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

A child with respiratory failure and cor pulmonale secondary to the obesity hypoventilation syndrome (OHS) was found to have abnormal beta-endorphin levels in cerebrospinal fluid (CSF) and serum. A single iv dose of 10 microgram/kg of naloxone early in the course of respiratory failure resulted in dramatic improvement which lasted approximately 3 to 4 h. The patient failed to response to progesterone, and because of deteriorating respiratory status a low-dose continuous infusion of naloxone, 2 microgram/kg.h, was begun and gradually increased to 10 microgram/kg.h, during which time there was a dramatic improvement in respiratory status and clinical condition. After 5 days, naloxone infusion was discontinued and progressive respiratory deterioration recurred. The child died of over-whelming sepsis and disseminated intravascular coagulation.
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PMID:Narcotic antagonist therapy of the obesity hypoventilation syndrome. 628 52

The association of acanthosis nigricans with pituitary tumors and insulin-resistant diabetes suggests that a pituitary peptide may promote papillomatosis and acanthosis characteristic of acanthosis nigricans. Although such a peptide has not been isolated, it may derive by sequential cleavage from the 31,000-dalton precursor peptide to ACTH and beta-lipotropin (beta-LPH). In order to evaluate the role of pituitary peptides in the pathogenesis of acanthosis nigricans, we compared plasma levels of beta-endorphin (beta-EP) and ACTH in plasma of 8 fasting patients with obesity-associated benign acanthosis nigricans and 7 fasting normal controls utilizing sensitive radioimmunoassay procedures. Mean plasma beta-EP levels for the acanthosis nigricans and control subjects were not significantly different (90 pg/ml vs. 140 pg/ml), nor was any significant difference observed between plasma ACTH levels of the 2 groups (42.3 and 31.2 pg/ml, respectively.) Our data indicate that plasma levels of the pituitary-derived peptides ACTH and beta-EP are not increased in obesity-associated benign acanthosis nigricans, and suggest that its proposed hormonal mediator might originate independently from the large peptide precursor of ACTH, beta-LPH and their fragments.
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PMID:Neuropeptides in the pathogenesis of obesity-associated benign acanthosis nigricans. 629 89

A 29-year-old woman presented with hirsutism, obesity, oligomenorrhea, and infertility caused by oligoovulation and tubal occlusion. Partial 21-hydroxylase deficiency of the adrenal was suggested by an abnormal adrenocorticotropic hormone (ACTH) stimulation test. The patient subsequently developed bilateral tuboovarian abscesses and underwent abdominal hysterectomy and bilateral salpingo-oophorectomy. Thus, an opportunity was presented to study the adrenal endocrine disorder in the absence of ovaries and to investigate the effect of human chorionic gonadotropin (hCG) on the adrenals. There was no change in the adrenal response to ACTH stimulation after oophorectomy. hCG stimulation resulted in an increase in dehydroepiandrosterone sulfate and 17 beta-estradiol levels, suggesting that hCG had a stimulatory effect on the adrenal. The ovarian-adrenal relationship and effects of adrenal stimulation in the absence of ovaries are discussed.
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PMID:Effect of adrenocorticotropic hormone and human chorionic gonadotropin before and after bilateral oophorectomy in a patient with acquired adult-onset adrenal hyperplasia: a case report. 629 2

The blood beta-endorphin and beta-lipotropin content was studied by radioimmunoassay in patients with obesity of different degree and healthy subjects with normal body weights. It was shown that the blood beta-endorphin concentration rises depending on the body weight growth, promoting the intensified insulin secretion and obesity development. beta-Lipotropin level was significantly augmented in patients with the 3d and 4th stages of obesity. The intensified beta-lipotropin secretion, stimulating lipolysis, may be considered as a compensatory mechanism, tending to return to normal fat metabolism in the originated pathological conditions. Comparison of beta-endorphin and beta-lipotropin levels in the blood of obese patients suggests that obesity is not only marked by hormonal disorders, producing obesity progression but also by the formation of adaptive mechanisms, directed at compensation of the pathological process.
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PMID:[Beta-endorphin and beta-lipotropin in the pathogenesis of obesity]. 630 Aug 30

Pituitary beta-endorphin content was measured in dormice during several distinct phases of the infradian body weight cycle. No significant differences in opiate content among groups were found. It appears unlikely that pituitary concentrations of beta-endorphin have etiological significance in the development of spontaneous obesity in hibernators.
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PMID:Pituitary beta-endorphin content during spontaneous food intake and body weight cycles in the dormouse, Glis glis. 631 9

Based on the findings of elevated circulating beta-endorphin (beta-END) levels in genetically obese (fa/fa) fats and the reversal of the overeating of genetically obese (ob/ob) mice by naloxone, circulating beta-END and beta-lipotropin (beta-LPH) levels were measured in 8 hirsute, hyperandrogenic, oligo-amenorrheic women of varying weights. Circulating beta-END and beta-LPH levels were significantly elevated (p less than .001) above the levels in nonobese control subjects and were positively correlated with body weight (p less than .025). Based on these data and indirect evidence in the literature, we propose a role may exist for beta-END and/or beta-LPH in human obesity and in adrenal androgen secretion.
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PMID:beta-Endorphin and beta-lipotropin plasma levels in hirsute women: correlation with body weight. 644 74

