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

Neonatal administration of monosodium glutamate (MSG) results in severe adenohypophyseal endocrine malfunction as a result of hypothalamic neurotoxic lesioning. The present study examined the effects of administration of MSG on the neurohypophyseal vasopressinergic (AVP) system and systolic blood pressure (SBP) in adulthood. Monosodium glutamate or hypertonic sodium chloride was administered to male and female rat pups on days 1, 3, 5, 7 and 9 after birth. MSG treatment produced several features characteristic of the MSG-toxicity syndrome, including obesity, anterior pituitary dysgenesis and hypogonadism. However, MSG did not alter neurohypophyseal AVP profiles: AVP content of the posterior pituitary and microdissected regions of the hypothalamus and brainstem were similar in MSG-treated and control rats. Furthermore, MSG treatment did not alter water intake, serum AVP concentration, or the ability to reduce urine output in response to water deprivation. Thus, despite insult to adenohypophyseal function by neonatal administration of MSG, the neurohypophyseal AVP system remained functionally intact. In contrast, neonatal treatment with MSG altered SBP in a sex dependent manner. Female MSG-treated rats, unlike male MSG-treated rats, exhibited consistent systolic hypotension when compared with the NaCl-treated or non-treated control rats at 6, 9 and 12 weeks of age. Despite this chronic hypotension in MSG-treated female rats, heart rate was not altered and serum AVP was not elevated. These observations suggest a resetting of the baroreflex, attributable to neonatal administration of MSG.
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PMID:Monosodium glutamate neurotoxicity: a sex-specific impairment of blood pressure but not vasopressin in developing rats. 375 44

The feeding responses induced by systemic administration of 2-deoxy-D-glucose (2-DG) and paraventricular hypothalamic injection of norepinephrine were assessed in Brattleboro rats deficient in vasopressin (VP). Controlling for the non-specific complications of diabetes insipidus, it was found that Brattleboro rats have a deficient 2-DG-feeding response, but an essentially normal noradrenergic-feeding response. Specific carbohydrate appetite abnormalities were also demonstrated. It is argued that VP influences 2-DG feeding by mobilizing endogenous energy stores following its acute release from the hypothalamoneurohypophysial system. A new function is thus ascribed for VP and the neural lobe of the pituitary. It is suggested that VP plays a role in stress-induced feeding and in specific aspects of carbohydrate appetite. The potential relevancy of vasopressin perturbations to bulimia nervosa and to the Prader-Willi obesity syndrome is also discussed.
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PMID:Vasopressin and glucoprivic-feeding behavior: a new perspective on an 'old' peptide. 377 90

A study was made of change in hormone secretion in 243 patients with alimentary-constitutional and hypothalamic obesity. Activation of the somatostatin mechanism, a decrease in somatotropic and thyrotropic function of the hypophysis, an increment of corticotropin, beta-lipotropin and vasopressin levels in the blood, disturbance of circadian fluctuations of hormone secretion, an increase in insulin and C-peptide secretion, a decrease in glucagon secretion and triiodothyronine and cortisol levels in the blood, activation of the renin-aldosterone system and cortisol secretion rate were equally expressed both in alimentary-constitutional and primary hypothalamic obesity. The central mechanisms of the regulation of endocrine functions were incorporated in a pathological process even in alimentary-constitutional obesity. Disorders of the hypothalamic regulation lay in the basis of both types of obesity.
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PMID:[Comparative evaluation of the hormonal changes in alimentaro-constitutional and hypothalamic obesity]. 395 72

