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

Arginine vasopressin (AVP) and prolactin (PRL) concentrations were measured in the plasma of grossly obese subjects to determine if abnormalities in salt and water homeostasis could be related to these hormones. Acute oral water loads and hypertonic saline infusions were administered during baseline obesity, after prolonged fasting, and after hypocaloric refeeding. Only 64.7%, 46.1%, and 70.1% of a water load was excreted during the respective three stages. Pre-water load plasma AVP levels were normal, but after the water load the obese failed to suppress AVP secretion in a normal fashion; this defect was corrected after fasting and with refeeding. Salt loading resulted in appropriate osmolality and AVP responses. Serum prolactin levels, normal at baseline during all phases, rose slightly after water loading during fasting. Hypertonic.saline produced no changes in prolactin levels in the obese or in the normal controls. In the disordered salt and water metabolism of the obese, persistently high AVP values during water loading appeared to be a factor in the delay of water excretion. In the observed water retentionduring dietary restriction and refeeding, secretion of AVP and PRL did not appear to have a major regulatory function.
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PMID:The role of vasopressin and prolactin in abnormal salt and water metabolism of obese patients before and after fasting and during refeeding. 31 25

The role of insulin and dopamine on blood pressure and renal sodium excretion was evaluated in 10 obese hypertensive patients. Essential hypertensive subjects (age 49.7 +/- 7.7) with at least 26.0kg/m2 obesity were hospitalized and a 2000k cal diet for 7 days (control periods) followed by a 800 k cal for 21 days were given. Salt intake was maintained at 10 g/day throughout this study. Mean blood pressure (MBP), plasma insulin (IRI), urinary dopamine and fractional excretion of sodium (FENa) were measured in both diet periods. Body mass index significantly decreased from 31.6 +/- 4.6kg/m2 to 28.6 +/- 4.1 kg/m2 after weight reduction (P < 0.001). MBP significantly lowered from 112.8 +/- 14.1 mmHg to 100.4 +/- 12.4 mmHg (P < 0.01) and IRI from 9.11 +/- 5.0 microU/ml to 6.3 +/- 5.5 microU/ml (P < 0.001) after weight loss. We observed a significant correlationship between delta MBP and delta IRI (r = 0.754, P < 0.01). Also, we observed a significant correlationship between delta MBP and delta FENa (r = -0.835, P < 0.01). A significant relationship was observed between urinary excretion of sodium and urinary excretion of dopamine (r = 0.507, P < 0.05). We concluded that sodium retention and increase of sympathetic nervous activity by hyperinsulinemia might play an important role of hypertension, and blood pressure reduction by weight loss resulted from decreased insulin and increased excretion of sodium in obesity hypertension.
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PMID:[Effect of weight loss on the reduction of blood pressure in obesity hypertension--hyperinsulinemia and renal sodium retention]. 129 71

Naltrexone, an opiate antagonist, was administered to young obese (ob/ob) and lean mice for five weeks. Animals had continuous access to food and received 10 mg/kg SC twice daily with equivalent volumes of saline given to controls. The effects on body weight, and pituitary and plasma levels of beta-endorphin-like material were measured. Naltrexone-injected obese animals gained weight more slowly over the first three weeks while the weight gain of lean animals was not affected by naltrexone. Plasma levels of beta-endorphin were shown to be significantly higher in untreated ob/ob mice and this difference increased with age (4-20 weeks). With naltrexone treatment, plasma levels in +/? mice rose and exceeded those in ob/ob. Saline treatment appeared to be a stress, and pituitary beta-endorphins rose 4-6 fold in ob/ob compared with +/?. While naltrexone reduced the levels of ob/ob pituitary towards normal, no effect on beta-endorphin levels in pituitary of lean mice was obtained. In vitro studies of effects of the opiate antagonists, naloxone, on insulin secretion by isolated islets provided additional evidence of resistance of lean mice to naloxone relative to ob/ob. (IRI secretion fell only in naloxone treated ob/ob islets). These observations support the contention that this form of genetic obesity is characterized by elevated endogenous opiate levels and an increased sensitivity to opiate antagonists such as naltrexone or naloxone.
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PMID:Naltrexone reduces weight gain, alters "beta-endorphin", and reduces insulin output from pancreatic islets of genetically obese mice. 627 40

