Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The STH level was studied in the blood of 105 patients with the hypothalamic pubertal syndrome (HPS). A tendency toward STH hyperproduction was revealed. A comparison of the STH level in the blood and the degree of obesity of the HPS patients showed a clear decrease of the growth hormone in Stage IV obesity. The STH level was almost the same in Stages I, II, III obesity. The STH secretion in the HPS patients correlated with age. The period of disease did not influence hypophysial somatotropic function in the HPS patients. No interrelationship between the content of hydrocortisone and STH in the blood was established. In most of the patients with the HPS, the growth hormone secretion in response to hypoglycemia was undisturbed. Preliminary results obtained with parlodel tests showed an opposite reaction in the HPS patients as compared to healthy ones. Our results confirmed once more that the HPS should not be interpreted as a variant of Icenko-Cushing's syndrome or constitutional obesity in which STH production was lowered.
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PMID:[Somatotropic function of the hypophysis in the hypothalamic puberty syndrome]. 388 63

The health consequences of obesity in adults encompass both metabolic and cardiovascular complications. Pregnancy in obese women also has a particular set of problems. For the obese pregnant woman, these include weight gain less than 5.4 kg, chronic hypertension and superimposed preeclampsia, gestational diabetes, multiple gestation, and the potential for a macrosomic child. The combination of obesity and maternal diabetes does not appear to have an additive effect on the excessive growth of infants of obese mothers. Furthermore, despite inadequate weight gain, hypertension, and multiple gestation, infants of obese mothers are usually born with a greater birth weight than those of nonobese women. In addition, the incidence of intrauterine growth retardation is lower after an obese pregnancy. Neonates born to obese mothers have increased risk for birth asphyxia and birth trauma. Recently infants born to obese women were noted to have transient neonatal fasting asymptomatic hypoglycemia. Hyperinsulinism is not present in the infants of obese mothers; thus, alternate fuel mobilization (free fatty acids, glycerol, ketones) may respond to the hypoglycemic stimulus. Suggestions and rationale for the management of the pregnant obese woman, fetus, and newly born infant are discussed in the text.
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PMID:Perinatal problems of the obese mother and her infant. 389 77

A low-carbohydrate diet, frequently used for treatment of reactive hypoglycemia, hypertriglyceridemia, and obesity may affect thyroid function. We studied the effects of replacing the deleted carbohydrate with either fat or protein in seven healthy young adults. Subjects were randomly assigned to receive seven days of each of two isocaloric liquid-formula, low-carbohydrate diets consecutively. One diet was high in polyunsaturated fat (HF), with 10%, 55%, and 35% of total calories derived from protein, fat, and carbohydrate, respectively. The other was high in protein (HP) with 35%, 30%, and 35% of total calories derived from protein, fat, and carbohydrate. Fasting blood samples were obtained at baseline and on day 8 of each diet. A meal tolerance test representative of each diet was given on day 7. The triiodothyronine (T3) declined more (P less than .05) following the HF diet than the HP diet (baseline 198 micrograms/dl, HP 138, HF 113). Thyroxine (T4) and reverse T3 (rT3) did not change significantly. Thyroid-stimulating hormone (TSH) declined equally after both diets. The insulin level was significantly higher 30 minutes after the HP meal (148 microU/ml) than after the HF meal (90 microU/ml). The two-hour glucose level for the HP meal was less, 85 mg/dl, than after the HF meal (103 mg/dl). Serum triglycerides decreased more after the HF diet (HF 52 mg/dl, HP 67 mg/dl). Apparent benefits of replacing carbohydrate with polyunsaturated fat rather than protein are less insulin response and less postpeak decrease in blood glucose and lower triglycerides. The significance of the lower T3 level is unknown.
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PMID:Effect of low-carbohydrate diets high in either fat or protein on thyroid function, plasma insulin, glucose, and triglycerides in healthy young adults. 390 Jan 81

