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

Intravenous insulin tolerance tests and thyrotropin-releasing hormone (T.R.H.) stimulation tests were performed in nine massively obese women and six lean female controls and the prolactin, growth hormone, and cortisol responses were measured. A combined pituitary function test (insulin, T.R.H., and gonadotropin-releasing hormone) was performed in eleven other massively obese women. In the obese women to whom insulin was given separately there was no prolactin release, and growth hormone and cortisol responses were impaired. T.R.H. stimulation produced a prolactin response which was subnormal. These changes were not apparent in the obese women in whom a combined pituitary function test was performed. The results suggest an alteration of hypothalamic function in massive obesity.
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PMID:Impaired hypothalamic control of prolactin secretion in massive obesity. 8 90

Obese Zucker rats were either pair-fed to their lean litter-mates or fed ad lib, to determine the effect of hyperphagia on serum hormone levels and tissue metabolism as indicated by enzyme activities and in vitro metabolite flux. Hyperphagia was shown to be non-essential for the elevation in serum insulin and suppression in serum growth hormone and prolactin in the genetically obese rat. It was also shown that the increased liver cell lipogenic rate was not dependent on hyperphagia in the obese rat and that adipose cell lipogenesis was not significantly altered in the pair-fed obese rat. The utilization of alanine for glucose synthesis in vitro was similar for both lean and obese rats, but its utilization for fatty acid synthesis was higher in the obese rat. Data is presented which suggest that the inhibitory effect of glucagon on liver lipogenesis is blunted in the obese rat.
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PMID:Serum hormone levels and tissue metabolism in pair-fed lean and obese Zucker rats. 19 81

Arginine vasopressin (AVP) and prolactin (PRL) concentrations were measured in the plasma of grossly obese subjects to determine if abnormalities in salt and water homeostasis could be related to these hormones. Acute oral water loads and hypertonic saline infusions were administered during baseline obesity, after prolonged fasting, and after hypocaloric refeeding. Only 64.7%, 46.1%, and 70.1% of a water load was excreted during the respective three stages. Pre-water load plasma AVP levels were normal, but after the water load the obese failed to suppress AVP secretion in a normal fashion; this defect was corrected after fasting and with refeeding. Salt loading resulted in appropriate osmolality and AVP responses. Serum prolactin levels, normal at baseline during all phases, rose slightly after water loading during fasting. Hypertonic.saline produced no changes in prolactin levels in the obese or in the normal controls. In the disordered salt and water metabolism of the obese, persistently high AVP values during water loading appeared to be a factor in the delay of water excretion. In the observed water retentionduring dietary restriction and refeeding, secretion of AVP and PRL did not appear to have a major regulatory function.
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PMID:The role of vasopressin and prolactin in abnormal salt and water metabolism of obese patients before and after fasting and during refeeding. 31 25

Diet and nutrition may be an indirect cause of human breast cancer. This review of the literature identifies high risk groups, geographic variables, experimental animal studies, and endocrinal research that link diet and obesity to aberant hormonal activity that can cause breast cancer. Studies of high risk groups indicate that some women are predisposed to breast cancer because of similar dietary habit that often cause obesity. Geographical factors influence the kinds of food available to a given population. As a result, people who live in areas that supply a rich diet of sugar, starches, and fats have a higher incidence of obesity and breast cancer than those people who have simple diets. Experimental studies on laboratory animals show that diets with reduced calories, fat, and proteins inhibit tumor development. The results of these studies, although intesting, are impractical for application to human subjects. Studies that address the relationship between breast cancer and specific hormones include investigations of androgens, estrogens and prolactin. At present, these studies are inconclusive and often conflicting. Many dietary factors appear to be causal of breast cancer, especially as they interact with each other. An individual's metabolism, synthesis of hormones, and amount of fat tissue can be predisposing factors for breast cancer. Future research should focus on these interacting factors so that workable, preventative health programs can be developed.
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PMID:Diet and breast cancer: a review. 36 82

