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

The possible involvement of Na+,K+-ATPase in the etiology of obesity in the obese (ob/ob) mouse was explored. The number of Na+,K+-ATPase enzyme units in skeletal muscle, liver, and kidneys from 4- and 8-wk-old obese and lean mice was estimated from saturable [3H]ouabain binding to particulate fractions. Neither phenotype nor age altered the Kd value for ouabain binding in these three tissue preparations. The total number of [3H]ouabain binding sites in hindlimb muscles was 35--55% lower in 4- and 8-wk-old obese mice than in their lean counterparts. However, the total number of [3H]ouabain binding sites in liver and kidneys of obese mice was similar to values observed in their lean counterparts. Because it has been suggested that ob/ob mice are hypothyroid, we investigated the response of Na+,K+-ATPase in these mice to thyroid hormone treatment (approximately 5 microgram thyroxine/day for 2 wk). The number of [3H]ouabain binding sites in the three tissues increased in both obese and lean mice injected with this relatively large dose of thyroxine, but the obese mice were 2--3 times more responsive than lean mice.
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PMID:Na+,K+-ATPase enzyme units in lean and obese (ob/ob) thyroxine-injected mice. 22 9

Preobese fetuses have elevated thyroid hormone levels and depressed growth hormone levels relative to lean fetuses. Therefore, we are studying various experimental fetal pig models to explore the relationship between endocrine status and onset of obesity. In the present study, intact and hypophysectomized (d 70) fetuses were implanted with thyroxine (T4) pellets on d 70 of gestation, and blood, adipose tissue, and skin samples were obtained upon removal of d 90 of gestation. Body weights were similar for all groups and T4 treatment reversed myxedema in hypophysectomized fetuses. Serum T4 levels were elevated (p less than 0.05) and skin and hair development were enhanced (p less than 0.05) to a similar degree by T4 treatment in intact and hypophysectomized fetuses. However, T4 did not influence adipose tissue development in intact fetuses, but markedly enhanced development in hypophysectomized fetuses. For instance, fat cell size and lipogenic enzyme activities in hypophysectomized fetuses were increased (p less than 0.05) by 5-mg and 15-mg T4 treatments, with a marked increase (p less than 0.05) in apparent fat cell number with the 15-mg T4 treatment. In contrast, there was no effect of T4 (15 mg) on these parameters in intact fetuses. Therefore, fetal obesity may be directly associated with elevated thyroid hormone levels and suppressed growth hormone levels, but not with elevated T4 levels alone.
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PMID:The influence of thyroxine on the differentiation of adipose tissue and skin during fetal development. 150 11

Hyperprolactinemia and prolactinoma in patients with long-term primary hypothyroidism have been recognized for decades. We report a case of 57-year-old female patient with lingual thyroid and cretinism who had a high serum prolactin level (greater than 200 ng/ml) and a pituitary tumor with suprasellar and parasellar extension. The tumor regressed to a size undetectable by CT scan after 2 years of thyroid hormone replacement therapy, but complete normalization of the hyperprolactinemia required additional bromocriptine therapy. This patient showed generalized short metacarpal and phalangeal bones, calcification of the basal ganglia and dentate nuclei bilaterally, and subcutaneous calcification at both gluteal regions, while serum calcium, phosphorus and c-PTH levels were all normal. Thus in addition to short stature, brachydactyly, a round face, and obesity, which are related to hypothyroidism, she also presented features uniquely mimicking the Albright's hereditary osteodystrophy seen in patients with pseudohypoparathyroidism and pseudopseudohypoparathyroidism. Since she had no family history of pseudohypoparathyroidism and had a normal level of Gs alpha protein on the membrane of the red blood cells, there is no evidence of pseudopseudohypoparathyroidism. The cause of the ectopic calcification remains unknown.
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PMID:Intracranial calcification and brachydactyly mimicking Albright's hereditary osteodystrophy in an adult patient with lingual thyroid and prolactinoma-like lesion. 167 15

