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

Endogenous Cushing's syndrome, obesity and chronic glucocorticod treatment are characterized by blunted GH secretion. The administration of GHRH is capable of stimulating a small but significant PRL increase in normal subjects. The current study was designed to determine plasma PRL levels in response to GHRH, studied in three different situations characterized by a blunted GH secretion. Obese patients (n = 6) with a weight over 30% of ideal body weight, patients with active Cushing's syndrome, and normal volunteers treated with dexamethasone 22 mg per os over two days before the pituitary challenge were studied. As a control group 18 normal subjects of similar age and sex were studied. GH and PRL was determined at intervals after GHRH (1 microgram/kg). GHRH-induced GH secretion was markedly reduced in patients with obesity, patients with endogenous Cushing's syndrome and volunteers treated with dexamethasone. In contrast, GHRH-induced PRL secretion was not affected in these three clinical situations. In summary, in three situations characterized for an impairment of the somatotroph cell, due to a primary intrinsic defect or to a functional hypothalamic alteration, there is a persistent GHRH-induced PRL secretion, suggesting that prolactin could be released by mammosomatotrophs that function normally in spite of hyposomatotropism.
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PMID:Persistent GHRH-induced PRL secretion in Cushing's syndrome, obesity and exogenous hypercortisolism. 788 70

Long term changes in the secretion of prolactin were monitored in groups of hypothalamo-pituitary disconnected rams (HPD rams, n = 8) and control rams (HPD sham-operated and unoperated, n = 8) while exposed to an artificial lighting regimen of alternating 16-weekly periods of long days (16L:8D) and short days (8L:16D) for 72 weeks, and during a treatment with subcutaneous constant-release implants of melatonin under long days. The HPD rams showed all the clinical characteristics of complete pituitary disconnection (diabetes insipidus, gonadal regression and slight obesity), and were unresponsive to a range of provocation tests (exposure to a barking sheep dog, cannulation of the jugular vein, injection of serotonin and NMDA) which caused acute changes in the blood plasma concentrations of prolactin in the controls. Nevertheless, there was a clearly defined cycle in the blood concentrations of prolactin in the HPD rams related to the imposed lighting regimen with values 10-fold higher under long days compared to short days (HPD mean +/- SEM: 90.1 +/- 24.7 vs 9.4 +/- 2.0 micrograms/l, long vs short day respectively, P < 0.001). The temporal pattern was very similar to that observed in the controls, although the concentrations of prolactin were higher in the HPD rams and more variable (control mean +/- SEM: 55.6 +/- 3.6 vs 3.0 +/- 0.5 micrograms/l, long vs short day, P < 0.001). There was a corresponding cycle in the growth and moulting of the wool in the HPD rams consistent with a biological response to the photoperiodically-induced changes in the secretion of prolactin. The diurnal rhythm in the blood concentrations of prolactin was absent in the HPD rams, but there was a normal rhythm in the secretion of melatonin. The treatment of the animals with constant-release implants of melatonin under long days caused a marked decrease in the blood concentrations of prolactin in both the HPD and control rams. The overall conclusion is that the endogenously generated daily melatonin signal which encodes daylength acts directly in the pituitary gland to mediate the effects of photo-period on the secretion of prolactin. The photo-period transduction pathway thus by-passes the hypothalamus.
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PMID:Photoperiodically-induced cycles in the secretion of prolactin in hypothalamo-pituitary disconnected rams: evidence for translation of the melatonin signal in the pituitary gland. 792 May 91

