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)

When newborn female rats were treated with monosodium glutamate, 4 mg/g body weight, on days 1 and 3 of life, circulating growth hormone concentrations were permanently reduced 75-85% in adulthood, whereas the feminine secretory profile characterized by frequent growth hormone pulses, separated by short-lived, measurable troughs, persisted. Associated with this reduction in growth hormone secretion was a mild obesity and a slight depression in peripubertal body weight. In contrast, expression of growth hormone-dependent, female-specific CYP2C12 was increased by almost 100% when measured at both its protein and mRNA levels. In agreement, this supraphysiological expression of CYP2C12 was reflected at a pharmacologic level by a simultaneous elevation in in vitro and in vivo hexobarbital metabolism. When growth hormone secretion was pulsatile (i.e. masculine) or was eliminated from the circulation (i.e. hypophysectomy), hepatic CYP2C12 protein and mRNA were undetectable. The present findings suggest that the normal levels of plasma growth hormone found in female rats are not necessarily optimum for the expression of female-specific CYP2C12.
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PMID:Subnormal concentrations in the feminine profile of circulating growth hormone enhance expression of female-specific CYP2C12. 801 Sep 84

The study was aimed at investigating the effect of monosodium glutamate administered during the perinatal period on the reproductive system of sexually mature male rats. Monosodium glutamate (at a dose of 4 mg/g of body weight) or hypertonic saline was administered subcutaneously to newborn rats at 2--nd, 4-th, 6-th, 8-th and 10-th day of life. At the age of four months the rats were killed and histological and morphometric examinations of testes, epididymis, seminal vesicles and ventral prostate were carried out. Blood serum levels of LH, FSH, testosterone and 17-beta-estradiol were determined by radioimmunoassay. The administration of monosodium glutamate caused inhibition of growth, obesity and decrease in weight of pituitary glands and testes. Blood serum levels of and FSH as well as the height of epithelial cells of accessory sexual glands remained unchanged, whereas testosterone level was lowered.
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PMID:[Effect of perinatal administration of monosodium glutamate (MSG) on the reproductive system of the male rat]. 805 18

Postprandial thermogenesis was estimated in 4-month-old male rats with glutamate induced obesity after being fed with 300, 450 and 600 kJ/kg0.75 of a pellet diet, respectively by indirect calorimetry in computer-controlled open circuit metabolic cages over 8 h. After an intake of 600 kJ/kg0.75 (above the maintenance energy requirement) postprandial thermogenesis was significantly reduced in the obese animals to about 40% of control rats (12.0 versus 31.5 kJ/kg0.75 x 8h). It is concluded that the glutamate obese rat can be accepted as an animal model with impaired facultative thermogenesis, mainly caused by a reduction of sympathetic adrenergic activity.
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PMID:Postprandial thermogenesis of rats with glutamate induced obesity in relation to energy intake. 809 1

Neonatal male and female mice were treated with monosodium glutamate (MSG) at either 2.0 or 4.0 mg/g body weight on alternate days during the first 9 days of life. As adults, mice were catheterized to obtain unstressed, serial blood samples for the determination of ultradian profiles of circulating growth hormone. In addition, monooxygenase levels (i.e. steroid hydroxylases and drug-metabolizing enzymes) were measured in hepatic microsomes. Generally, both doses of MSG produced the same developmental defects. Mice neonatally exposed to the amino acid developed a syndrome characterized by retarded growth, obesity and reduced organ weights. While vehicle-treated mice secreted growth hormone in sexually dimorphic patterns defined by pulse frequency (i.e. F > M), hormone concentrations in plasma samples obtained during 8 continuous hr of serial blood collections from both male and female MSG-treated mice were barely detectable at best, and exhibited no pulsatility. Approximately 15% of the measured monooxygenases were male-predominant, 35% were female-predominant and 50% had no sex differences. The enhanced expression of the hepatic monooxygenases in response to MSG-induced depletion of plasma growth hormone indicates that the hormone basically functions as a suppressor of the murine enzyme system.
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PMID:Effects of neonatally administered monosodium glutamate on the sexually dimorphic profiles of circulating growth hormone regulating murine hepatic monooxygenases. 816 51

