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

1. Body weight and total body potassium were measured in 23 hyperthyroid patients before and at various stages during treatment and in 19 athyreotic patients who were being treated with high-dose L-thyroxine. 2. In the hyperthyroid patients the total body potassium rose by 23 +/- 2.8% (SEM) within a few weeks of restoring the blood thyroid hormone levels to normal. The body potassium values after treatment were close to that expected in these individuals if they were healthy indicating that a considerable loss of body potassium is usual in hyperthyroidism. 3. The gain of total body potassium in hyperthyroidism averaged 71 +/- 8 mmol for each kg of body weight gained (compared with muscle potassium concentration of about 92 mmol/kg). In contrast, weight loss produced by dietary treatment of obesity caused very little change of body potassium (maximum averaged was 14 +/- 4 mmol/kg wt. loss). 4. Among the patients with hyperthyroidism, the greatest muscular weakness was present in those with the greatest body potassium loss and these patients regained a large amount of potassium relative to weight on recovery. 5. Total body potassium changes were closely related to total plasma tri-iodothyronine concentrations but unrelated to the thyroxine levels.
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PMID:Total body potassium in relation to thyroid hormones and hyperthyroidism. 723 44

Empty sella syndrome (ESS) is a multicausal entity. The incidence of primary empty sella syndrome (PESS) in children with neuroendocrine dysfunction is not known. In the pediatric age group, frequency seems to have been underestimated. A total of 117 cases of neuroendocrine disorders, including complete growth hormone deficiency, primary hypothyroidism with pituitary resistance to thyroid hormone, obesity, central precocious puberty, hypothalamic hypogonadism and central diabetes insipidus, have been studied with computed tomography and/or magnetic resonance imaging of sellar region for etiologic evaluation. Twenty-one patients were found to have PESS. We noted a high incidence of PESS in children with neuroendocrine dysfunction (17.9%). Children with neuroendocrine dysfunction should be investigated with respect to PESS, and children with PESS recognized coincidentally should be studied with the particular consideration of subclinical neuroendocrine dysfunction.
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PMID:Association of empty sella and neuroendocrine disorders in childhood. 764 85

P1 is a nuclear protein found exclusively in rat liver and binds to a motif that spans nucleotides -310 to -288 of the thyroid hormone responsive gene, S14. We expect P1 to play an important role in regulating gene expression because the binding motif for this factor is contained within a DNase I-hypersensitive site of S14 chromatin. In this report, we have attempted to define the function of P1 by correlating its DNA binding activity with levels of mRNA-S14 in response to aging and obesity. Results of all studies revealed inverse relationships between the activity of P1 and levels of mRNA-S14, thus suggesting that P1 may function as a repressor of S14 gene expression. Accordingly, we tested the repressor hypothesis using cell-free transcription and transient transfection assays to measure the activity of reporter constructs with and without the P1 binding motif. In the presence of the P1 motif, S14 promoter activity was repressed and the negative effect on gene transcription was further enhanced by thyroid hormone. These observations are consistent with P1 being a repressor of S14 gene transcription.
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PMID:A liver-specific nuclear protein represses transcription of the S14 gene in vitro and in vivo. 769 31