There is a close epidemiological association between obesity and elevated blood pressure for all age groups, although not every obese individual becomes hypertensive. In populations without age-related increases in body weight, an elevation of blood pressure with age is not seen. Mechanisms included in the development of hypertension in obesity are hyperinsulinemia, insulin induced sodium retention and increased sympathetic tone. Overnutrition with over intake of sodium and lack of physical exercise contribute to the metabolic syndrome of obesity. Thus, weight reduction by decreased energy uptake and increased physical exercise is recommended in the treatment of hypertension in obese patients. The resulting fall in insulin levels may lead to decreased sodium absorption in the kidney. Although treatment of obesity by weight loss decreases blood pressure substantially, a minority of patients do not respond to the weight loss. Blood pressure generally decreases before normal weight is achieved. Salt intake reduction does not appear to explain why weight reduction lowers blood pressure. Reduced levels of plasma renin activity, serum aldosterone levels, catecholamine levels and serum insulin levels may be involved in the blood pressure lowering associated with weight loss. Since the risk of cardiovascular disease in the hypertensive patient is not only determined by the blood pressure, an overall treatment which aims at reduction of other risk factors such as glucose intolerance and hyperlipoproteinemia is advocated. Thus, in any obese hypertensive patient normalization of excess body weight and increased physical activity appears to be the first and most important step of any rational therapeutic strategy.
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PMID:Obesity and hypertension: epidemiology, mechanisms, treatment. 636 45

The effects of mazindol on the salivary secretion of dogs was investigated. Mazindol (2 mg/kg, i.v.) decreased the volume and pressure of salivary secretion induced by either chemical (carpronium) stimulation or electrical nerve stimulation. It also reduced spontaneous salivary secretion. Secretion velocity in the mazindol treated group was significantly less than in the physiological saline administered control group at 4 to 6 min after injection. Saline and mazindol produced no significance differences in Na+, Cl- or K+ concentrations in the saliva or serum. Thus mazindol inhibition of salivary secretion was not caused by ion transport. The existence of some other inhibitory mechanism is suggested. The effects of mazindol on the peripheral and central control of gastric acid secretion was also investigated in rats. Gastric acid secretion induced by direct application of cholinergic agents on oxyntic cells was not affected by mazindol. Gastric acid secretion induced by insulin and/or 2-DG, on the other hand, was markedly inhibited by intra-hypothalamic injection or systemic (i.v.) injections of mazindol. Electro-osmotic mazindol mimicked the effects of glucose in the lateral (inhibition) and ventromedial (excitation) hypothalamus. The results suggest that the inhibitory effects of mazindol on salivary secretion may be through the hypothalamic feeding control centers. Mazindol also directly affected gastric acid secretory neurons in the lateral hypothalamus. It might thus be expected to be effective in the treatment of obesity.
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PMID:[Mazindol effects on the salivary and gastric acid secretory mechanisms]. 674 6

There is a close epidemiological association between obesity and blood pressure for all age groups, although not every obese individual becomes hypertensive. In populations without age-related increases in body weight, an elevation of blood pressure with age is not seen. Treatment of obesity by weight loss decreases blood pressure substantially; however, in a minority of patients blood pressure does not fall with weight loss. Blood pressure generally decreases before normal weight is achieved. Blood pressure after weight loss remains reduced as long as there is no marked regain of body weight. Salt intake reduction does not appear to explain why weight reduction lowers blood pressure. Reduced levels of plasma renin activity, serum aldosterone levels, catecholamine levels, and serum insulin levels may be involved in the blood pressure lowering associated with weight loss. Since the risk to the hypertensive patient is not only determined by the blood pressure, an overall treatment that aims at reduction of all risk factors is advocated. Some risk factors, e.g., glucose intolerance, may be normalized only when desirable weight is achieved. Thus, in any obese hypertensive patient with other risk factors, normalization of excess body weight appears to be the first the most important step of any rational therapeutic strategy.
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PMID:Obesity and hypertension: cardiovascular response of weight reduction. 704 31

Two blood pressure (BP) measurements separated by 3 months were performed according to international guidelines on 2976 students (11 to 19 years) of different economic levels. Obesity was defined based upon height and weight. With the first measurements, 59th and 95th percentile value distribution curves were defined. Systolic hypertension (SH) was found in 9.5%; 10.2% were males and 8.9% females. The sample showed that 8.1% were obese (240 cases); among them the incidence of SH increased to 28.8% (69 cases) (p less than 0.01). In the entire sample, diastolic hypertension (DH) was 4.3%; males, 2.7%, and females, 5.5% (p less than 0.01). Among obese students, DH increased to 8.3% (20 cases) (p less than 0.01), and showed prevalence figures of 5.8% for obese males and 10.3% (14 cases) for obese females. After a second measurement, DH for the sample decreased to 1.8%. Salt intake and familial antecedents of high BP showed differences between hypertensive and normal populations.
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PMID:Blood pressure levels in urban school-age population in Chile. 729 40

