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

The effects of chronic growth hormone deficiency on the growth hormone-dependent, sexually dimorphic hepatic drug-metabolizing enzymes were studied in adult rats of both sexes. Neonatal administration of monosodium L-glutamate produced the expected syndrome characterized by stunted growth, obesity, prolonged vaginal estrus, and an inhibition in the growth of the pituitaries, adrenals, gonads, sexual accessory organs, and kidneys. Associated with these abnormalities was a 90% reduction in the concentration of serum growth hormone in male and female rats. In contrast, the activities of hepatic aniline hydroxylase, total cytochrome P-450, and the Michaelis constants and maximal velocities for hexobarbital hydroxylase and UDP-glucuronosyltransferase were unaffected by the profound deficiency in growth hormone.
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PMID:Normal levels of hepatic drug-metabolizing enzymes in neonatally induced, growth hormone-deficient adult male and female rats. 287 66

Inbred mice with the mutation diabetes C57BL/KsJ db+/db+ and the mutation obese C57BL/6J ob/ob displayed a total liver mitochondrial capacity to oxidize glutamate or succinate which was approximately eight times greater than the capacity of the C57BL/6J +/+ control mice. This increase in oxidation capacity was estimated by multiplying the observed twofold increase in each of the following components: total liver weight, the mitochondrial protein content per gram of liver, and glutamate or succinate respiration activity per milligram of liver mitochondrial protein. No significant difference in liver mitochondrial function and capacity for oxidation was observed between db+/db+ and ob/ob mutants, which indicated that these results may be primarily mediated by the genetic factors responsible for obesity and hyperphagia in these mutants, and not by the genetic traits associated with diabetes. These findings may provide a biochemical foundation in support of the thrifty gene hypothesis.
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PMID:Influence of genetic predisposition to diabetes and obesity on mitochondrial function. 287 79

Adipsin expression at the protein and mRNA levels is greatly reduced in several distinct syndromes of obesity in the mouse: genetic obesity due to the db/db and ob/ob genes, and a chemically induced model secondary to neonatal exposure to monosodium glutamate. We considered first the possibility that the adipsin gene might be identical to the db or ob locus and the lowered expression of this protein might result from a mutation in this gene. We show here that the adipsin structural gene is located on chromosome 10 and hence is physically distinct from any obesity genes so far identified in the mouse. A major role for the adrenal gland and adrenal glucocorticoids in the aberrant regulation of adipsin in these models of obesity is indicated by several experiments. Adrenalectomy of the ob/ob mouse raises the circulating levels of adipsin protein and the amount of this mRNA in epididymal fat pads (5-fold), although neither is increased to the levels seen in lean controls. Exogenous administration of corticosterone completely blocks the effects of adrenalectomy on adipsin, suggesting that the effect of this endocrine ablation is through reduction of adrenal glucocorticoids. Corticosterone administration also causes suppression in the levels of adipsin mRNA and protein in lean mice, although this decrease is never as severe as that seen in obese mice. The effect of exogenous corticosterone in lean mice occurs within 2 days and hence is not secondary to the obesity which these hormones eventually elicit. These results indicate that glucocorticoids can regulate adipsin expression in vivo and strongly suggest that the hyperglucocorticoid state seen in certain obese models plays a significant role in lowering adipsin mRNA and protein levels. Quantitative analysis of these experiments suggests that other as yet unknown neuroendocrine factors also function to suppress adipsin in obesity.
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PMID:Adrenal glucocorticoids regulate adipsin gene expression in genetically obese mice. 291 85

Administration of monosodium glutamate to neonate rats causes hypothalamic lesions in the region of the nucleus arcuatus and the eminentia mediana, followed by massive accumulation of triglycerides, diminished secretion of growth hormone, reduced body length and organ weights and diminished number of adipocytes (hypoplastic-hypertrophic obesity). Locomotor activity of obese animals is reduced by about 50%. Food intake is increased by about 10% during growth and development of obesity but decreased beneath the level of that in control animals in the stationary phase of obesity. Hyperinsulinemia coupled with insulin resistance develops in the stationary phase of obesity, i.e. when adipocyte diameter has reached approximately 100 microns. The effects of reduced secretion of growth hormone are considered to be a main factor of fat accumulation in this type of obesity.
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PMID:Development of hypothalamic obesity in growing rats. 306 67

Obesity was induced in neonatal mice by subcutaneous injections of monosodium glutamate (MSG) at an early neonatal stage. The process of adipocyte formation was studied comparatively in the developing epididymal adipose tissue of the MSG-treated mice and in normal mice during the period from the 6th to the 100th postnatal day. Tritiated thymidine autoradiographic studies showed that cell proliferation activity was the highest on the 6th postnatal day both in the MSG-treated and the control mice. In normal mice, however, cell proliferation took place less frequently after 6 days and had almost ceased after 49 days. In the obese mice, as evidenced by relatively high labeling indices, cell proliferation continued to occur even after 49 days. Ultimately there was no difference in the number of adipocytes counted by Hirsch's method in the MSG-treated and the control mice at the 100th postnatal day. The storage of fat droplets became more noticeable in obese mice than in normal mice after 35 days. The mean size of fat droplets of the obese mice was twice as large as that in normal mice on the 49th postnatal day. These results indicate that the MSG-induced obesity is of the hypertrophic type.
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PMID:Development of the epididymal adipose tissue in monosodium glutamate-induced obese mice. 318 80