Zinc is known to be an essential trace metal which is necessary for health and growth, and is also essential for the function and activity of over 200 metalloenzymes. A relationship between zinc and obesity was first found in obese patients and obese mice (genetically and dietary obese) to that the obese had lower blood zinc levels than their lean controls, and the zinc level was inversely related to the degree of obesity. The therapeutic effect of zinc on obesity is still a controversial subject. This study was to investigate the alterations of tissues zinc distribution, dietary zinc effect in obese mice, and the interactive combinations of zinc and endocrine factors in obese patients. Zinc and body fat contents were determined by atomic absorption spectrometer and gravimetrically, respectively. The results indicated that dietary zinc treatment increased body fat deposition in obese mice. Obese mice carried markedly low zinc levels in most of the peripheral tissues, but retained a great amount of zinc in liver and adipose tissues compared with lean mice. Clinically, zinc was found to be correlated with thyroid hormone conversion and insulin resistance. Although the true metabolic role of zinc in obesity is still obscure, the relationships between zinc, endocrine factors, and neurotransmitters, and interactions with other trace metals are needed to throw light on the subject. These approaches to thermoregulation and metabolic mechanisms of obesity and diabetes mellitus may be of great interest in the future.
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PMID:[Investigation of the relationships between zinc and obesity]. 179 13

Thyroid hormone preparations comprised over 1% of all prescriptions filled by retail pharmacies during 1988 in the conterminous United States, i.e., the 48 contiguous states. Their large market share gives the patterns of their use substantial public health importance. This article describes prescription thyroid hormone use in the United States from 1960 through 1988, using pharmaceutical marketing research data collected from panels of retail pharmacies and office-based physicians. Although the use of natural products has declined by over 50% since 1960, about one fourth of all thyroid hormone prescriptions were for natural preparations as recently as 1988. Per capita thyroid mentions (i.e., patient-physician contacts during which a thyroid agent of any kind was recommended, prescribed, dispensed, administered, ordered to be given by a hospital, or given as a sample) doubled during this period among those over 59 years old. Per capita mentions for synthetic thyroid products increased fourfold and tenfold among men and women in this age group, respectively. Use for weight loss, despite the label's boxed warning indicating it to be ineffective and potentially dangerous, has diminished but persists. Obesity was second only to hypothyroidism among the diagnoses underlying thyroid product mentions.
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PMID:Thyroid hormone use: trends in the United States from 1960 through 1988. 184 27

Circulating TRH-immunoreactive levels, the thyrotropin response to a TRH intravenous stimulation (200 micrograms) and thyroid hormone concentrations have been determined in 43 overweight subjects (body mass index 45 +/- 12 kg/m2, mean +/- s.d.) and 46 (body mass index 22 +/- 2 kg/m2) normal weight controls. The TRH levels measured by a recently developed, highly specific radioimmunoassay were similar among both groups (44 +/- 16 vs 40 +/- 12 fmol/ml, n.s.). The pattern of response of TSH to TRH was normal in the obese and no significant difference was observed between the peak TSH values of the obese and the normal group (8.3 +/- 2.8 vs 8.7 +/- 2.2 microU/ml, n.s.). No correlations were found between the degree of obesity and the concentrations of TRH, TSH and peripheral thyroid hormone levels. Three obese patients showed a delta-TSH of 18, 19 and 21 microU/ml at normal thyroid hormone concentrations as sign of latent hypothyroidism. These data indicate that in obesity: (a) the TSH response to i.v. TRH is not impaired, (b) circulating TRH-IR levels are not significantly changed and (c) the incidence of overt hypothyroidism is not increased.
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PMID:Thyrotropin releasing hormone (TRH) immunoreactivity and thyroid function in obesity. 190 Dec 99

