Growth, endocrinological and behavioral deficits after monosodium l-glutamate in the neonatal rat: possible involvement of arcuate dopamine neuron damage

Nemeroff, Charles B.; Grant, Lester D.; Bissette, Garth; Ervin, Gregory N.; Harrell, Lindy E.; Prange, Arthur J.

doi:10.1016/0306-4530(77)90023-3

Cited by 110 publications

(62 citation statements)

References 44 publications

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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%

“…Energy expenditure includes basal metabolism, diet-induced thermogenesis and physical activity. It was reported that the MSG-treated mice had lower spontaneous activity after 30 days of age (5,20) and that the growth hormone (6-8) and thyroid hormone (5-9), which affect energy expenditure including basal metabolism, were also reduced in the blood. In addition to these findings, we have confirmed that most of the important organs with major physiological functions became hypoplastic in the MSG-treated mice.…”

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. …”

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confidence: 99%

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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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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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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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“…Monosodium L-glutamate (MSG) administration in neonatal rats is recognized to mainly damage hypothalamic arcuate nucleus (ARC) neurons. [1][2][3] MSG-induced partial hypothalamic denervation alters several neuroendocrine-metabolic functions. It has been proposed that early loss of hypothalamic neurotransmitters induced by MSG, namely in the ARC, 1,4,5 is responsible for such abnormalities.…”

Section: Introductionmentioning

confidence: 99%

Impact of transient correction of increased adrenocortical activity in hypothalamo-damaged, hyperadipose female rats

et al. 2005

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Objective: To explore the effects of transient correction of enhanced corticoadrenal activity in monosodium L-glutamate (MSG)-damaged female rats on peripheral insulin sensitivity and in vitro retroperitoneal (RP) adipocyte function. Designs: A dose of 4 mg/g body weight (BW) of MSG or vehicle (CTR) was i.p. injected, once every 2 days, between days 2 and 10 of age, in female rats. Intact and 21 day-operated (sham or adrenal enucleation (AE)) rats from both (CTR and MSG) groups were used for experimentation on day 120 of age. Circulating levels of several hormones, in basal and after i.v. high-glucose load conditions, and RP adiposity morphology and function were then evaluated. Results: MSG rats developed increased adrenocortical function, hyperadiposity, hyperleptinemia, hyperinsulinemia and decreased peripheral insulin sensitivity. These characteristics were fully reversed after transient correction of corticoadrenal hyperactivity induced by AE. In addition, in vitro experimentation with isolated RP adipocytes indicated that cells from intact MSG animals displayed decreased sensitivity to insulin and dexamethasone stimulation of leptin secretion. Interestingly, adipocyte dysfunction in MSG rats was fully abrogated after AE-induced transient correction of insulinemia, leptinemia and adrenocortical activity. Importantly, the reversion of these metabolic abnormalities, induced by AE for 21 days, in MSG animals did occur, despite no significant changes in BW values. Conclusion: Our results support that the changes in adipocyte characteristics and peripheral insulin resistance, developed in this pseudo-obese female rat model, are mainly due to increased glucocorticoid production. Importantly, appropriate correction of the enhanced adrenocortical activity fully reversed these abnormal functions.

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“…On the other hand, intraperitoneal administration of monosodium glutamate (MSG) to rats in the neonatal stage destroys the VMH and ARC in the hypothalamus, producing neonatally MSG-treated obese (MSG-OB) rats whose sympathetic nerve activity decreases with growth [10,34,45,46]. Hypothalamic obesity animal models may thus be easily prepared through destruction of the VMH by systemic administration of MSG.…”

Section: Introductionmentioning

confidence: 99%

Effects of Chronic Administration of Sibutramine on Body Weight, Food Intake and Motor Activity in Neonatally Monosodium Glutamate-Treated Obese Female Rats: Relationship of Antiobesity Effect with Monoamines

et al. 2000

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When the hypothalamic ventromedial nucleus and arcuate nucleus were destroyed in rats by treatment with monosodium glutamate in the neonatal stage, increase in the Lee index (body weight 1/3 /body length) and in retroperitoneal fat as well as decreases in spontaneous motor activity, food consumption and growth hormone secretion function associated with hypothalamic low body length obesity (monosodium glutamatetreated obesity; MSG-OB) were observed as these rats grew. Treatment with sibutramine at 3 and 10 mg/kg p.o. once a day continuously for 14 days improved these parameters, and the degree of improvement was dose related. The plasma lipid values in MSG-OB rats, which were the same as those in normal rats, were decreased by consecutive administration of sibutramine. Levels of hypothalamic monoamines (MAs) such as norepinephrine, 5-HT (serotonin) and dopamine and their metabolites DOPAC, HVA and 5-HIAA were decreased in MSG-OB rats, and further decrease in them, though slight, was observed with consecutive daily administration of sibutramine, probably as a result of the feedback attributable to an increase in MA in synapses caused by inhibition of MA uptake by sibutramine. These results suggest that sibutramine can activate the MA nervous system by MA uptake inhibition in regions of the brain such as the lateral hypothalamic area and the paraventricular nucleus, which control food intake and sympathetic nerve activity, and the nigrostriatal area related to the extrapyramidal motor system, and thereby exhibit anti-obesity effects in the MSG-OB rat.

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Growth, endocrinological and behavioral deficits after monosodium l-glutamate in the neonatal rat: possible involvement of arcuate dopamine neuron damage

Cited by 110 publications

References 44 publications

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

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

Impact of transient correction of increased adrenocortical activity in hypothalamo-damaged, hyperadipose female rats

Effects of Chronic Administration of Sibutramine on Body Weight, Food Intake and Motor Activity in Neonatally Monosodium Glutamate-Treated Obese Female Rats: Relationship of Antiobesity Effect with Monoamines

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