Rats treated with monosodium glutamate (MSG) during the neonatal period show hypothalamic lesions and multiple neuroendocrine alterations manifested as a remarkable increase in levels of circulating corticosterone and obesity. Paw edema induced by local injection of carrageenin was significantly reduced in MSG-treated rats compared to normal rats. In contrast, both adrenalectomized rats and adrenalectomized, MSG-treated rats showed an increased response to carrageenin relative to controls. These results suggest that glucocorticoids are important modulators of inflammation in this phase of the process.
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PMID:Inflammatory edema induced by carrageenin in monosodium glutamate-treated rats. 324 Mar 79

Lesions of the circumventricular regions of the brain induced by neonatal administration of monosodium L-glutamate (MSG) are associated with chronic hypophagia and deficits in response to a variety of feeding challenges. These deficits occur despite the fact that, at least at high doses, MSG can produce obesity. The cause of the feeding deficits in MSG-treated animals is unknown. However, the circumventricular regions that are damaged by MSG contain high concentrations of insulin binding sites. In order to determine whether the MSG lesion alters responsiveness to circulating insulin, we have investigated the response of non-obese MSG-treated mice to doses of exogenous insulin designed either to stimulate feeding or to induce hypoglycemic convulsions. We report that MSG produces a dose-related decrease in hypoglycemic convulsions and glucoprivic feeding, suggesting that a loss in sensitivity to insulin may contribute to the MSG syndrome.
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PMID:Monosodium L-glutamate lesions reduce susceptibility to hypoglycemic feeding and convulsions. 329 94

Adipsin, a serine protease homolog, is synthesized and secreted by adipose cells and is found in the bloodstream. The expression of adipsin messenger RNA (mRNA) and protein was analyzed in rodents during metabolic perturbations and in several experimental models of obesity. Adipsin mRNA abundance is increased in adipose tissue during fasting in normal rats and in diabetes due to streptozotocin-induced insulin deficiency. Adipsin mRNA abundance decreased during the continuous infusion of glucose, which induces a hyperglycemic, hyperinsulinemic state that is accompanied by an increased adipose mass; it is suppressed (greater than 100-fold) in two strains of genetically obese mice (db/db and ob/ob), compared to their congenic counterparts, and is also reduced when obesity is induced chemically by injection of monosodium glutamate into newborn mice. Circulating adipsin protein is decreased in these animal models of obesity, as determined by immunoblotting with antisera to adipsin. Little change in adipsin expression is observed in a model of obesity obtained by pure overfeeding of normal rats (cafeteria model). These data suggest a possible role for adipsin in the above-mentioned disordered metabolic states, and raise the possibility that adipsin expression may be used to distinguish obesities that arise from certain genetic or metabolic defects from those that result from pure overfeeding.
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PMID:Severely impaired adipsin expression in genetic and acquired obesity. 329 6

The content and turnover of norepinephrine was measured in the interscapular brown adipose tissue (BAT), white adipose tissue (WAT) and heart of lean and monosodium glutamate treated obese rats (GOR). An HPLC-ECD method was used for efficient separation and sensitive detection of catecholamines with an appropriate sample preparation, especially for lipid rich tissues. The lower basal norepinephrine level and the slower norepinephrine turnover in organs of the glutamate obese rats indicate a diminished activity of the sympathetic nervous system which may be a reason for a reduced thermogenic response and in this way contributes to the development of obesity.
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PMID:Measurement of tissue catecholamines of obese rats by liquid chromatography and electrochemical detection. 344 8

Monosodium glutamate and bipiperidyl mustard both produce mediobasal hypothalamic lesions and have been reported to alter the subsequent feeding behavior and/or insulin levels of treated animals. In our previous studies bipiperidyl mustard alone had no effects on insulin levels or feeding, but in combination with glutamate produced hyperphagic obesity. Administration of exogenous cholecystokinin octapeptide also has been shown to affect feeding behavior and plasma insulin. In order to determine if endogenous cholecystokinin played a role in the effects of glutamate or bipiperidyl mustard, concentrations of cholecystokinin in the pituitary glands of lesioned rats were measured. Bipiperidyl mustard alone increased cholecystokinin content while combined lesioning with glutamate prevented the increase. The potential role of cholecystokinin-containing elements of the hypothalamus and pituitary in modulation of feeding is discussed.
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PMID:Hypothalamic neurotoxins alter the content of immunoreactive cholecystokinin in pituitary. 356 52


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