the effects of marked weight loss (at least 30% of excess body weight) induced by a low-energy (600 Kcal), normal sodium diet in severely obese patients, on blood pressure at rest and during sympathetic stimulation. Eight of the 20 patients initially recruited for the study were able to reach the therapeutical goal and brought their body weight from 107 +/- 6 to 91 +/- 4 kg. Their blood pressure (BP) at rest was at the same time reduced from 137/81 +/- 5/4 to 122/74 +/- 4/4 mmHg. Also, blood pressure measured during three different stimuli (cold pressor test, handgrip and mental arithmetic test) was lowered by this nonpharmacological means. These effects are related solely to weight reduction, since no change in salt intake occurred, as demonstrated by measurements of the 24-h sodium excretion test (191 +/- 13 vs 185 +/- 10 mEq/24 h). In conclusion, these results support the hypothesis that a drastic weight loss, independently of salt restriction, significantly reduces BP at rest and during stimulation of the adrenergic nervous system.
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PMID:Weight reduction lowers blood pressure independently of salt restriction. 150 18

Changes of colonic temperature were investigated to examine a mechanism of hypothermia in the obese rats which received subcutaneous administration of intermediate type-insulin (8 U/day) for 8 weeks. Although diurnal rhythmicity of colonic temperature levels was maintained similarly with those of vehicle-injected controls, the overall colonic temperature levels were significantly lowered in insulin-treated animals. In the condition of cold exposure at 5 degrees C, colonic temperature levels of insulin-treated animals were immediately and significantly decreased at 60 minutes after the start of cold exposure. The data obtained herein demonstrated that hyperinsulinemia accompanying with hyperphagia should be profoundly involved in hypothermia, observed in various experimental models of obesity.
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PMID:Hypothermia in insulin-treated obese rats. 163 26

Adipsin gene expression is severely diminished in certain forms of genetic and acquired rodent obesity. Common to many of these models of obesity is decreased sympathetic nervous system (SNS) activity. In addition, treatment of MSG obese mice with the sympathomimetic drug mixture ephedrine and caffeine restores adipsin deficiency to normal, while reversing obesity. Based on these observations, we hypothesized that adipsin gene expression might be regulated through changes in SNS activity with deficient adipsin gene expression in obesity being the result of impaired SNS activity. In the present study we used three models to assess the role of the SNS in regulating adipsin gene expression. First we exposed mice to the cold (4 degrees C), a potent activator of SNS activity. Second, we chemically sympathectomized mice with 60H-dopamine. Third, we treated mice with BRL 26830A, an atypical beta adrenoreceptor agonist. In contrast to our initial hypothesis, these studies demonstrate that alterations of SNS activity do not affect adipsin gene expression in normal mice. Neither increased SNS activity secondary to cold exposure nor decreased SNS activity resulting from sympathectomy alter serum adipsin concentration or adipsin mRNA levels in white (WAT) and brown adipose tissue (BAT). Surprisingly, treatment of lean mice with BRL 26830A decreases both adipsin serum concentrations and adipsin mRNA levels, suggesting a potential role for atypical beta adrenoreceptors in pathways that suppress adipsin expression in vivo. The significance of this observation with respect to adipocyte physiology is unclear at present. Future studies will be aimed at defining the molecular mechanisms by which BRL 26830A suppresses adipsin gene expression and the physiological significance of this effect.
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PMID:Alterations in sympathetic nervous system activity do not regulate adipsin gene expression in mice. 164 81