We propose a rational regimen for management of non-insulin-dependent pregnant diabetics (NIDD), using appropriately constituted calorie-restricted diets with the oral agents metformin and glibenclamide as may be necessary, with rapid recourse to insulin if the latter do not produce excellent control of blood glucose. Using this regimen between June 1974 and December 1983 we have managed 423 new diabetics (ND, diagnosed during pregnancy) with a perinatal mortality (PNM) of 14 per 1000 and 268 established diabetics (known diabetics, KD) with a PNM of 70/1000 (57/1000 since 1978). A further 80 NIDDs were 'untreated', i.e., not seen by us until near term; these suffered a PNM of 313/1000. Side-effects of the drugs have been few and mild, they are not teratogenic; 'starvation ketosis' does not occur; neonatal hypoglycaemia is preventable by using continuous insulin infusion during delivery. We suggest that the regimen outlined here is acceptable to the patients, is safe, gives excellent results and furthermore teaches the diabetic mother proper dietary control and combats lifelong obesity. It should be useful especially in developing countries in which pregnant, overweight NIDDs are common. Precise control of the blood glucose is essential.
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PMID:The management of non-insulin-dependent diabetes during pregnancy. 393 18

Estimation of plasma glucose and immunoreactive insulin concentrations in normal subjects after an overnight fast showed that subjects with high basal plasma glucose levels tended to have high plasma insulin concentrations. A similar correlation between glucose and insulin levels was seen in patients with obesity and various endocrine disorders. The suppression of plasma insulin levels associated with hypoglycaemia was used to derive an "amended insulin-glucose ratio," which appeared to be a good discriminant for the diagnosis of insulinomas. In normal subjects the ratio was less than 30 muU insulin/mg glucose, in obese subjects less than 50 muU/mg, and most of the patients with insulinomas had values over 200 muU/mg.
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PMID:Control of basal insulin secretion, with special reference to the diagnosis of insulinomas. 432 38

The available data show that GIP is at present the strongest candidate for the insulin-secreting factor of the gut named incretin. Its release is triggered by the absorption of ingested nutrients. GIP acts on the B-cells of the pancreas by potentiating glucose-induced insulin secretion. The role of GIP as an enterogastrone is less well established. The release of GIP from the gut cells seems to be regulated by the composition and the amount of the ingested food, by the rate of absorption of nutrients by neural factors (vagal), and by feedback control mediated by insulin. In addition, the adaptation of the intestine to individual eating habits influences the response of the GIP cells. It is suggested that an overactive enteroinsular axis, i.e. enhanced GIP secretion, participates in the development of the hyperinsulinaemia of obesity and maturity onset diabetes mellitus. In gastrointestinal diseases accompanied by malabsorption the GIP response is diminished. In gastrointestinal disorders with rapid gastric emptying (duodenal ulcer) or with accelerated passage of the nutrients through the intestine, hypersecretion of GIP and insulin occurs. This may be significant for the reactive hypoglycaemia of these conditions.
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PMID:Gastric inhibitory polypeptide. 610 91

The responses of pituitary hormones and venous catecholamine concentrations to insulin hypoglycaemia were studied in 12 formerly obese women with familial obesity who had lost about 30 kg by dieting. These responses were compared with those of 10 lean women. The post-obese women showed an exaggerated response in cortisol output but an impaired release of growth hormone. 6 of the post-obese women had in addition both an impairment in prolactin output and a failure to increase their venous noradrenaline concentrations during hypoglycaemia. These results suggest that an alteration in hypothalamic control, displayed by limited responses in pituitary hormone secretion and by reduced sympathetic activity, may be an innate feature of people with familial obesity
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PMID:Altered hypothalamic and sympathetic responses to hypoglycaemia in familial obesity. 612 54

