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

The role of dopamine (DA) in the secretion of gonadotropic hormones was studied in women with obesity and normal body mass. Tests with sulpiride (peripheral antagonist of DA-receptors), sulpiride LH-RH and thyroliberin were made. Basal and LH-RH-stimulated secretion of gonadotropins and prolactin (PRL) was studied to reveal the relationship of their secretion with the status of the hypothalamohypophyseal system. It was shown that the blockade of peripheral DA receptors did not result in an increase in the basal and LH-RH-stimulated secretion of LH either in healthy women or in women with obesity at the normal basal level of gonadotropic hormones. Hyperprolactinemia caused by sulpiride or LH-RH, did not lower LH secretion during the entire period of investigation. There were no differences either in the basal level of gonadotropic hormones or in their ejection in response to LH-RH administration in women with normal and excess body mass. Stimulation of PRL secretion in response to LH-RH was found in patients with exogenous-constitutional obesity and minimum signs of diencephalic pathology. Slight inhibition of PRL secretion after LH-RH administration was noted in women with obesity of hypothalamic type and unstable type of disorder of EEG. The absence of changes in PRL secretion was noted in women with strongly marked hypothalamic signs of the disease.
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PMID:[The effect of luliberin and sulpiride on the secretion of gonadotropic hormones and prolactin in patients with obesity]. 220 52

Human growth hormone releasing hormone (GHRH) was originally extracted from two pancreatic tumours in patients with acromegaly, and is now known to consist of a 44 residue amidated peptide or its C-terminal-shortened derivatives. The sequence of rat GHRH has also been determined; this 43 residue peptide shows approximately 70% homology with human GHRH, and is located mainly in the arcuate nucleus of the hypothalamus. Pulsatile GH release in the rat is principally a consequence of the pulsatile release of hypothalamic GHRH, although this appears to be associated with a transient suppression of somatostatin release. Exogenous GHRH specifically increases circulating GH in many species, and in the long term may increase growth. In normal man, several analogues of GHRH have been shown to be safe, sensitive and specific stimuli to GH release; although there may be a variable prolactin response, this is usually of small magnitude. Continuous infusion of GHRH leads to a decrement in responsiveness, due at least in part to changes in hypothalamic somatostatin. The GH response to GHRH is also modulated by obesity, blood sugar, free fatty acids, and GH itself. Many children with 'GH deficiency' (idiopathic, radiation-induced, or secondary to hypothalamopituitary tumours) respond to intravenous GHRH with an acute rise in serum GH. Early studies also indicate that long-term therapy with subcutaneous GHRH may increase growth velocity in some of these children. It is concluded that analogues of GHRH are useful in the investigation of the hypothalamopituitary axis, and may be important in the therapy of short stature.
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PMID:Growth hormone releasing hormone. 242 96

In order to study the hypothesized impairment of the serotoninergic system in human obesity, an insulin tolerance test (ITT) was carried out on 12 obese normoprolactinemic women and on 6 normal-weight women before (A) and after (B) the administration of a serotoninergic drug, fenfluramine (60 mg twice a day per os for 7 days). After a washout period, a new ITT (C) followed the administration of fenfluramine at the same dose, associated with a specific S2 blocker receptor agent, ritanserin (30 mg/day for the first 2 days and 20 mg/day for a further 5 days). In obese subjects, the prolactin (PRL) response to ITT A was reduced as compared to the controls: in 6 patients ('nonresponders') the PRL levels did not change, while in the other 6 ('responders') they increased (p less than 0.003) but less than in the controls (p less than 0.02). In normal-weight subjects, the administration of fenfluramine alone or with ritanserin did not modify the PRL response to ITT. In the responders, the serotoninergic drug normalized the PRL response to ITT while significantly improving it in the nonresponders; these effects were not antagonized by ritanserin. In conclusion, our data suggest that the serotoninergic system of obese patients is impaired and that the different secretory pattern observed in the two groups before and after fenfluramine may reflect differing degrees of this impairment.
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PMID:Effects of fenfluramine and ritanserin on prolactin response to insulin-induced hypoglycemia in obese patients: evidence for failure of the serotoninergic system. 250 Dec 8