A comprehensive review of what was known of the epidemiology of breast cancer as of the early 1970s was published by MacMahon et al. in 1973. This review covers the major aspects of the epidemiology of breast cancer included in the 1973 review and, additionally, emphasizes recently reported work. Attention is directed to the following: magnitude of the problem in the U.S.; demographic characteristics of breast cancer cases; international variation; laterality of breast cancer; reproductive variables; benign breast diseases; multiple primary cancers involving the breast and other sites; familial aggregation and genetics; endogenous hormones (estrogens, progesterone, prolactin, androgens, and thyroid); exogenous estrogens; diet; body build; radiation; exposure to radiation in screening for breast cancer; mammographic parenchymal patterns; viruses; other exposures of current interest (reserpine, hair dyes); and breast cancer in males. The high incidence and mortality rates and the detrimental impact on the quality of life of those affected indicate that breast cancer in the U.S. continues to be a serious problem for women. An annual age-adjusted incidence rate of 84.9/100,000 women was reported for the 1973-1976 years; the annual age-adjusted mortality rate among women in the U.S. was 27.7/100,000 over this same time period. From these figures, it may be estimated that each year in the U.S. almost 100,000 cases of breast cancer are diagnosed, and over 30,000 deaths occur. Age specific incidence rates increase rapidly with age until about 45-50 years of age, after which they continue to increase but at a slower rate. In addition to age, a few other risk factors, including a history of bilateral premenopausal breast cancer in a 1st degree relative, a history of breast cancer in the contralateral breast, and residence from an early age in North America compared to Asia, are associated with large relative risks. Other risk factors, including whether or not an oophorectomy has been performed, age at 1st birth, a history of fibrocystic disease, previous exposure to high levels of radiation in the chest, socioeconomic status, obesity, and a previous cancer in the ovary or endometrium are associated with relative risks of at least 2 but less than 4-fold. Finally, age at menarche, age at menopause, marital status, place of residence, and the white compared to the black race are associated with small but real differentials in risk.
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PMID:A review of the epidemiology of human breast cancer. 39 70

We studied secretion of growth hormone (GH), insulin, and prolactin in eight women with anorexia nervosa and nine women with refractory obesity before and during treatment with bromocriptine, 10 mg/day. In the anorexic patients the raised plasma GH concentrations occurring during an oral glucose tolerance test fell significantly while on bromocriptine treatment, but there was no change in plasma insulin or blood glucose concentrations. In the obese patients, however, plasma GH concentrations remained low during the oral glucose tolerance test, and were not modified by bromocriptine. Blood glucose and plasma insulin concentrations were also unchanged. Plasma GH and plasma 11-hydroxycorticosteroid responses to insulin-induced hypoglycaemia were unaffected. Serum prolactin concentrations which were raised in five anorexic patients and marginally raised in two obese subjects, fell significantly in both groups during treatment. We observed no consistent weight changes in either groups.
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PMID:Growth hormone, insulin, and prolactin secretion in anorexia nervosa and obesity during bromocriptine treatment. 57 73

A patient, who has been followed for thirteen years, developed the first symptoms of progressive hypothalamic atrophy at the age of 39. The diagnosis was confirmed by pneumoencephalography five years after onset. Hypothalamic dysfunction was manifested clinically by loss of libido, impotence, obesity, polydypsia, somnolence, and rage attacks. Assessment of endocrinologic function demonstrated low serum levels of testosterone, FSH, and LH, a diabetic glucose tolerance curve, decreased basal and hypoglycemic stimulated levels of HGH, and progressively increasing levels of serum prolactin. Repeated pneumoencephalography revealed an initial, and then progressive, enlargement of the third ventricle which was later associated with generalized, but proportionately less severe, atrophy of the cerebellum and cerebral hemispheres. Analysis of the physiologic and endocrinologic mechanisms underlying these abnormalities suggests diffuse hypothalamic damage, especially in the ventromedial area. The decreased somnolence and increased libido and potency which accompanied therapy with levodopa suggest damage to dopaminergic and noradrenergic pathways. Slowly progressive hypothalamic atrophy, confirmed by pneumoencephalography, but without specific etiology, has not been reported previously. This article describes such a patient followed over thirteen years, and the efficacy of therapy with levodopa in ameliorating certain aspects of his disease.
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PMID:Hypothalamic atrophy. 58 Feb 84