The present study was designed to determine whether the diminution of growth hormone (GH) secretion that occurs in obese Zucker rats is related to alterations of GH-releasing factor (GRF) or somatostatin (SRIF) pituitary binding sites. Cold saturation studies were performed in pituitary homogenates of 4-month-old lean and obese rats, using [125I-Tyr10]hGRF(1-44)NH2 as radioligand and [127I-Tyr10]hGRF-(1-44)NH2 as competitor, and in pituitary membrane preparations, using [125I-Tyr0, D-Trp8]SRIF14 as radioligand and [127I-Tyr0, D-Trp8]SRIF14 as competitor. In lean rats, analysis of the curves by the Ligand program revealed the presence of two distinct classes of GRF binding sites, the first being of high affinity (0.74 +/- 0.11 nM) and low capacity (118 +/- 31 fmol/mg protein), the second being of lower affinity (880 +/- 240 nM) and higher capacity (140 +/- 35 pmol/mg protein), and of a single class of SRIF binding sites (affinity: 0.40 +/- 0.12 nM; capacity: 24 +/- 6 fmol/mg protein). In obese rats, no difference was observed in GRF binding parameters for both classes of sites, but the concentration of somatostatin binding sites was reduced by 67% when compared to their lean littermates. These findings suggest that the SRIF pituitary receptors are down-regulated in obese Zucker rats and indicate that no alteration of GRF pituitary binding sites contribute to the blunted GH secretion observed in this model of obesity.
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PMID:Alteration of somatostatin but not growth hormone-releasing factor pituitary binding sites in obese Zucker rats. 168 74

The effects of acute cold exposure on rectal temperature (Tr) and circulating thyrotropin (TSH), thyroxine (T4) and triiodothyronine (T3) levels were examined in fed and food-deprived obese (ob/ob) and lean (?/+) C57BL/6 mice. At 23 degrees C, obese mice had lower body temperatures but higher TSH, T4 and T3 values than lean mice while male mice of both phenotypes had similar body temperatures and higher levels of all three hormones than females. Obese mice became severely hypothermic during 4 h cold exposure (8 degrees C) although TSH and T4 concentrations declined equally in obese and lean mice and T3 values were unaffected by cold. Male and female mice exhibited similar Tr responses to cold, while males continued to have higher values of TSH and thyroid hormones than females. When allowed food during cold exposure, both obese and lean mice displayed higher Tr although obese mice remained hypothermic. Thyroid hormones in all groups were increased by feeding but only male mice exhibited increased TSH values. These data show that the acute feeding, metabolic and thermogenic responses of mice to low ambient temperatures are not closely associated with altered systemic levels of TSH, T4 or T3. Furthermore, since ob/ob mice did not display lower hormone levels or defective hormone responses to cold or feeding, the data suggest that their apparent hypothyroidism is largely independent of hormone availability to target tissues.
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PMID:Effects of phenotype, feeding condition and cold exposure on thyrotropin and thyroid hormones of obese and lean mice. 176 7

A close correlation between body weight and blood pressure has been frequently observed in both clinical and epidemiological studies. The aim of this clinical trial was to evaluate whether, in obese patients, there is any relationship between blood pressure, at rest or during sympathetic stimulation, and blood glucose and serum insulin, both while fasting and during an oral glucose challenge. Twenty obese patients (age 26-65 years, body weight 97 +/- 16 kg, 11 normotensive and 9 hypertensive) entered the study. After a 4-week run-in period on an isocaloric diet with normal intake of sodium, blood pressure and heart rate were measured at rest and during sympathetic stimulation induced by cold and isometric testing. Responses of glucose and insulin to a standardized 75 g oral glucose tolerance test were also evaluated. The responses of glucose and insulin to glucose challenge were not statistically different in normotensive and hypertensive obese patients. Levels of insulin in the serum in the serum in the fasting state and during glucose load were significantly correlated with the response of blood pressure to cold and isometric exercise, but not to blood pressure at rest. The response of heart rate to cold was closely related to insulin only in the subgroup of normotensives. The present findings support the hypothesis that the sympathetic nervous system, which influences secretion of insulin and regulation of blood pressure, is involved in the pathophysiology of the association of obesity and hypertension.
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PMID:Responses of serum insulin and blood pressure to cold and handgrip in obese patients. 179 Oct 88

