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

Most metabolic disorders of genetically obese Zucker rats are reversed by adrenalectomy and are restored by corticosterone treatment, thus suggesting that a functional hypercorticosteronemic state is involved in the pathogenesis of the obesity syndrome in fa/fa rats. However, the hormone content and morphology of the hypothalamo-pituitary-adrenal axis of this animal model have to our knowledge not yet been described. We, thus, investigated morphologically and morphometrically the hypothalamic regions involved in CRF synthesis and secretion in male fa/fa rats. To ascertain if the brain is selectively or uniformly affected, we studied the main nuclei of the lateral and mediobasal hypothalamus, i.e. arcuate, lateral hypothalamic, and ventromedial nucleus and the parvicellular portion of the paraventricular nucleus. Moreover, after immunocytochemical labeling, we analyzed densitometrically the CRF-bearing axons of the median eminence and the ACTH-containing cells of the anterior and intermediate lobe of the pituitary gland. Finally, we investigated the adrenal glands by qualitative light microscopy. In fa/fa rats most hypothalamic nuclei were structurally changed. Furthermore, hypothalamic CRF and anterior pituitary ACTH contents as well as adrenal weight were increased, the zona fasciculata of the adrenal cortex was hypertrophic, and the ACTH content of the intermediate lobe was reduced. In conclusion, our results demonstrate that the obesity syndrome in genetically obese fa/fa rats is associated with lesions of the hypothalamo-pituitary-adrenal axis consistent with hyperadrenocorticism due to hyperactivity of the whole adrenal axis. Alterations also occur in the hypothalamic nuclei controlling glycemia, insulinemia, and circadian corticosterone secretion.
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PMID:Changes in the hypothalamo-pituitary-adrenal axis of genetically obese fa/fa rats: a structural, immunocytochemical, and morphometrical study. 231 48

This study was performed on four groups of subjects, including 10 patients with Cushing's disease, 10 patients with simple obesity, 8 patients with hypopituitarism and 13 normal subjects. The study was conducted by measuring the sequential changes of plasma ACTH, serum cortisol, 24-h UFC, 24-h 17 KS and 24-h 17 KGS following aminoglutethimide (AG) administration. The results suggest that normal subjects showed sequential changes of hypothalamic-pituitary-adrenal hormone concentrations with normal feedback regulation of the axis following AG administration. Patients with Cushing's disease had obvious autonomy in the production of ACTH from the pituitary. Patients with simple obesity might display abnormality to some degree in the production from the pituitary. Patients with hypopituitarism lost the capacity of ACTH production in various degrees because of pituitary lesions.
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PMID:Effects of aminoglutethimide on hypothalamic-pituitary-adrenal functions. 256 55

We have previously reported that the hypothalamo-pituitary-adrenal response to insulin-induced hypoglycaemia is normal while the cortisol release to pituitary stimulation by corticotrophin releasing factor (CRF-41) is reduced in obesity. Impaired growth hormone (GH) secretion is also found in obesity which may result from altered central levels of somatostatin (SMS). We have investigated, by giving a simultaneous infusion of SMS to six volunteer normal weight men during a CRF test, whether it is possible for SMS to modify pituitary-adrenal function. Each subject received intravenous CRF-41 (0.5 micrograms/kg) on two occasions during an infusion of isotonic saline or SMS (4 micrograms/min) in a randomized double-blind study. Plasma GH, cortisol, ACTH and SMS were measured. Three subjects demonstrated GH peaks during saline infusion but no peaks were seen in any subject during SMS infusion. No significant difference was found between peak cortisol responses during saline or SMS infusion (SMS cortisol 443 +/- 61 nmol/l, saline cortisol 485 +/- 52 nmol/l); neither was there any difference in the ACTH responses. We conclude that SMS does not alter the pituitary response to CRF in normal weight men and is thus less likely to be responsible for the altered pituitary-adrenal function seen in obesity. Further studies of alternative mechanisms are required to explain the cause of this abnormality.
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PMID:The pituitary-adrenal response to CRF-41 is unaltered by intravenous somatostatin in normal subjects. 257 84