Hourly integrated concentrations (IC) of growth hormone (GH), prolactin (PRL) and cortisol were determined by a continuous sampling procedure in six obese women, before and at the end of a 12 day fast, and in eight normal controls under basal conditions. Hormonal 24 h IC and nyctohemeral variations were calculated from these data. Nyctohemeral rhythms were investigated by the periodogram method. A significant increase over basal values of 24 h IC of PRL, GH and cortisol was observed at the end of the fasting period. Nyctohemeral variations--but not nyctohemeral rhythm--of IC-GH were found in normal subjects. They were abolished in obese patients under basal conditions but restored during fasting. The circadian rhythm of cortisol was not altered in obesity. A shift of the normal nyctohemeral rhythm of PRL was observed in obese patients, but the normal pattern was restored during fasting.
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PMID:Simultaneous study of cortisol, growth hormone and prolactin nyctohemeral variations in normal and obese subjects. Influence of prolonged fasting in obesity. 67 99

During pregnancy estrogen-medicated augmented prolactin secretion is presumably responsible for a 10-20 fold increase in circulating plasma prolactin; significant differences in basal levels between nursing and nonnursing women persist into the puerperium, reflecting the influence of sucking on maternal plasma prolactin. The release of prolactin is induced via a neurogenic pathway from nipple to hypothalamus and it is proportionate to the length of nursing and to the intensity of the stimulus. There is evidence supporting catecholamine/serotonin control of prolactin release, and the influence of changes in hypothalamic dopamine turnover. The composition of human milk is dependent on various factors; overall, fat composition is 2-5% and protein 9% at 3 weeks and 5% thereafter; milk delivers 20-25 calories per ounce; total fluid and nutritional requirements of the newborn can be met by breastfeeding up to 6 months postpartum. Maternal malnutrition negatively affects lactation; gestational, rather than progestational, food intake influences lactation. Immunity in the newborn is provided also by breast milk through immunoglobulins, thus enhancing the child's protection against internal pathogens. The incidence of gastrointestinal disorders is 1.5/1000 in breastfed infants, and 84.7/1000 in bottle fed infants; the incidence of respiratory infection is .4/1000 and 48/1000, respectively. Prolactin may exert an inhibitory influence on ovarian steroidogenesis, and gonadotropin secretion is disrupted by nipple stimuation; this may account for the low percentage of ovulation among nursing mothers. Lactational amenorrhea has been proven to have great demographic impact; dramatic variations in fertility on the basis of variations in lactational amenorrhea have been described in rural areas of Latin America, Asia, and Africa. Reduction of lactational amenorrhea results not only from changes in sociocultural patterns, but from improved maternal nutrition, often through nutrition programs. When nursing has to be interrupted because of complications full lactation may be restored by oral administration of thyrotropin-releasing hormone. Breastfeeding is possible in 99% of women; the denial of lactation may cause the retention of unwanted weight, which can be compounded by the use of oral contraceptives. Moreover, infantile obesity may stem from the lack of a satiety signal in bottle fed newborns.
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PMID:Mechanisms of puerperal lactation. 83 86

Mice with the recessively inherited obese-hyperglycemic syndrome (ob/ob) and their nonobese litter mates were studied over a 26-week period. The body weights and serum glucose levels of ob/ob mice began to rise markedly at 5-6 weeks of age and remained elevated throughout the period of study. Obese mice were significantly heavier (P less than .001) and had higher serum glucose levels (P less than .001) than lean mice, but obese mice had variably lower serum growth hormone (GH) and prolactin (PRL) levels (P less than .001) than lean litter mate controls after 4-5 weeks of life. A 24 h rhythm study performed on 15-week-old mice revealed a relatively unaltered but attenuated pattern of GH and PRL secretion in ob/ob mice. During and after the development of the obese-hyperglycemic syndrome, the low levels of these two hormones probably indicates an altered hypothalamic regulation of pituitary function.
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PMID:Serum growth hormone and prolactin during and after the development of the obese-hyperglycemic syndrome in mice. 94 10


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