A fictitious patient with obesity, hirsutism and polycystic ovary syndrome is discussed by 3 British general practitioners to illuminate management of this type of case. The patient is 24 years old, expects to marry next year, has irregular menses averaging 6 weeks apart, and is requesting an explanation for her irregular periods as well as oral contraception. The 1st physician would exclude hypothyroidism, then evaluate polycystic ovary syndrome by assaying testosterone, LH, FSH and prolactin, next find out the significance of the patient's questions in her mind and finally prescribe a triphasic pill. The 2nd doctor would withhold the pill on the grounds that it might compromise future fertility if she has a primary endocrine imbalance. She would check rubella status, assay progesterone, LH, FSH, prolactin and testosterone on Day 19 of the cycle, and probably prescribe Marvelon oral contraceptives. The 3rd doctor would use a hirsutism score, investigate the polycystic ovary syndrome by ultrasound and an essay of sex hormone binding globulin and the LH:FSH and prolactin, next find out the significance of the patient's questions in her mind and finally prescribe a triphasic pill. The 2nd doctor would withhold the pill on the ground that it might compromise future fertility if she has a primary endocrine imbalance. She would check rubella status, assay progesterone, LH, FSH, prolactin and testosterone on Day 19 of the cycle, and probably prescribe Marvelon oral contraceptives. The 3rd doctor would use a hirsutism score, investigate the polycystic ovary syndrome by ultrasound and an assay of sex hormone binding globulin and the LH:FSH ration between Days 2-6 of the cycle, and rule out congenital adrenal hyperplasia with an assay for 17-alpha-OH-progesterone. Since the patient might be anovulatory because of obesity, major long-term weight lose is a priority. Prescription of pills would depend on family history, smoking, and the degree of hirsutism and endocrine status. The most likely prescription would be a reverse sequential of cyproterone acetate 50 or 100 mcg from Days 5-15, and ethinyl estradiol 30 mcg on Days 2-25.
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PMID:Contraception and irregular menses. 259 23

Administrations (injections and in feed) of bromocriptine, a dopamine agonist that inhibits prolactin secretion, reduced body fat stores and plasma total cholesterol and triglyceride concentrations in several rodent species (Syrian hamsters, Djungarian hamsters, Swiss Webster mice and obese Zucker rats). Body fat indices were reduced by at least 50% in the hamsters and mice within 10-15 days of treatment and by 29% in 8 weeks in the rats. Bromocriptine reduced total plasma cholesterol concentration by 17% in Syrian hamsters, 41% in mice and 30% in rats fasted before blood sampling. In nonfasted obese rats, bromocriptine dramatically reduced both cholesterol (from 440 to 130 mg/dl) and triglyceride (from 1570 to 540 mg/dl) levels compared with controls. These findings offer further evidence for a primary role of prolactin in lipid metabolism and indicate that bromocriptine may be useful for treating obesity and lipid-based cardiovascular disorders.
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PMID:Reductions of body fat stores and total plasma cholesterol and triglyceride concentrations in several species by bromocriptine treatment. 260 78

A 32-year-old man is reported with the Morgagni-Morell-Stewart syndrome with hypertension, diabetes, obesity, emotional lability, irritability and thickening of the internal lamina of the frontal bone in radiogram, which is the phatognomonic sing for the syndrome. The syndrome is rarely observed in men. Hormonal determinations showed increased serum concentrations of prolactin and thyrotropic hormone.
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PMID:[Morgagni-Stewart-Morel syndrome in a young man]. 263 53

As is obvious from the previous discussions, obesity is associated with a wide variety of changes in endocrine parameters (Table 1). Some of these changes, such as the reduction in SHBG without change in serum free testosterone levels, reflect merely laboratory abnormalities that may influence interpretation of diagnostic tests but have no important physiologic relevance. Other abnormalities have major clinical impact, such as hyperestrogenemia-endometrial carcinoma and hyperlipidemia-coronary artery disease. In some cases, endocrine changes in obesity are beneficial--that is, hyperestrogenemia leading to lower incidence of osteoporosis. In other cases, such as the profound suppression of growth hormone output in obesity, the physiologic relevance is unknown. Several endocrine changes in obesity, such as the impaired response of many hormones (growth hormone, prolactin, vasopressin, corticotropin) to insulin-induced hypoglycemia and elevated endorphin levels, suggest hypothalamic dysfunction. Furthermore, the failure of all of these abnormalities to be normalized after weight reduction raises the possibility of an underlying disorder leading to both endocrine dysfunction and obesity, rather than the endocrine dysfunction being simply a consequence of the obesity. Successful elucidation of the pathogenesis of obesity, which might then lead to much needed specific treatment modalities, may be advanced if we can solve some of these puzzles.
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PMID:Endocrine aspects of obesity. 264 1