The tripeptide hormone, TRH, is metabolized by three enzymes, the most specific of which is pyroglutamyl peptide hydrolase-II (also termed thyroliberinase), a metalloenzyme present in serum and brain. Because pyroglutamyl peptidase-II activity in rat serum is regulated by thyroid hormone levels, we tested the hypothesis that this activity is similarly altered in humans. We studied serum pyroglutamyl peptidase-II activity in 6 patients with hyperthyroidism, 18 patients with hypothyroidism, and 31 euthyroid, normal weight volunteers. Because TRH [or its metabolite cyclo(His-Pro)] is believed to be an important hormone regulating appetite and metabolism, we also evaluated pyroglutamyl peptidase-II activity in 27 euthyroid patients with obesity. Serum pyroglutamyl peptidase-II activity was elevated in patients with hypothyroidism (mean +/- SEM, 33.9 +/- 3.7 nmol/mL.h) compared to that in euthyroid, normal weight volunteers (24.5 +/- 2.8 nmol/mL.h; P < 0.05), but not that in patients with hyperthyroidism (28.3 +/- 4.1 nmol/mL.h; P = NS). Euthyroid obese patients had the highest pyroglutamyl peptidase-II activity (43.6 +/- 2.8 nmol/mL.h; P < 0.0001 vs. normal weight volunteers). Pyroglutamyl peptidase-II activity was positively correlated with body mass index (r2 = 0.30; P < 0.0001). After correction for body mass index, there were no difference in pyroglutamyl peptidase-II activity in hypothyroid, hyperthyroid, and euthyroid individuals. We conclude that serum pyroglutamyl peptidase-II activity is regulated by, or regulates, body weight.
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PMID:Pyroglutamyl peptidase-II ("thyroliberinase") activity in human serum: influence of weight and thyroid status. 771 73

Several reports have focused on the clinical features of the untreated GH-deficient adult and the effect of GH therapy. The results reported are strikingly unanimous. Untreated GH-deficient adults have been shown to have increased cardiovascular mortality, reduced exercise capacity, reduced muscle strength, subnormal glomerular filtration rate and renal plasma flow, defective sweat secretion and defective thermoregulation, reduced energy expenditure and basal metabolic rate, abnormal thyroid hormone metabolism, reduced myocardial function and clinical signs of premature atherosclerosis. Body composition has been found abnormal with increased fat mass, decreased lean body mass, decreased muscle fat ratio, visceral obesity, reduced extracellular fluid volume and reduced bone mineral content. Furthermore, two independent groups have reported impaired psychological wellbeing as compared to normal subjects. Apart from the observation on total mortality, all the above-reported abnormalities improve during GH substitution. The only recognisable side effects so far has been fluid retention, which is usually transient and dose-dependent. It is concluded that GH deficiency has distinct clinical consequences all of which can be totally or partially alleviated by GH replacement therapy.
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PMID:Adult growth hormone deficiency. 786 79

In addition to various psychosocial and metabolic factors, food intake is also influenced by gastrointestinal mechanisms that trigger both the initiation and termination of eating behaviors. Although gastric distension is one of the most obvious signs of "fullness" and clearly plays a role in controlling food intake, its effects are only temporary and are distinct from the feelings of satiety generally associated with a meal. Such postprandial sensations appear to be related to the activation of intestinal chemoreceptors. Other evidence indicates that the release of cholecystokinin and perhaps other transmitters as well may contribute to satiety. Although the stomach probably does not expand or shrink in response to different levels of food intake, nutrient receptors in the small intestine probably do adapt to changes in food intake. Intestinal adaptation also occurs in response to thyroid hormone, insulin, and cortisol as well as to obesity, pregnancy, and illness, which all may have an important bearing on changes in eating behavior in these situations.
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PMID:The role of the gut in regulating food intake in man. 813 94

