Late Endocrine Effects of Administering Monosodium Glutamate to Neonatal Rats

Bakke, John L.; Lawrence, Natasha J.; Bennett, J. P.; Robinson, S.; Cy, Bowers

doi:10.1159/000122829

Cited by 94 publications

(46 citation statements)

References 4 publications

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“…Regarding the BW of MSG rats, we observed that they were lighter than respective control animals, which was the characteristic phenotype of this model as described by Remke et al (1988), Dolnikoff et al (2001), and Schoelch et al (2002). Although there were no overweight rats, the MSG-obese rats were found to have more fat pad stores as compared with control animals (Bernardis & Patterson 1968, Bray & York 1998, which was correlated with lower growth hormone (Bakke et al 1978, Acs et al 1982 and reduced basal metabolic rate (Arndt et al 1991).…”

Section: Discussionmentioning

confidence: 64%

HPA axis and vagus nervous function are involved in impaired insulin secretion of MSG-obese rats

Miranda

Torrezan

Oliveira

et al. 2016

Journal of Endocrinology

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Neuroendocrine dysfunctions such as the hyperactivity of the vagus nerve and hypothalamus–pituitary–adrenal (HPA) axis greatly contribute to obesity and hyperinsulinemia; however, little is known about these dysfunctions in the pancreatic β-cells of obese individuals. We used a hypothalamic-obesity model obtained by neonatal treatment with monosodiuml-glutamate (MSG) to induce obesity. To assess the role of the HPA axis and vagal tonus in the genesis of hypercorticosteronemia and hyperinsulinemia in an adult MSG-obese rat model, bilateral adrenalectomy (ADX) and subdiaphragmatic vagotomy (VAG) alone or combined surgeries (ADX–VAG) were performed. To study glucose-induced insulin secretion (GIIS) and the cholinergic insulinotropic process, pancreatic islets were incubated with different glucose concentrations with or without oxotremorine-M, a selective agonist of the M3muscarinic acetylcholine receptor (M3AChR) subtype. Protein expression of M3AChR in pancreatic islets, corticosteronemia, and vagus nerve activity was also evaluated. Surgeries reduced 80% of the body weight gain. Fasting glucose and insulin were reduced both by ADX and ADX–VAG, whereas VAG was only associated with hyperglycemia. The serum insulin post-glucose stimulation was lower in all animals that underwent an operation. Vagal activity was decreased by 50% in ADX rats. In the highest glucose concentration, both surgeries reduced GIIS by 50%, whereas ADX-VAG decreased by 70%. Additionally, M3AChR activity was recovered by the individual surgeries. M3AChR protein expression was reduced by ADX. Both the adrenal gland and vagus nerve contribute to the hyperinsulinemia in the MSG model, although adrenal is more crucial as it appears to modulate parasympathetic activity and M3AChR expression in obesity.

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Section: Discussionmentioning

confidence: 64%

HPA axis and vagus nervous function are involved in impaired insulin secretion of MSG-obese rats

Miranda

Torrezan

Oliveira

et al. 2016

Journal of Endocrinology

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“…In the MSG-treated mature animals, reduction of the growth hormone (6-8) and thyroid hormone (5)(6)(7)(8)(9) in the blood as well as an imbalance in the autonomic nervous system (5-9) were reported. Moreover, irreversible hypothalamic lesions by MSG histologically were manifested immediately after the treatment (18,19), suggesting possible functional disturbance in the hypothalamus-hypophysis system and a subsequent functional imbalance in the nervous, endocrine and metabolic systems.…”

Section: Discussionmentioning

confidence: 99%

“…In the same report, he mentioned that the animals with MSG-induced hypothalamic lesions became apparently obese in and after adolescence even without hyperphagia and that these MSG-induced obese animals remained short throughout their lives (1)(2)(3)(4). MSG-induced obese animals have been mainly investigated biochemically in order to clarify the mechanism of obesity (5)(6)(7)(8)(9) In the present study, the growth pattern of the visceral organs together with the changes in body weight gain, morphological findings and cell proliferative kinetics was investigated in MSG-induced obese mice. …”

mentioning

confidence: 99%

Morphological and cell proliferative study on the growth of visceral organs in monosodium L-glutamate-treated obese mice.

