Plasma Levels of Insulin-Like Growth Factor-l Are Reduced at One Week of Age in Monosodium L-Glutamate-Treated Mice.

Yamamoto, Toru; Matsuo, Seiichiro; Ueshima, Yasuo; Inoue, Fumio; Kinugasa, Akihiko; Sawada, Tadashi

doi:10.1507/endocrj.40.461

Cited by 12 publications

(11 citation statements)

References 18 publications

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“…Our results confirm other researches [7, 9, 35]in which neonatal treatment with MSG caused obesity in mice. Lee index used as biometrics data to evaluate obesity shows that the neonatal treatment provoked obesity installation at age 30 days and continues till 60 and 90.…”

Section: Discussionsupporting

confidence: 92%

“…Ninety-day-old MSG-obese mice presented moderate glycemia and severe hyperinsulinemia, already shown by other researchers [9, 35]. Hyperinsulinemia is a common phenomenon to several obesities caused by hypothalamic injuries [9, 10, 11, 12, 13, 35, 36]. The pancreatic islets isolated from MSG-obese mice disclose high insulin secretion when perifused with glucose 5.6 m M , which is held to be a blood glucose concentration before food intake [32].…”

Section: Discussionsupporting

confidence: 73%

“…Rodents treated with MSG present low levels of GH [6]. However, the efficacy of the treatment may be due to the MSG dose applied in neonatal mice [7, 9, 35]. Ninety-day-old MSG-obese mice presented moderate glycemia and severe hyperinsulinemia, already shown by other researchers [9, 35].…”

Section: Discussionmentioning

confidence: 97%

“…However, the efficacy of the treatment may be due to the MSG dose applied in neonatal mice [7, 9, 35]. Ninety-day-old MSG-obese mice presented moderate glycemia and severe hyperinsulinemia, already shown by other researchers [9, 35]. Hyperinsulinemia is a common phenomenon to several obesities caused by hypothalamic injuries [9, 10, 11, 12, 13, 35, 36].…”

Section: Discussionmentioning

confidence: 99%

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Insulin Secretion and Acetylcholinesterase Activity in Monosodium <i>L</i>-Glutamate-Induced Obese Mice

et al. 2000

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Objective: Pancreatic islets isolated from mice treated neonatally with monosodium L-glutamate (MSG) were used to study insulin secretion. Material and Methods: Total acetylcholinesterase (AchE) activity of tissue extract was measured as a cholinergic activity marker. Obesity recorded in 90-day-old MSG mice (OM) by Lee index reached 366.40 ± 1.70, compared to control mice (CM) 324.40 ± 1.10 (p < 0.0001). Glucose 5.6 mM induced insulin secretion of 36 ± 5 pg/15 min from islets of CM and 86 ± 13 from OM (p < 0.001). When glucose was raised to 16.7 mM, islets from OM secreted 1,271 ± 215 and 1,017 ± 112 pg/30 min to CM. AchE activity of pancreas from OM was 0.64 ± 0.02 nmol of substrate hydrolyzed/min/mg of tissue and 0.52 ± 0.01 to CM (p < 0.0001). Liver of obese animals also presented increase of AchE activity. Results: These indicate that OM insulin oversecretion in low glucose may be attributed, at least in part, to an enhancement of parasympathetic tonus.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionsupporting

confidence: 73%

Section: Discussionmentioning

confidence: 97%

Section: Discussionmentioning

confidence: 99%

See 2 more Smart Citations

Insulin Secretion and Acetylcholinesterase Activity in Monosodium <i>L</i>-Glutamate-Induced Obese Mice

et al. 2000

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“…31,32 The resulting obesity is accompanied by reductions in many pituitary hormones (such as growth hormone) and a stunted somatic growth rate. 33 GTG injected intraperitoneally (ip) into adult mice, causes neuronal loss in the VMH (a satiety center) 4 and thereby induces a period of robust overeating. 34 There are also genetic lines of obese mice characterized by high leptin levels.…”

Section: Introductionmentioning

confidence: 99%

Role of neuropeptide Y in diet-, chemical- and genetic-induced obesity of mice

1998

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OBJECTIVE: The goal of this study was to ascertain whether neuropeptide Y (NPY) is required in mice for the development of obesity induced by a high-fat diet (HFD), chemical lesions of the hypothalamus caused by monosodium glutamate (MSG) or gold thioglucose (GTG), impaired brown adipose tissue (BAT) due to a diphtheria toxin transgene driven by the uncoupling protein 1 promoter (UCP-DTA) or the lethal yellow agouti mutation (A y ). BACKGROUND: The obesity syndrome of the leptin-de®cient (ob/ob) mouse can be partially reversed by the genetic removal of NPY. In the murine models of obesity examined in this study, the animals become obese despite increased serum leptin levels, indicating that they are resistant to the weight-limiting actions of leptin. The role of NPY in these obesity models with elevated leptin levels is unknown. EXPERIMENTAL DESIGN: Mice lacking NPY due to genetic disruption of the gene and wildtype littermates were made obese by allowing them access to a highly palatable HFD, by treatment with MSG, or GTG, or by inheriting the dominant UCP-DTA or A y alleles. Food consumption, body weight and dissectable fat pad weights were measured and compared to values obtained from non-obese littermates. RESULTS: In each model of obesity tested, NPY-de®cient mice achieved the same food intake, body weight and fat content as wildtype littermates. CONCLUSION: NPY is not necessary for the progressive development of obesity exhibited by multiple murine models with leptin resistance.

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Swim training of monosodium l-glutamate-obese mice improves the impaired insulin receptor tyrosine phosphorylation in pancreatic islets

et al. 2012

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The goal of the present study was to investigate changes on glucose homoeostasis and of the insulin receptor (IR) and insulin receptor substrate-1 (IRS-1) signalling in pancreatic islets from MSG-obese mice submitted to or not submitted to swim training. Swim training of 90-day-old MSG mice was used to evaluate whether signalling pathways of the IR and IRS-1 in islets are involved with the insulin resistance and glucose intolerance observed in this obese animal model. The results showed that IR tyrosine phosphorylation (pIR) was reduced by 42 % in MSG-obese mice (MSG, 6.7 ± 0.2 arbitrary units (a.u.); control, 11.5 ± 0.4 a.u.); on the other hand, exercise training increased pIR by 76 % in MSG mice without affecting control mice (MSG, 11.8 ± 0.3; control, 12.8 ± 0.2 a.u.). Although the treatment with MSG increased IRS-1 tyrosine phosphorylation (pIRS-1) by 96 % (MSG, 17.02 ± 0.6; control, 8.7 ± 0.2 a.u.), exercise training also increased it in both groups (control, 13.6 ± 0.1; MSG, 22.2 ± 1.1 a.u.). Current research shows that the practice of swim training increases the tyrosine phosphorylation of IRS-1 which can modulate the effect caused by obesity in insulin receptors.

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Plasma Levels of Insulin-Like Growth Factor-l Are Reduced at One Week of Age in Monosodium L-Glutamate-Treated Mice.

Cited by 12 publications

References 18 publications

Insulin Secretion and Acetylcholinesterase Activity in Monosodium <i>L</i>-Glutamate-Induced Obese Mice

Insulin Secretion and Acetylcholinesterase Activity in Monosodium <i>L</i>-Glutamate-Induced Obese Mice

Role of neuropeptide Y in diet-, chemical- and genetic-induced obesity of mice

Swim training of monosodium l-glutamate-obese mice improves the impaired insulin receptor tyrosine phosphorylation in pancreatic islets

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