Hepatic plasma membranes of female obese mice C57 BL-6 orl ob/ob (ob/ob mice) completely lack vasopressin (VP) receptors of the V1 type whereas kidney VP receptors are normally expressed and functionally coupled to adenylate cyclase. To discover if these alterations are linked to a genetic defect of the V1 receptor, we have studied the binding of VP on liver and kidney membranes of two other models, female diabetic mice C57 BL-6 orl db/db (db/db mice) and female Zucker rats Fatty/orl fa/fa (fa/fa rats), which exhibit different temporal pattern of obesity, hyperinsulinemia and insulin resistance. In addition, since VP is known to exert its vascular response through stimulation of V1 receptors, we have studied the reactivity of VP of isolated tail artery in the three different models, ob/ob and db/db mice and fa/fa rats, and in their respective controls. In all cases, VP kidney receptors and VP vascular reactivity are normal. db/db mice exhibit a marked decrease in hepatic VP receptors whereas a 50% decrease was observed in 32 week fa/fa rats. Angiotensin II and prazosin binding sites are still present as well as the adenylate cyclase response to glucagon. These results suggest that the specific alteration in liver VP receptors is not related to a defect in V1 receptor genetic expression but is specific for liver and appears to parallel the level of hyperinsulinemia and/or insulin resistance.
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PMID:Reduction in hepatic but not in renal and vascular vasopressin receptor number in hyperinsulinemic mice and rats. 609 84

Experimental obesity produced in rats by stereotaxic lesions of the ventromedial hypothalamus (VMH) resulted in hyperphagia, polydipsia, polyuria, decreased urine osmolality, and enhanced excretion of total solute and urea. A 24-h water deprivation test revealed the inability of VMH-lesioned rats to increase urine antidiuretic hormone (ADH) excretion. Thus, destruction of the VMH area appears to be accompanied by impairment of ADH secretion, resulting in a diabetes insipidus syndrome that is partially masked by food restriction and improved by treatment with exogenous ADH.
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PMID:Abnormal water turnover associated with hypothalamic obesity. 700 48

Although insulin resistance and hypertension are commonly associated, the underlying cause for this association remains unknown. Plasma concentrations of the recently described hormone amylin, which is cosecreted with insulin by the pancreatic beta cell, are reported to be elevated in various states of insulin resistance, including hypertension and obesity. Preliminary studies by our group have suggested that there are amylin binding sites in the kidney. In nine healthy humans an infusion of human amylin that resulted in steady state plasma amylin levels in the subnanomolar range led to significant increases in plasma renin and aldosterone concentrations. These changes occurred in the absence of significant changes in plasma electrolytes, catecholamines, vasopressin, total renin, or osmolality. Diastolic pressure at 30 minutes and plasma glucose at 60 minutes rose modestly. Since amylin has both metabolic and renal actions, this peptide may be an important link between hypertension, insulin resistance, and the renin-angiotensin system.
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PMID:Amylin stimulates plasma renin concentration in humans. 764 82

Animal experiments have shown that the parvocellular oxytocin (OXT) neurons of the hypothalamic paraventricular nucleus (PVN) inhibit food intake. In the present study, the PVN and its OXT neurons have been investigated in an extreme human eating disorder, i.e. the Prader-Willi syndrome (PWS). PWS patients are characterized by gross obesity, insatiable hunger, hypotonia, hypogonadism, and mental retardation. The PVN of 5 PWS patients (2 males and 3 females), varying in age between 22-64 yr, and 27 controls (14 males and 13 females) without any primary neurological or psychiatric diseases was morphometrically investigated after conventional staining with thionine and immunocytochemical staining for OXT and vasopressin (AVP). The thionine-stained volume of the PVN was 28% smaller in PWS patients (P = 0.028), and the total cell number was 38% lower (P = 0.009). The immunoreactivity for OXT and AVP was decreased in PWS patients, although the variability within the groups was high. A strong and highly significant decrease (42%; P = 0.016) was found in the number of OXT-expressing neurons of the PWS patients. The volume of the PVN-containing OXT-expressing neurons decreased by 54% (P = 0.028) in PWS. The number of AVP-expressing neurons in the PVN did not change significantly. The OXT neurons of the PVN seem to be good candidates for playing a physiological role in ingestive behavior as "satiety neurons" in the human hypothalamus.
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PMID:Alterations in the hypothalamic paraventricular nucleus and its oxytocin neurons (putative satiety cells) in Prader-Willi syndrome: a study of five cases. 785 23

Measurements of blood lipids and hormones (plasma renin, aldosterone, vasopressin, prolactin, atrial natriuretic peptide, beta-endorphin, thyrotropin, thyroid hormones) in two groups of patients suffering from obesity (group 1: 64 patients with arterial hypertension and group 2: 26 patients with normal arterial pressure) have brought the authors to a conclusion that arterial hypertension in young obese patients is an early manifestation of essential hypertension. Hormonal dysfunction in obese patients is conducive to early development of essential hypertension in cases when there is a hereditary predisposition to it.
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PMID:[Hormonal aspects of the pathogenesis of arterial hypertension in young obese patients]. 810 42