Some results suggesting the existence of gluco- and/or insulin-sensitive sites within the central nervous system (CNS) are recalled. In summary, it seems that when these sites are activated by the presence of glucose or insulin, there is an activation of the parasympathetic nervous system which is responsible for an increased peripheral insulin secretion and/or an hypoglycemia. This could possibly favour glucose disposal. Inversely, when the CNS lacks energy substrates, a cascade of events occurs which tend to increase peripheral glycemia. Bilateral lesions of the ventromedial hypothalamus (VMH) bring about a very early occurring hypersecretion of insulin which can be rapidly and completely abolished by vagotomy. It has also been shown that genetically pre-obese rats (fa/fa) do hypersecrete insulin in response to an i.v. glucose load. This suggests that hypersecretion of insulin of these animals could play a causative role in the development of their obesity. Moreover, this hypersecretion of insulin observed in genetic pre-obesity is abolished by acute atropine administration indicating the involvement of the parasympathetic nervous system in the development of their hyperinsulinemia and subsequent obesity. Cephalic phase insulin secretion seems to "optimalize" insulin secretion that occurs following a meal, as it appears to permit adequate glucose utilization and therefore glucose tolerance. Indeed, animals which are lacking cephalic phase insulin secretion do hypersecrete insulin while remaining hyperglycemic for a longer period of time when compared to animals which have a cephalic phase insulin secretion. Hypothalamic factors present in the ventromedial or the ventrolateral hypothalamus have been shown to have insulin secretion promoting activity when administered in vivo or in vitro to donor rats. It remains to be shown whether such factors are indeed released into the blood (humoral factors) or whether they are neuromodulators and/or neurotransmitters.
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PMID:[The central nervous system-endocrine pancreas axis]. 614 77

An increase in the basal cortisol level in the blood plasma or the adrenal cortex reaction to insulin hypoglycemia was seen in patients in the early periods of diabetes mellitus (latent, initial manifest type). No considerable differences were found between the adrenals of juvenile and adult diabetic patients. Combined diabetes mellitus and obesity led to a significant rise in the indices studied. An intensification of the adrenocortical glucocorticoid function is not accompanied by an enhancement of the hypophysis adrenocorticotropic function.
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PMID:[Adrenal cortex glucocorticoid function in the early stages of the development of different forms of diabetes mellitus]. 625 84

Forty patients with the Prader-Willi syndrome have been examined. The typical features begin in gestational life with poor fetal vigor and difficulties with birth and post-partum feeding. The classical features of hypotonia, small hands and feet, cryptorchidism can be identified at this time. The delayed milestones, mental retardation and obesity become more prominent later. The average height of the patients in this series who were admitted to the Clinical Study Center was 149 cm and their weight was 114 kg. The weight and height curves show that Prader-Willi individuals are consistently shorter and heavier than normal children. Tests of endocrine function showed normal glucose tolerance. Insulin secretion was increased in relation to obesity. The rise in growth hormone (hGH) after injecting insulin to induce hypoglycemia and after the infusion of arginine was comparable to other obese individuals but was low in comparison to normal weight subjects. There was no rise in growth hormone with L-dopa administration, but there was a rise in hGH with the administration of 2-deoxy-D-glucose. The hypoglycemia produced by insulin was greater in the Prader-Willi patient than in obese controls. The rise in TRH (thyrotropin-releasing hormone) following the injection of TSH (thyrotropin stimulating hormone) was greater in the Prader-Willi patients than in the obese controls. Hypogonadism was routine in this series, and the response to LRH (luteinizing releasing hormone) was absent in all tested subjects. Treatment with clomiphene for 30 to 90 days significantly increased the response to LRH in three adult individuals who had not been treated with gonadal steroids previously and who were hypogonadal. Rectal temperature declined in three of the five Prader-Willi patients during exposure to an ambient temperature of 4 degrees C, but none of the three obese controls showed a decline. Food intake averaged 5167 kcal/d when six patients were given trays containing more food than they could eat. Food intake was not reduced when tryptophan was added to the diet. Salivary secretion was reduced in the Prader-Willi patients. A number of pulmonary function tests were significantly reduced in the study patients compared to obese or normal weight controls. The anatomic findings in four autopsied patients with the Prader-Willi syndrome showed no significant differences from those of obese subjects without this syndrome. The chromosomal pattern showed a deletion or translocation at chromosome 15 in 3 of 12 patients in whom this test was performed. These findings in 40 patients with the Prader-Willi syndrome have been compared with the information contained in 159 reports published in the medical literature.
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PMID:The Prader-Willi syndrome: a study of 40 patients and a review of the literature. 633 43


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