Digoxin was studied to see whether it impairs adrenal function and feminizes male subjects by changing plasma sexual hormones; both have been reported on previously. In eight healthy male subjects neither estrone (38.7 +/- 7.7 vs 35.4 +/- 3.2 pg/ml) nor estradiol (35.8 +/- 6.4 vs 32.2 +/- 3.9 pg/ml) nor testosterone (6.32 +/- 0.74 vs 6.45 +/- 0.73 ng/ml) were found to be altered by digoxin administration (plasma levels 1.55 +/0- 0.27 ng/ml) lasting 35 days. The same was true of free testosterone (147 +/- 24 vs 142 +/- 19 pg/ml) and free estradiol (657 +/- 77 vs 615 +/- 78 fg/ml). Even maximal stimulation of the adrenal and gonadal glands by adrenocorticotropic hormone (ACTH) and human chorionic gonadotropin (hCG) did not exhibit any digoxin-induced alterations in the synthesizing capacity of steroid hormones, as shown by plasma cortisol (increase from 128 +/- 18 to 389 +/- 18 ng/ml) and testosterone (from 5.96 +/- 0.90 to 10.33 +/- 1.19 ng/ml). Furthermore, seven subjects on digoxin were observed over a period of 150-210 days; they did not show any increase of estrogens. This was also found in three subjects when estrogen levels were elevated initially due to extreme obesity. Also, 35 patients who took beta-methyldigoxin (n = 8), beta-acetyldigoxin (n = 20) and digitoxin (n = 7) from 1 to 9 (mean: 1.9) years demonstrated normal plasma concentrations of gonadal and adrenal steroids, irrespective of duration of application or the digitalis compound.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[No effect of digitalis on sex and adrenal hormones in healthy subjects and in patients with congestive heart failure]. 670 91

A 37-year-old woman presented with acute psychosis and cognitive impairment. Skull x-ray showed an enlarged sella turcica with erosion of the floor. Endocrinologic workup suggested the diagnosis of Cushing's disease and hyperprolactinemia. She had no cushingoid feature, and the only physical sign was mild generalized obesity. She showed a paradoxic response to dexamethasone suppression, and underwent trans-sphenoidal resection of a pituitary macroadenoma. Electron microscopy showed the tumor to be a Crooke's cell adenoma. Results of immunohistochemical staining were positive only for ACTH and beta-endorphin. The neuropsychiatric manifestations resolved after surgery.
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PMID:Occult Cushing's disease presenting with acute psychosis. 671 82

Pituitary and central beta-endorphin have been implicated in the regulation of food intake. It has been suggested that an elevation in hypophyseal beta-endorphin represents the genetic defect in the obese mutant Zucker rat. Both pituitary and central beta-endorphin systems appear to interact with dopamine. We have therefore examined hypophyseal, hypothalamic, and basal forebrain levels of beta-endorphin in the obese Zucker rat, its lean littermate, and lean littermates sustaining neurotoxic lesions of the A10 dopamine cell group in the ventral mesencephalon. The obese mutant exhibits elevated pituitary, but not central, beta-endorphin levels relative to lean littermates. A10 lesions result in a marked increase in both pituitary and hypothalamic beta-endorphin levels, and tend to decrease the amount of the peptide in the basal forebrain. These lesions do not result in either increased food intake or body weight. These data therefore suggest that elevated pituitary beta-endorphin levels do not mediate obesity in the Zucker rat, and also demonstrate that both central and pituitary beta-endorphin are modulated by a dopamine system originating in the ventral mesencephalon.
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PMID:Mesencephalic dopamine modulation of pituitary and central beta-endorphin: relation to food intake regulation. 686 61

Neuropeptide Y (NPY), a major brain neurotransmitter, is expressed in neurons of the hypothalamic arcuate nucleus (ARC) that project mainly to the paraventricular nucleus (PVN), an important site of NPY release. NPY synthesis in the ARC is thought to be regulated by several factors, notably insulin, which may exert an inhibitory action. The effects of NPY injected into the PVN and other sites include hyperphagia, reduced energy expenditure and enhanced weight gain, insulin secretion, and stimulation of corticotropin and corticosterone release. The ARC-PVN projection appears to be overactive in insulin-deficient diabetic rats, and could contribute to the compensatory hyperphagia and reduced energy expenditure, and pituitary dysfunction found in these animals; overactivity of these NPY neurons may be due to reduction of insulin's normal inhibitory effect. The ARC-PVN projection is also stimulated in rat models of obesity +/- non-insulin diabetes, possibly because the hypothalamus is resistant to inhibition by insulin; in these animals, enhanced activity of ARC NPY neurons could cause hyperphagia, reduced energy expenditure, and obesity, and perhaps contribute to hyperinsulinemia and altered pituitary secretion. Overall, these findings suggest that NPY released in the hypothalamuss, especially from the ARC-PVN projection, plays a key role in the hypothalamic regulation of energy balance and metabolism. NPY is also found in the human hypothalamus. Its roles (if any) in human homeostasis and glucoregulation remain enigmatic, but the animal studies have identified it as a potential target for new drugs to treat obesity and perhaps NIDDM.
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PMID:Neuropeptide Y, the hypothalamus, and diabetes: insights into the central control of metabolism. 747 13


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