A 62-year-old male with small cell lung cancer (SCLC) associated with Cushing's syndrome and diabetes insipidus (DI) is reported. The patient was referred to our hospital for treatment of SCLC. A diagnosis of paraneoplastic Cushing's syndrome was made on the basis of an elevated serum ACTH (623.5 pg/ml) level, elevated excretion of urinary 17-OHCS (18.01 mg/day), obesity, hypertension, hyperglycemia, persistent hypokalemia, alkalosis, and no history of diabetes mellitus. He was also diagnosed as having DI based on polyuria and polydipsia, low specific gravity of the urine (1.007-1.010), low serum ADH (1.4 pg/ml) level, normal plasma osmolarity (29 mOsm/kg H2O), and the results of water deprivation test. DI and a left visual field defect was suggestive of metastasis to the pituitary region, but no lesion was detected by either CT scan or MRI scan. The patient failed to show a good response to intensive chemotherapy, and died of the tumor five months after commencing chemotherapy. Post-mortem examination revealed metastases to the hypothalamic-neurohypophyseal region, lungs, liver, adrenal glands, bone, bone marrow, and hilar and mediastinal lymph nodes.
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PMID:[A case of small cell lung cancer associated with diabetes insipidus and Cushing's syndrome]. 839 May 89

In a previous study, we demonstrated that premenopausal women with visceral obesity have hyperactivity of the hypothalamic-pituitary-adrenal (HPA) axis, characterized by an exaggerated hormone response to corticotropin-releasing factor (CRF) and corticotropin (ACTH) stimulation. The hypothalamic peptide flow that stimulates the pituitary, particularly after a physiological stress challenge, involves not only CRF, but also arginine-vasopressin (AVP), which synergizes the CRF capacity to stimulate pituitary hormone secretion. Previous studies in humans have demonstrated that combining AVP with CRF permits maximal stimulation of the pituitary, providing a more appropriate method of assessing pituitary hormone reserve. We therefore investigated the response of the HPA axis to combined CRF and AVP stimuli in obese women with different obesity phenotypes. Moreover, we examined hormonal and cardiovascular responses to several mental stress tasks, according to previously standardized procedures. Two groups of age-matched premenopausal eumenorrheic obese women with visceral (V-BFD) or subcutaneous (S-BFD) body fat distribution and a group of normal-weight healthy controls were investigated. All women randomly underwent the following protocol: (1) a combined CRF/AVP test (100 micrograms plus 0.3 IU intravenously [IV], respectively); (2) a standardized stress test, which consisted of completing two puzzles and a mental arithmetic test; and (3) a control saline test. Blood samples for ACTH and cortisol determinations were obtained before and during each test, and measurements of arterial blood pressure and pulse rate were made at regular intervals during the stress test. After combined CRF/AVP administration, ACTH and cortisol were significantly higher in V-BFD than in the other two groups. In contrast, no significant hormonal variation was found in either group during stress tasks. During the stress test, pulse rate (but not arterial blood pressure) significantly increased after 8 and 15 minutes in the V-BFD group, whereas no significant variation was found in S-BFD and control women. A significant correlation was present between the pulse rate and change in cortisol level during the stress test at minutes 8 (r=.54, P<.05) and 15 (r=.57, p<.01) in all women considered together. Subjective emotional involvement during stressful tasks was measured by a two-dimensional short verbal scale, which revealed that the stress section had a more significant impact in obese V-BFD than in S-BFD and control women. These data therefore confirm that women with visceral obesity have hyperactivity of the HPA axis, and that the combined CRF/AVP stimulation may offer a good tool for investigating pituitary reserve in this obesity phenotype. Moreover, the results indicate that these women probably have a hyperreactive sympathetic response to acute stress that seems interrelated to that of the HPA axis.
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PMID:Hypothalamic-pituitary-adrenal axis activity and its relationship to the autonomic nervous system in women with visceral and subcutaneous obesity: effects of the corticotropin-releasing factor/arginine-vasopressin test and of stress. 860 43


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