Low-calorie diet therapy (LCDT) was used to treat obesity in 74 females aged 18-49 in four regimens: short-term (up to 7 days), of middle duration (10-14 days), long-term (up to 21-24 days) and fractionated. Middle duration of LCDT proved most favourable. Long-term fasting may bring unstable effects or complications. LCDT results in electrolyte unbalance, hypokalemia, hypokaligestia. Relevant correction is necessary on the diet day 5-6. Red cell count, blood levels of sugar and protein, lipidogram, nitrogenous metabolism, coagulation activity changed insignificantly. Obese patients on LCDT exhibited reduced hyperinsulinism responsible for body mass decrease, hyperproduction of hydrocortisone and prolactin enhancing fat synthesis. They also developed T3-hypothyrosis reducing thermogenesis. The changes in the body mass depended on these factors.
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PMID:[Clinical, metabolic and hormonal changes in patients with obesity on low-calorie diet therapy]. 797 33

The detection of clinical hyperandrogenism in women presenting with infertility requires detailed hormonal investigations using the decisional plan suggested here. Initial studies including measurement of plasma androgen, gonadotrophic hormones and prolactin levels, may be sufficient to reveal an adrenal origin or pure ovarian origin. Non-tumor androgenic hypercorticism is seen classically in late-presenting enzyme deficits, but also in other situations: excessive adrenarche, hyperprolactinemia, obesity, chronic stress. The immediate Synacthene test can then eliminate diagnostic uncertainties if it leads to the discovery of appearances of 21- or 11-hydroxylase or 3 beta-ol dehydrogenase blocks. Intense virilisation in a woman with a testosterone level above 2 ng/ml (7 nM/l) should lead to suspicion of an androgen-secreting tumor of the ovary or adrenal. CT scan of the abdomen and true pelvis is essential here since it may reveal the presence of an adrenal or ovarian mass. If no morphological abnormality is shown by this investigation, an endocrine lesion of a small ovary should be strongly suspected, the demonstration of which requires isotope techniques and/or catheterisation of the ovarian veins. Two situations also exist which are responsible for severe hyperandrogenism but less alarming in terms of their course and significance: certain homozygous forms of 21-hydroxylase deficit diagnosed late and ovarian hyperthecosis. It may happen that these hormonal investigations do not suffice alone to determine the precise origin of hyperandrogenism and its cause. The dexamethasone adrenal suppression test is useful in the diagnosis of type II micropolycystic dystrophy, in order to define the essentially ovarian, adrenal or mixed origin of hyperandrogenism.
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PMID:[Diagnostic strategy in infertility due to hyperandrogenism. Development of a decision tree]. 803 86

The neural regulation of food intake seems to be quite similar in birds and mammals. The ventromedial hypothalamic syndrome produced by lesions within the mediobasal hypothalamus of both birds and mammals is composed of several independent physiological and behavioral changes. Other neural sites known to be important in mammals for regulating food intake need to be examined in birds including the paraventricular nucleus, nucleus tractus solitarius and parabrachial nucleus. Members of the opioid and pancreatic polypeptide families are effective in stimulating food intake in avian species. Both prolactin and growth hormone are also efficacious in stimulating food intake. In contrast, cholecystokinin inhibits food intake when administered intracerebroventricularly. The autonomic and endocrine hypothesis developed to explain obesity in mammals appears to be quite applicable to genetic strains of commercial birds selected for meat production. Specifically the commercial broiler appears to display an imbalance of the autonomic nervous system. The parasympathetic nervous system dominates as a consequence of intense genetic selection for growth rate.
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PMID:Central neuroanatomical systems involved in the regulation of food intake in birds and mammals. 806 84

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 case of hypothalamic dysfunction in a girl with a twelve-year follow-up is reported. Onset occurred at the age of three with severe obesity, hypothermia, hypersomnia, and lethargy. Somatotropic, gonadotropic, and thyrotropic hormones were low, whereas prolactin was increased. Imaging techniques failed to disclose any lesion of the hypothalamus or pituitary. Clomipramine improved the vegetative disorders. The literature on clinical and hormonal disorders of hypothalamic dysfunction is reviewed.
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PMID:[Hypothalamic syndromes. Review of clinical and endocrinal semiology]. 823