Overweight and obesity may develop in individuals with genetically determined low resting energy expenditure. Drugs are among the recognised precipitating factors. The obesity promoting impact of beta-blockers is, however, less well known. Resting energy expenditure, and thermogenesis induced by stimuli such as meals, cold and heat exposure, stress and anxiety, have a facultative component mediated by the sympathoadrenal system through catecholamines working on beta-adrenoceptors. Treatment with beta-blockers reduces the facultative thermogenesis by 50-100 kcal/d, which corresponds to the weight gain of 2-5 kg/year reported in clinical trials. Treatment with beta-blockers also results in insulin resistance, which may aggravate existing diabetes and elicit diabetes in predisposed patients. Overweight and obesity are frequently complicated with hypertension and angina pectoris, which are often treated with beta-blockers. Obesity is associated with a defective sympathetic activity, and treatment with beta-blockers may further reduce facultative thermogenesis and promote weight gain. The consequence may be aggravation of hypertension, insulin resistance and other atherogenic factors. The causal therapy of android overweight and obesity complicated with diabetes or hypertension is a sufficient weight loss. If pharmacological treatment is inevitable, combined treatment with diuretics and ACE-inhibitors are most appropriate.
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PMID:[Obesity and diabetes as side-effects of beta-blockers]. 197 28

Reduced thermogenesis in brown adipose tissue (BAT) may contribute to increased energetic efficiency and obesity in rats with ventromedial hypothalamic (VMH) lesions. Thermogenic activity of BAT is a function of the environmental temperature. If a relationship exists, it follows that the increased energetic efficiency of VMH-lesioned rats likewise should be governed by temperature. We have therefore investigated the energy balance of normal and VMH-lesioned rats housed at 30 degrees C and 10 degrees C. Experiments at differing feeding levels allowed calculation of maintenance energy requirements and the net energetic efficiencies of each group. VMH-lesioned rats at thermoneutrality (30 degrees C) accumulated more body fat at all feeding levels than did normal rats. Maintenance energy requirement was reduced, but the net energetic efficiency did not differ significantly from normal. The reduced maintenance energy requirement of lesioned rats persisted at 10 degrees C. Net energetic efficiency decreased in normal rats acclimated to cold but increased in the lesioned group. The difference was significant (P less than 0.05). The cold-induced increase in interscapular brown adipose tissue (IBAT) oxidative capacity of VMH-lesioned rats was only half that of normal rats. Differences in BAT thermogenesis may be the basis for the differing temperature effects on net energetic efficiency.
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PMID:Opposite effect of cold on energetic efficiency in normal and obese Wistar rats with hypothalamic lesions. 200 9

Energy expenditure for thermogenesis in brown adipose tissue (BAT) serves either to maintain body temperature in the cold or to waste food energy. It has roles in thermal balance and energy balance, and when defective, is usually associated with obesity. BAT can grow or atrophy; it is usually atrophied in obese animals. Control of BAT thermogenesis and growth is by the sympathetic nervous system, with integration of signals in the hypothalamus. Sensory nerves may also be involved. Understanding the control of growth and differentiation of BAT is important for discovering how to reactivate it is obesity. Studies on control of gene expression in BAT are concentrating on thermogenically important components such as the uncoupling protein (which allows BAT mitochondria to operate in a thermogenic uncoupled mode), lipoprotein lipase (which allows BAT to compete with white adipose tissue for dietary lipid), and thyroxine 5'-deiodinase (which allows endogenous triiodothyronine generation, part of the control of differentiation and growth of BAT). Differentiation of BAT cell precursors in culture has recently been achieved. BAT is present in adult humans and some anti-obesity drugs are targeted to stimulation of BAT thermogenesis. However, extrapolation to humans of results of studies of BAT requires the development of novel approaches to the noninvasive assessment of amount and function of human BAT.
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PMID:Brown adipose tissue thermogenesis: interdisciplinary studies. 219 86


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