We investigated glucose transporters (GLUT 1 and GLUT 4) in subcellular membrane fractions of white adipose tissue (WAT) of insulin-resistant obese aurothioglucose (AuTG)- or monosodium glutamate (MSG)-treated mice. In vivo insulin stimulation (0.75 U/kg, EV) promoted, 10 min later, no significant change on glycemia of both AuTG and MSG obese mice, but control mice showed a decrease of 30% (p < 0.001). Basal GLUT 4 content in WAT of obese mice was reduced by 40% (p < 0.001) when compared to that of nonobese mice. Insulin-stimulated GLUT 4 content was significantly (p < 0.01) higher in plasma membrane fraction and lower in microsomal fraction when compared to respective basal values, in all groups. Although the absolute values of GLUT 4 were lower in membrane fractions of obese mice, the relative changes stimulated by insulin were similar among the groups. No effect of obesity or insulin stimulation was observed upon GLUT 1 content. We conclude that WAT of insulin-resistant obese AuTG- and MSG-treated mice has a decreased GLUT 4, but not GLUT 1, content, and the in vivo insulin-stimulated GLUT 4 translocation is preserved.
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PMID:Reduced content and preserved translocation of glucose transporter (GLUT 4) in white adipose tissue of obese mice. 819 Jul 86

We assessed the content of two isoforms of glucose transporter (GLUT 1 and GLUT 4) in insulin-sensitive tissues of hypothalamic obese mice treated with either aurothioglucose (AuTG) or monosodium glutamate (MSG). The animals were studied when obesity had reached a plateau, and they were clearly insulin resistant. We studied different membrane fractions from white adipose tissue (WAT), such as fat-free extract (FFE), plasma membrane (PM) and microsomal (M) fractions. GLUT 4 expressed per protein content displayed a decrease of 50% (p < 0.001) in all membrane fractions of AuTG- and MSG-treated mice. The PM GLUT 4 content, expressed per cell surface area, was reduced by 70% (p < 0.001) in obese mice, and the total FFE GLUT 4, expressed per total fat mass, was 5 times reduced in obese mice. Compared to control mice, obese mice showed a reduction (p < 0.01) of the GLUT 4 amount by 30% (AuTG) and by 40% (MSG) in total membrane fraction (TM) of skeletal and cardiac muscles. Similarly, a reduction of the GLUT 4 amount by 40% (AuTG) and by 45% (MSG) in FFE of brown adipose tissue was observed. The GLUT 1 content in FFE of WAT and TM of skeletal muscle showed no significant difference among the different animal groups. These results confirm a decreased expression of GLUT 4, but not of GLUT 1, in insulin-sensitive tissues, which may contribute to the impaired glucose utilization in these obese animals.
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PMID:Decreased glucose transporter (GLUT 4) content in insulin-sensitive tissues of obese aurothioglucose- and monosodium glutamate-treated mice. 822 98

The neurotoxic effects of monosodium glutamate (MSG) on certain parts of the central nervous system (CNS) and endocrine functions are well documented. MSG-treated rats exhibit stunted growth, obesity and decrease in sexual behavior. The present study was designed to evaluate how neonatal administration of MSG affects sex-odor attractivity and approach behavior, and to investigate factors limiting copulation in MSG-treated rats. In this experiment, subcutaneous injections of MSG (400 mg MSG/ml normal saline/0.1 Kg B.W.) were given to Long-Evans pups on days 1 and 3 after birth, whereas the control groups received normal saline injections of equal volume (1 ml/0.1 kg B.W.). When the rats were 3 months old, sex-odor attractivity and approach behavior were tested. Two points were displayed by MSG-treated rats: (a) attenuated the attractivity of sex-odor. (b) decreased performance of sexual approach to partners. From our results and those of a previous study, we suggest that the deterioration of sex-odor attractivity and approach behavior to partners is attributed to a decline in sexual hormones. Furthermore, we concluded that this decrease in behaviors is to some extent responsible for reduced copulatory behavior.
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PMID:[The effects of neonatal monosodium glutamate treatment on sex-odor attractivity and approach behavior in rats]. 832 Jul 57