Sodium (Na) intake is one of the important environmental factors influencing the development and maintenance of high blood pressure (BP). Patients with essential hypertension can be divided into two groups: "salt-sensitive" and "non-salt-sensitive", according to BP response to salt loading, suggesting the heterogeneity of salt sensitivity of BP. Salt-sensitive patients had greater increases in BP by salt loading, associated with greater Na retention. Although the precise mechanism for impaired renal Na handling in salt-sensitive patients is still unknown, the sympathetic nervous system in the kidney may play an important role in the decreased renal function of Na excretion and the increased salt sensitivity. Moreover, there are several pieces of evidence indicating that increased renal sympathetic nerve activity is intimately related to the abnormal central noradrenergic systems. In addition, the renin-angiotensin system, insulin, and so on, may modulate salt sensitivity of BP. Some ions influence the hypertensinogenic effect of Na: Chloride ion facilitates it, while potassium, calcium and magnesium antagonize it. Moreover, obesity and a stressful environment increase salt sensitivity of BP.
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PMID:[Role of electrolytes in the development and maintenance of hypertension]. 795 91

Correction of the obese state induced by genetic leptin deficiency reduces elevated levels of both blood glucose and hypothalamic neuropeptide Y (NPY) mRNA in ob/ob mice. To determine whether these responses are due to a specific action of leptin or to the reversal of the obese state, we investigated the specificity of the effect of systemic leptin administration to ob/ob mice (n = 8) on levels of plasma glucose and insulin and on hypothalamic expression of NPY mRNA. Saline-treated controls were either fed ad libitum (n = 8) or pair-fed to the intake of the leptin-treated group (n = 8) to control for changes of food intake induced by leptin. The specificity of the effect of leptin was further assessed by 1) measuring NPY gene expression in db/db mice (n = 6) that are resistant to leptin, 2) measuring NPY gene expression in brain areas outside the hypothalamus, and 3) measuring the effect of leptin administration on hypothalamic expression of corticotropin-releasing hormone (CRH) mRNA. Five daily intraperitoneal injections of recombinant mouse leptin (150 micrograms) in ob/ob mice lowered food intake by 56% (P < 0.05), body weight by 4.1% (P < 0.05), and levels of NPY mRNA in the hypothalamic arcuate nucleus by 42.3% (P < 0.05) as compared with saline-treated controls. Pair-feeding of ob/ob mice to the intake of leptin-treated animals produced equivalent weight loss, but did not alter expression of NPY mRNA in the arcuate nucleus. Leptin administration was also without effect on food intake, body weight, or NPY mRNA levels in the arcuate nucleus of db/db mice. In ob/ob mice, leptin did not alter NPY mRNA levels in cerebral cortex or hippocampus or the expression of CRH mRNA in the hypothalamic paraventricular nucleus (PVN). Leptin administration to ob/ob mice also markedly reduced serum glucose (8.3 +/- 1.2 vs. 24.5 +/- 3.8 mmol/l; P < 0.01) and insulin levels (7,263 +/- 1,309 vs. 3,150 +/- 780 pmol/l), but was ineffective in db/db mice. Pair-fed mice experienced reductions of glucose and insulin levels that were < 60% of the reduction induced by leptin. The results suggest that in ob/ob mice, systemic administration of leptin inhibits NPY gene overexpression through a specific action in the arcuate nucleus and exerts a hypoglycemic action that is partly independent of its weight-reducing effects. Furthermore, both effects occur before reversal of the obesity syndrome. Defective leptin signaling due to either leptin deficiency (in ob/ob mice) or leptin resistance (in db/db mice) therefore leads directly to hyperglycemia and the overexpression of hypothalamic NPY that is implicated in the pathogenesis of the obesity syndrome.
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PMID:Specificity of leptin action on elevated blood glucose levels and hypothalamic neuropeptide Y gene expression in ob/ob mice. 860 77

A clinical evaluation of the Easy-Flow External Condom Catheter (Delphi Medical Products) was performed on incontinent patients of the Salt Lake City VA Medical Center. All 20 subjects were experienced users of condom catheters prior to entering the study. Use of the experimental device reduced frequency of change for 10 patients, increased daytime dryness for 13 patients, and improved nighttime dryness for 10 patients. All except one of the 20 subjects found the Easy-Flow Catheter easier to apply and all rated it easiest to remove. Overall, 13 of the 20 patients indicated that they preferred the Easy-Flow Catheter to all others used in the past. Although obesity and presence of a small penile shaft were observed to reduce satisfaction with the new device, the Easy-Flow Catheter may improve patient satisfaction for many patients who experience problems with other external condom catheters.
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PMID:Clinical evaluation of the easy-flow catheter. 910 48


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