Naturally obese female Syrian hamsters were injected daily with prolactin at 0 or 12 h after cortisol injections for 10 days while held in constant light. Controls were similarly injected with saline. Animals were then held on short daylengths (10 h light:14 h darkness) for 10 weeks. They were allowed free access to food and water from birth to time of death. Ten weeks after treatment, retroperitoneal fat stores, plasma concentrations of insulin and glucose, and hypoglycaemic responsiveness to exogenous insulin were determined. The control groups as well as the 12-h hormone treatment group were obese, hyperinsulinaemic and insulin resistant. However, the 0-h treatment dramatically reduced retroperitoneal fat stores (41-55%), plasma insulin concentration (60-70%) and the insulin to glucose ratio (63-68%) compared with controls. Values for these parameters in the 0-h treatment groups were similar to those of their lean litter-mates. Furthermore, the 0-h group but not the 12-h group was more sensitive than control animals to the hypoglycaemic effects of exogenous insulin at doses 0.2 and 2.0 U/kg body weight. These results demonstrate that timed daily injections of cortisol and prolactin in specific temporal relationships can produce marked reductions in obesity, hyperinsulinaemia and insulin resistance in the Syrian hamster that persist long after the termination of treatment. This study also suggests an important role for the interactions of circadian neuroendocrine systems in the regulation of these metabolic states.
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PMID:Properly timed injections of cortisol and prolactin produce long-term reductions in obesity, hyperinsulinaemia and insulin resistance in the Syrian hamster (Mesocricetus auratus). 264 90

Excess body fat has been clearly associated with an increased risk of oligo-ovulation and endometrial/breast carcinoma. The connection has been assumed to lie within derangements of the metabolic/endocrine compartments, particularly of estrogens and androgens. To differentiate the effect of obesity from its related disease process, an attempt has been made to define the reproductive-endocrinologic alterations encountered in otherwise asymptomatic obese women. Androgen metabolism is accelerated in obesity. It is not clear whether the increased clearance precedes or follows the accelerated production of androgens. A servocontrol mechanism appears to be operative in these asymptomatic individuals, maintaining plasma steroid levels normal. The unbound fraction of T may be somewhat increased in overweight women with predominantly upper body fat deposition. The increased clearance of androgen may arise from an obesity-related depression in SHBG concentration (e.g., for T, E2, delta 5-diol, etc.). Adipose tissue, by virtue of the lipid solubility of most of these steroids, concentrates androgens, estrogens, and progesterone. This steroid sequestration not only contributes to the obesity-related increase in androgen clearance but also leads to an extremely enlarged total body steroid pool. Fat tissue sequestration also increases the concentration of androgens in the vicinity of adipose stromal cells, possibly encouraging their aromatization. Adipose tissue also has a moderate degree of 17-hydroxysteroid dehydrogenase activity, which appears to stimulate the conversion of A to T. Finally, alterations in peripheral and hepatic conjugation and an accelerated urinary excretion may contribute to the elevated clearance of androgens. The accelerated PR of androgens may simply result as compensation for the elevated MCR in obesity. Nonetheless, evidence of alteration(s) in adrenocortical steroidogenesis has been presented suggesting a selective obesity-related enhancement in adrenal androgen secretion. These remain to be confirmed. Nonetheless, adrenocortical abnormalities may arise secondary to the influence of other circulating and intra-adrenal factors, including insulin, prolactin, estrogens, and androgens. It is not known whether the accelerated androgen metabolism or the aberrant adrenal steroidogenesis improve with weight reduction. Excess body fat increases androgen aromatization which, together with an obesity-related decrease in SHBG, is associated with mildly elevated levels of E1 and free E2 in postmenopausal women. Although premenopausal obese individuals have the same tendency, the far greater ovarian estrogen secretion overshadows any differences. The bulk of aromatization activity in fat lies in the stromal comportment. The major substrate for peripheral estrogen production is A. Testosterone also contributes to the estrogen pool via its conversion to E2.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Reproductive endocrinologic alterations in female asymptomatic obesity. 268 Jun 25

The secretion of growth hormone (GH) is abnormal in genetically obese Zucker rats. Measurements of pulsatile GH release and circulating GH levels in lean (Fa/?) and obese (fa/fa) rats have shown that both are reduced in the latter. We have studied pituitary GH gene expression in order to understand the role of GH synthesis in this abnormality. Obese animals have lower pituitary GH mRNA levels than lean controls. Within each genotype a sex difference was observed with the female animals having lower GH mRNA levels than the males. It is unlikely that the GH abnormality is due to a generalized pituitary defect because prolactin mRNA levels were the same in all four groups of rats.
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PMID:Obesity- and sex-related alterations in growth hormone messenger RNA levels. 277 63


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