Neonatal exposure to monosodium glutamate (MSG) permanently blocks growth hormone (GH) secretion, which results in the development of a well-defined syndrome characterized by stunted body growth, obesity and impaired drug metabolism. We have found that restoration of the normal masculine circulating profile of GH (i.e., six daily pulses) by use of an external pumping apparatus is ineffective in restoring the normal expression of hepatic cytochrome P450 2C11, a major GH-dependent drug and steroid metabolizing enzyme that is eliminated by MSG treatment. Moreover, administering GH at two, four or seven plasma pulses per day with amplitudes ranging from physiologic to 7 times normal were similarly ineffective in restoring the expression (at both an activity and mRNA level) of the cytochrome. Additionally, multicytochrome P450-dependent hexobarbital hydroxylase was also unresponsive to GH administration in the MSG-treated rats. Because GH replacement was unable to correct the enzyme defects, our results suggest that the developmental abnormalities produced by neonatal MSG are not simply a result of a GH deficiency per se, but are due to an irreversible insensitivity of the target cell to GH.
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PMID:Irreversible suppression of growth hormone-dependent cytochrome P450 2C11 in adult rats neonatally treated with monosodium glutamate. 849 38

Glucose transporter (GLUT 4) was assessed in subcellular membrane fractions of white adipose tissue (WAT) from obese insulin-resistant aurothioglucose (AuTG)- or monosodium glutamate (MSG)-treated mice. Obesity was demonstrated by increased body weight and/or Lee index, as well as by the heavier WAT and brown adipose tissue in relation to similar weights of gastrocnemius and heart. In vivo insulin-resistance in obese animals was suggested by moderate hyperglycemia and severe hyperinsulinemia. Morphological analyses of adipose cells showed a > 10-fold increase in cell volume of obese mice. Subcellular fractionation indicated a reduced (P < 0.01) protein membrane content in the fat-free extract (FFE) from obese mice. However, the specific activity of 5'nucleotidase, a plasma membrane (PM) marker, in FFE and PM did not differ among groups. In addition, the total PM enzyme activity per unit of cell surface area was also unchanged. The GLUT 4 content, assessed by Western blotting and expressed per microgram membrane protein, was reduced by approximately 50% (P < 0.01) in all membrane fractions from obese animals. However, the total FFE GLUT 4 content per cell was increased (P < 0.01), from 23.5 +/- 1.8 in controls to 62.4 +/- 7.6 and 47.4 +/- 5.9 cpm cell-1 10(-3) in AuTG and MSG, respectively, but the total PM GLUT 4 content per unit of cell surface area was highly reduced (P < 0.01), from 165.1 +/- 16.7 in controls to 53.8 +/- 10.9 and 32.0 +/- 5.3 cpm microns-2 10(-9) in AuTG and MSG, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effect of adipose cell size on the measurement of GLUT 4 in white adipose tissue of obese mice. 852 May 34

Neonatal treatment with monosodium glutamate (MSG) decreases proopiomelanocortin (POMC) peptides and results in obesity. The yellow mouse is a model of obesity induced by the viable yellow (Avy) gene at the agouti locus on Chromosome 2, which results in overproduction of a POMC receptor antagonist. Thus we hypothesized that MSG, when imposed on the genetically susceptible model, would alter the development of obesity. Both yellow obese (Avy) and black lean (alpha/alpha) males were injected on Postnatal Days 1, 3, 5, 7, and 9 with 2.0 mg/g body weight MSG or saline SC. Their food intake, growth parameters, and neurochemical status were examined. Paradoxically, MSG interacted with the yellow phenotype to delay the rapid rate of weight gain characteristic of this model (p < 0.05). Food intake was decreased (p < 0.05) in both phenotypes treated with MSG, as was hypothalamic content of dopamine (p < 0.05) and of the POMC peptide, beta-endorphin (p < 0.001). The yellow obese phenotype was more sensitive than the black lean phenotype to the neurochemical effect of early postnatal MSG administration. Recent reports suggest the agouti locus protein is an antagonist of the receptor for another POMC peptide, melanocyte-stimulating hormone (MSH). Therefore, the balance of functional activity between various POMC peptides appears to be an important factor in the development of both acquired and genetic obesity.
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PMID:Neonatal MSG reduces hypothalamic DA, beta-endorphin, and delays weight gain in genetically obese (A viable yellow/alpha) mice. 880 53


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