Hamaoka

Kusunoki

1986

Journal of Nutritional Science and Vitaminology, J Nutr Sci Vit

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SummaryThe growth pattern of visceral organs was investigated in monosodium L-glutamate (MSG)-treated obese mice with hypothalamic lesions. Male Jcl-ICR strain mice were subcutaneously injected with MSG, 2mg/g of body weight daily, for five days after birth. The MSG-treated mice became obese after 4 weeks of age. According to patterns of weight gain compared with those in the control mice, the visceral organs in the MSG-treated mice were classified into three groups as follows: The first group of organs (heart, lungs, spleen, pancreas, kidneys, testes, brain and submandibular glands) remained absolutely lower in weight throughout their growth. The second group of organs (liver and stomach) was low in weight until 12 weeks of age, but became identical to that of the control mice after 16 weeks of age. The third group of organs (epididymal fat, small intestine and colon) showed lower weight until 4 weeks of age and were significantly heavier than those in the control mice after 8 weeks of age. The heart in the first group of organs apparently had hypertrophic muscle cells after 8 weeks of age and became significantly hypoplastic due to decreased cell production as was revealed by the continuous suppression of mitotic activity and DNA synthesis by [3H]thymidine autoradiography. The liver in the second group of organs became significantly hypoplastic due to decreased cell production and showed the same weight with the control mice due to the development of fatty liver. The small intestine in the third group of organs became hypoplastic due to decreased cell production in the crypts until 4 weeks of age, and became hypertrophic and hyperplastic by the acceleration of cell production in the crypts from 4 to 8 weeks of age. From these findings, in the MSG-treated mice with specific growth patterns of visceral organs, it is suggested that low energy expenditure results in a relatively excessive energy supply and leads to obesity, because most of the important organs with major physiological functions became 395

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“…It is well known that GH is more affected by MSG treatment than other hormones, but this treatment also produced hypogonadism [33, 34, 41], probably because of alterations in GnRH release regulation [42, 43]. Differences in the gonadal axis of males and females were found in response to GH deficiency and GH administration.…”

Section: Discussionmentioning

confidence: 99%

Sexual Dimorphism in Growth as Measured by Microknemometry: Different Responses to GH Deficiency and Exogenous GH Administration

Rol

Perez-Romero²,

Hermanussen³

et al. 1998

Neuroendocrinology

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To monitor growth, a novel noninvasive leg length measurement technique, called microknemometry, which allows daily observation of tibial growth rate, was used. The rat exhibits a striking sex-related difference in postpubertal growth. Exogenous GH administration results in a sexually dimorphic response, affecting growth in normal young female rats but not in males. Here we investigated how chronic GH deficiency affects male and female rat growth patterns. The degree of growth rate recovery was investigated after exogenous GH administration to chronically deficient males and females. The deficiency was induced by neonatal monosodium glutamate (MSG) treatment. Since the neonatal gonadal environment plays an important role in the dimorphic growth pattern, neonatal androgenization of female rats with testosterone or neonatal feminization of male rats by castration was performed and the growth pattern monitored. MSG treatment decreased pituitary GH content and plasma IGF I levels in both sexes, but caused a less marked reduction of female rat tibial growth and body weight gain than in males. Additionally, only MSG-treated males showed decreased pituitary LH content, so that the dimorphic action of MSG on the gonadal axis may contribute to the observed differences in growth rate. GH administration was able to increase leg length in all MSG-treated rats but was more effective in females, despite a similar restoration of plasma IGF I levels in both sexes. Although neonatal castration of male rats resulted in a reduction of tibial growth rate and body weight, and neonatal testosterone administration to female rats caused a slight increase in body weight, a complete modification of the gender-dependent growth pattern was not achieved, indicating that appropriate steroid environment is also needed in puberty and adulthood.

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Late Endocrine Effects of Administering Monosodium Glutamate to Neonatal Rats

Cited by 94 publications

References 4 publications

HPA axis and vagus nervous function are involved in impaired insulin secretion of MSG-obese rats

HPA axis and vagus nervous function are involved in impaired insulin secretion of MSG-obese rats

Morphological and cell proliferative study on the growth of visceral organs in monosodium L-glutamate-treated obese mice.

Sexual Dimorphism in Growth as Measured by Microknemometry: Different Responses to GH Deficiency and Exogenous GH Administration

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