The effects of a combined treatment with supraphysiological doses of the thyroid hormone T3 (15 micrograms/kg BW/day, s.c.) and high doses of a predominant beta 1-blocker (atenolol, 12.5 and 25 mg/kg BW, 3X/day, s.c.) or a non-specific beta-blocker (propranolol, 5 mg/kg BW s.c. and 33 mg/kg BW p.o., each 3X/day) on energy intake, body composition and the heart were studied in overfed rats with an increased body fat content. The goal of the study was to investigate whether the above treatment constitutes a therapy for obesity in that T3 causes weight and fat loss and the beta-blockers prevent the unwanted T3-effects on the heart (tachycardia and increased heart weight). T3 did not increase energy intake above the level seen in overfed animals. It caused loss of body weight due to loss of fat but not protein, an increase in interscapular brown adipose tissue (IBAT) weight and fat, tachycardia and an increase in heart weight. Atenolol and propranolol blocked T3-induced tachycardia. With the exception of the highest propranolol dose which abolished the T3-induced increase in IBAT fat content, the beta-blockers did not modify the other T3 effects. Thus, in spite of the weight and fat loss and the lack of significant protein loss and tachycardia observed under T3/high dose beta-blockers treatment, the T3-induced increase in heart weight makes this treatment unsuitable as a therapy for obesity.
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PMID:T3 plus high doses of beta-blockers: effects on energy intake, body composition, bat and heart in rats. 198 82

The manifestations of endocrine derangements in the musculoskeletal system in infancy and childhood are disturbances in growth and maturation and in adulthood are disturbances in maintenance and metabolism. Hypercortisolism during skeletal immaturity suppresses growth. In the adult, hypercortisolism leads to osteoporosis, osteonecrosis, and muscle wasting. Deficiency of growth hormone during skeletal development results in short stature. An excess of growth hormone in a skeletally immature individual results in gigantism, an excess in a skeletally mature individual results in acromegaly. Patients with gigantism have extreme height with normal body proportions. Musculoskeletal manifestations of acromegaly include soft-tissue thickening, vertebral body enlargement, characteristic hand and foot changes, and enthesal bony proliferation. Hyperthyroidism causes catabolism of protein and loss of connective tissue, which manifest as muscle wasting. Deficient levels of thyroid hormone cause defects in growth and development. Severe growth retardation from congenital hypothyroidism is rare because neonatal screening recognizes the disorder and leads to early treatment. The skeletal manifestation of hypergonadism in children is precocious growth and early skeletal maturation. Although the initial precocious growth spurt results in a tall child, early closure of the growth plates results in a short adult. Hypogonadism in the prepubertal child results in delayed adolescence and delayed skeletal maturation. Diabetes mellitus in childhood results in decreased growth, a phenomenon presumed to be secondary to nutritional abnormalities. Generalized osteoporosis and short stature are common. In the adult, generalized osteoporosis may accompany insulin-dependent diabetes mellitus if obesity is absent. Calcification of interdigital arteries of the foot is common in diabetics and uncommon in other conditions. Additional skeletal manifestations relate to complications of diabetes such as peripheral neuropathy and diabetic foot disease.
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PMID:Radiologic manifestations in the musculoskeletal system of miscellaneous endocrine disorders. 198 24

Some major pathways of lipid metabolism are under control of thyroid hormones. Thyroxine changes the lipid composition of different cell membranes. Modification of thyroid hormone metabolism during ontogenesis is one of the reasons of changes in lipid composition and function of cell nuclei and its other structures. Atherosclerosis and obesity may be a result of the thyroid dysfunction and modulation of the cellular lipid metabolism.
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PMID:[Thyroid hormones and lipid metabolism]. 266 Dec 74

The overall prevalence of thyroid hormone use in an unselected population of older adults (n = 2575; average age, 68.6 years) was 6.9% (10.0% in women and 2.3% in men). Eighty-one percent of women taking it were doing so for appropriate indications, eg, hypothyroidism, while 12% were not, eg, for obesity or high serum cholesterol; more men (29%) were taking it inappropriately. Inappropriate use was associated with desiccated thyroid more than with thyroxine. After follow-up averaging 6.9 years, 58% of inappropriate users were still taking it. Underuse also occurred. Thirty-seven percent of those definitely hypothyroid had a clearly elevated serum thyrotropin level (greater than 10 mU/L) despite thyroid therapy. Thyroid therapy is common in the elderly; most is appropriate. When inappropriate use occurs, it is more common in men and more often associated with desiccated thyroid, still commonly used in this age group. In chronic users of thyroid hormone, it is important to review currently appropriate indications and to measure serum thyrotropin levels to assess the adequacy of treatment of primary hypothyroidism.
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PMID:The aging thyroid. The use of thyroid hormone in older persons. 270 45


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