The prevalence of obesity is increasing in the developed as well as underdeveloped countries. Obesity in women is associated with reproductive disorders. The levels of estrone and androgens are higher in obese women along with a reduction in the levels of sex hormone binding globulin ( SHBG ). The pituitary secretion of hormones is altered either due to a deficient peripheral feedback regulation or a concomitant central defect in the obese. Luteinizing hormone ( LH ) level may increase in some of the obese subjects. The secretion of LH in response to luteinizing hormone releasing hormone ( LHRH or GnRH ), clonidine and naloxone may be altered in obese women. The levels of circulating prolactin may fall along with a delay in the nocturnal surge of the hormone. The secretion of prolactin in response to thyrotropin releasing hormone ( TRH ), insulin-induced hypoglycemia, arginine and chlorpromazine is altered. Similarly growth hormone secretion in response to growth hormone releasing hormone ( GHRH ), clonidine, naloxone and arginine is also altered in obesity. The literature suggests an alteration in the autonomic nervous system activity and the metabolism of carbohydrates and fats in the obese. Steroid hormones could affect the distribution of fat in the various regions of the body, and the distribution of body fat is linked with the severity of hyperandrogenism and metabolic disorders in obese subjects. However, it is heartening to note that many of the endocrinological and reproductive disorders are reversible with weight reduction in the obese subjects.
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PMID:Reproductive functions in obese women. 837 28

A role for circadian neuroendocrine rhythms in the age-related development of obesity and insulin resistance was investigated in the male Sprague-Dawley rat. The phases and amplitudes of the plasma rhythms of several metabolic hormones (i.e., corticosterone, prolactin, insulin, and triiodothyronine) differed in lean, insulin-sensitive (3-week-old rats), insulin-resistant (8-week-old rats) and obese, insulin-resistant (44-week-old rats) animals. Simulation of the daily rhythms of endogenous corticosterone and prolactin by daily injections of the hormones at times corresponding to the peak levels found in 3-week-old rats reversed age-related increases in insulin resistance and body fat in older (5-6-month-old) rats. Ten such daily injections of corticosterone and prolactin in 12-14-week-old rats produced long-term reductions in body fat stores (30%), plasma insulin concentration (40%), and insulin resistance (60%) (determined by a glucose tolerance test) measured 11-14 weeks after the treatment. Alterations in circadian neuroendocrine rhythms may account for age-related changes in carbohydrate and lipid metabolism in the male Sprague-Dawley rat, and resetting of these rhythms by appropriately timed daily injections of corticosterone and prolactin may help maintain metabolism characteristic of younger animals.
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PMID:Circadian neuroendocrine role in age-related changes in body fat stores and insulin sensitivity of the male Sprague-Dawley rat. 840 68

Previous reports have shown that long-term administration of typical and atypical neuroleptics induced obesity in female but not in male rats. It has been suggested that impaired ovarian steroidogenesis related to neuroleptic-induced hyperprolactinemia is necessary to observe the body weight changes. This hypothesis was tested with clozapine, an atypical neuroleptic that produces in rats a shorter increase in serum prolactin levels than do other neuroleptics. The effects of clozapine on body weight and food intake were assessed in female and male rats under treatment with any of the following doses: 0.5, 1, 2.5, 5, 10, and 20 mg/kg IP for 21 days. Vaginal cycle under clozapine treatment, as an indirect indicator of ovarian steroidogenesis, was also assessed. Obesity was not observed in any group. By contrast, clozapine at the doses of 10 and 20 mg/kg significantly decreased body weight and feeding in male rats. Clozapine at the doses of 5 and 10 mg/kg IP induced permanent diestrus. The failure of clozapine to induce obesity in female rats, despite impaired vaginal cycle, can be considered indirect evidence that drug-induced hyperprolactinemia is not sufficient to observe neuroleptic-induced obesity in rats.
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PMID:Effects of long-term administration of clozapine on body weight and food intake in rats. 851 72


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