As the hypothalamic gonadotropin-releasing hormone (GnRH) pulse generator is an integrator of hormonal, metabolic, and neural signals, it is not surprising that the function of the hypothalamogonadal axis is subject to the influence of a large array of environmental factors. Before puberty, the central nervous system (CNS) restrains the GnRH pulse generator. Undernutrition, low socioeconomic status, stress, and emotional deprivation, all delay puberty. During reproductive life, among peripheral factors that effect the reproductive system, stress plays an important role. Stress, via the release of corticotropin-releasing factor (CRF), eventually triggered by interleukin 1, inhibits GnRH release, resulting in hypogonadism. Effects of CRF are probably mediated by the opioid system. Food restriction and underweight (anorexia nervosa), obesity, smoking, and alcohol all have negative effects on the GnRH pulse generator and gonadal function. Age and diet are important determinants of fertility in both men and women. The age-associated decrease in fertility in women has as a major determinant chromosomal abnormalities of the oocyte, with uterine factors playing a subsidiary role. Age at menopause, determined by ovarian oocyte depletion, is influenced by occupation, age at menarche, parity, age at last pregnancy, altitude, smoking, and use of oral contraceptives. Smoking, however, appears to be the major determinant. Premature menopause is most frequently attributable to mosaicism for Turner Syndrome, mumps ovaritis, and, above all, total hysterectomy, which has a prevalence of about 12-15% in women 50 years old. Premature ovarian failure with presence of immature follicles is most frequently caused by autoimmune diseases or is the consequence of irradiation or chemotherapy with alkylating cytostatics. Plasma estrogens have a physiological role in the prevention of osteoporosis. Obese women have osteoporosis less frequently than women who are not overweight. Early menopause, suppression of adrenal function (corticoids), and thyroid hormone treatment all increase the frequency of osteoporosis. Aging in men is accompanied by decreased Leydig cell and Sertoli cell function, which has a predominantly primary testicular origin, although changes also occur at the hypothalamopituitary level. Plasma testosterone levels, sperm production, and sperm quality decrease, but fertility, although declining, is preserved until senescence. Stress and disease states accelerate the decline on Leydig cell function. Many occupational noxious agents have a negative effect on fertility.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Environment, human reproduction, menopause, and andropause. 824 11

Hypothyroidism is the condition most commonly treated with exogenous thyroid hormone. The goal of therapy is to normalize levels of serum thyrotropin (thyroid-stimulating hormone), which should be monitored by a high-sensitivity test. Adjustments in optimal dose may be necessary for a number of physiologic reasons (eg, decreased gastrointestinal absorption, pregnancy). Thyroid hormone therapy is also appropriate after surgery for thyroid cancer and for patients with goiter or benign thyroid nodules. In the absence of hypothyroidism, such treatment should not be used for obesity, fatigue, irregular menses, or infertility.
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PMID:Thyroid hormone therapy. What, when, and how much. 841 59

The steroid hormone intermediate, DHEA, has been proposed as a therapeutic agent for the treatment of obesity. Its effects on lipogenesis, substrate cycling, peroxisome proliferation, mitochondrial respiration, protein synthesis, and thyroid hormone function have been reported. The results of these studies suggest that the antiobesity function of DHEA is not simply one of inhibiting fat synthesis and deposition but is one of affecting a number of pathways that contribute to the maintenance of the isoenergetic state rather than the promotion of positive energy balance.
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PMID:Is dehydroepiandrosterone an antiobesity agent? 846 83

A low resting metabolic rate (RMR) for a given body composition has been identified as a risk factor for weight gain and obesity, and has also been reported in formerly obese individuals with the genetic predisposition for obesity. The possible role of thyroid hormone in low RMR was studied in a large sample of postobese women. RMR was measured by indirect calorimetry in 28 weight-stable postobese women with a family history of obesity (PO group) and in a control group of 28 nonobese women closely matched for age, fat mass, and fat-free mass. RMR was 8% lower in the PO than in the control group [[symbol: see text]; 95% Cl:5856 (5520, 6214) compared with 6408 kJ/d (6096, 6768 kJ/d), P < 0.02], and the group difference remained unchanged after fat-free mass and fat mass were adjusted for (552 kJ/d, P < 0.015). The PO group had lower plasma free triiodothyronine [2.4 (1.9, 3.0) compared with 3.4 pmol/L (2.9, 3.9 pmol/L), P < 0.01], whereas plasma androstenedione only tended to be lower in the PO than in the control group. Adjustment for differences in androstenedione did not reduce the difference in RMR, whereas adjustment for differences in plasma free triiodothyronine eliminated the group difference (96 kJ/d, P = 0.59). The present study shows that RMR for a given body composition is lower among postobese than among matched never-obese control subjects. Statistically, the lower plasma free triiodothyronine concentrations of the postobese subjects could explain their lower RMRs, but it remains to be established whether these findings are causally related.
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PMID:Low resting metabolic rate in subjects predisposed to obesity: a role for thyroid status. 864 81


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