The patient was a 16-month-old girl, born by mature natural delivery and weighing 3,320 g. Hirsutism was noted on birth. Development of pubic hair and hypertrophy of the labia minora were noted after 8 months. At the time of admission, the height was 80 cm and body weight 14.5 kg. Systemic obesity, facial acne, systemic hirsutism, low pitched voice and hypertrophied clitoris were observed. Androstenedione, dehydroepiandrosterone-sulfate and cortisol showed high levels in the blood, and the urinary 17-KS was obviously high, along with an increase in urinary 17-OHCS. The subject did not respond to either the dexamethasone inhibition test or ACTH load test. The abdominal CT revealed a tumor in the front upper position of the left kidney, and adrenal scintigraphy disclosed an obvious accumulation image in the adrenal gland on the left side. Based on the diagnosis of a left adrenal tumor, left adrenalectomy was performed. The tumor measured 5.0 x 4.5 x 3.7 cm, and weighed 57 g. Histopathologically it was diagnosed as adrenocortical adenoma. The infantile virilizing adrenocortical tumor is reported together with some discussion of the literature.
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PMID:[A case of infantile virilizing adrenocortical tumor]. 261 Jan 80

The relationship between sex hormones and the skin is increasingly considered to be very important. The skin has appropriately been called "A peripheral endocrine gland". In this review some aspects of the cutaneous metabolism of oestrogens, progestogens and particularly androgens are analyzed. Production of skin collagen is markedly enhanced by oestrogens. Progestogens with strong androgenic activity and especially androgens have a powerful stimulating action on all skin elements particularly the epidermis and the dermis the sebaceous glands and the hair. The skin manifestations of hyperandrogenism and disturbances of reproductive functions such as anovulation, oligoamenorrhoea and polycystic ovarian disease are usually the consequences of three main aetiopathogenic factors: the first is an abnormality of GnRH pulsatility related to central nervous system dysfunction and seemingly mediated by an increase in beta Endorphin, possibly related to some extent to changes in body weight and hyperinsulinism. The second aetiopathogenic approach is hyperaestronaemia secondary to obesity. Finally adrenal hyperandrogenism caused by different types of congenital adrenal hyperplasia or by increased sensitivity to ACTH may be implicated in these various clinical manifestations.
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PMID:[Sex hormones and the skin]. 269 19

A study was made of the psychoendocrine factor of pathogenesis of patients suffering from cerebral obesity with a hyperphagic reaction to stress and without it. The purpose was to study the hypothalamo-hypophyseo-adrenal system, emotional-personality features and motivation sphere in patients with cerebral obesity as compared to a control group. The following methods of examination were used: cliniconeurological examination, psychological methods--MIL test, Spilberger's test, a radioimmunoassay for determination of the blood levels of ACTH, STH, prolaction and cortisol at rest and under experimentally simulated stress. These methods were followed by mathematical processing of the obtained data with a correlation analysis of psychological and hormonal indices. The conclusions were based on statistically significant results only. A variable psychohormonal complex of reaction to stress was revealed in the patients with relation to the presence or absence of a hyperphagic reaction to stress. In a hyperphagic reaction to stress an increase in the body mass under an emotional stress resulted mainly from inadequate psychomotivation shifts with further overeating. In the absence of such a reaction a body mass increase under a stress was associated mainly with the neuroendocrine factor with retardation of lipolysis.
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PMID:[Psycho-endocrine interrelations in patients in a state of emotional stress during cerebral obesity]. 271 71

In Zucker obese rats (fa/fa) there are disturbances in the regulation of ACTH and corticosterone. In addition, beta-endorphin concentrations are higher in the pituitary and hypothalamus in obese than in lean rats. Since ACTH and beta-endorphin are thought to be controlled by corticotropin releasing factor (CRF), these effects may be due to abnormalities in CRF regulation. This possibility was investigated by immunizing rats against CRF. Obese rats immunized against CRF developed higher titer antibodies than lean rats. Hypothalamic CRF concentrations were higher in CRF-immunized obese but not lean rats compared with those of control rats, suggesting that compensation for sequestration of peripheral CRF developed in obese rats. In obese, but not lean rats, immunization against CRF decreased weight gains during weeks 1-4 and increased gains during weeks 9-12 and food intakes were decreased during weeks 5-8 compared with those for obese rats immunized against bovine serum albumin (BSA). Adrenal glands weighed 30% less in both obese and lean rats immunized against CRF compared with those immunized against BSA. These responses to immunization against CRF occurred even though plasma, hypothalamic and pituitary concentrations of ACTH and beta-endorphin were unaffected at the end of the study.
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PMID:Weight gain and food intake in corticotropin releasing factor immunized Zucker rats. 282 27

Periodic hormonogenesis has been described in patients with ACTH-dependent hypercorticism, and fluctuations of cortisol secretion have also been observed in patients with adrenal tumors. In this report, we studied a 41-year-old white male who presented with hypertension, central obesity, and muscle weakness of 2-years duration. His plasma cortisol was low (4.5 micrograms) in the morning and high in the evening (29.3 micrograms). Urinary free cortisol was 750 micrograms/day. A 24-hour cycle demonstrated highest values at noon and in late afternoon. This pattern was not suppressed by dexamethasone. When the patient was kept fasting, plasma cortisol remained low all day, and became elevated immediately after meal administration overnight. A left-sided adrenal mass was demonstrated and removed. In vitro, the adenylate cyclase activity of tumor tissue demonstrated more significant response to vasopressin than to ACTH; other tested peptides were inactive. We propose that a humoral factor induced by eating was responsible for the periodic hormonogenesis, directly stimulating the adrenal secretion of cortisol.
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PMID:Cushing syndrome with food-dependent periodic hormonogenesis. 283 Oct 1

In order to evaluate the role of beta-endorphin in the pathogenesis of obesity and essential hypertension 44 subjects were investigated: 12 nonobese hypertensives, 11 obese hypertensives, 11 obese normotensives and 10 normal subjects. Plasma concentrations of beta-endorphin and cortisol were measured by radioimmunological and ACTH by immunoradiometric methods. The plasma concentrations and the circadian rhythms of ACTH and cortisol secretion were normal in all groups investigated. A circadian rhythm of beta-endorphin secretion was demonstrated in nonobese hypertensives and in normal subjects. The plasma concentrations of beta-endorphin were twice higher than those in nonobese subjects. Also, in all obese patients the circadian rhythm of beta-endorphin secretion was blunted. The increased concentrations and the altered circadian rhythm of beta-endorphin in all obese subjects may point to a role of beta-endorphin in the pathogenesis of obesity rather than in that of essential hypertension.
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PMID:The possible role of beta-endorphin in pathogenesis of obesity and essential hypertension. 283 3

The use of a standard CRF test, using 100 micrograms i.v. synthetic ovine CRF-41, has been assessed in 22 patients with surgically-proven Cushing's disease and one patient with the ectopic ACTH syndrome secondary to a bronchial carcinoid. Three of the 22 patients, and the single patient with the ectopic ACTH syndrome, failed to produce a rise in serum cortisol to above the normal range in response to CRF-41. However, 18/22 patients with Cushing's disease had an enhanced cortisol response to CRF, including four patients who were resistant to high-dose dexamethasone. One patient with Cushing's disease responded to CRF-41 with an excessive cortisol response on one occasion, and a rise within the normal range on a second. Ten patients with simple obesity (mean weight 101 kg) were given CRF 0.5 microgram/kg, and their results compared to a control group of seven normal weight females (mean weight 58 kg). Peak serum cortisol responses to CRF were significantly less than in the control group, even when the dose was increased to 1 microgram/kg in six of the obese patients. Peak plasma ACTH responses were not significantly different between control and patient groups. It is concluded that the serum cortisol response to CRF is enhanced in the majority (but not all) of patients with Cushing's disease, and is attenuated in simple obesity. The reason for this attenuation requires further study.
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PMID:The use of CRF-41 in the differential diagnosis of Cushing's syndrome and obesity. 283 93


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