Effects of Monosodium Glutamate‐induced Obesity in Mice on Carbohydrate Metabolism in Insulin Secretion

Cameron, Donald P.; Cutbush, L.; Opat, F.

doi:10.1111/j.1440-1681.1978.tb00650.x

Cited by 39 publications

(20 citation statements)

References 19 publications

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“…The hyperinsulinemia noted in MSG-treated mice has already been reported both in fasting and ad libitum-fed states at 10 weeks of age [19]. Hyperinsulinemia is considered to be due to a lesion of the ventromedial nucleus which is observed in MSG-treated mice [2].…”

Section: Discussionmentioning

confidence: 99%

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

et al. 1993

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Abstract. Administration of monosodium L-glutamate (MSG) to neonatal mice produces a hypothalamic syndrome consisting of stunted growth and later development of obesity. We assayed plasma insulin (IRI), thyroxine (T4) and insulin-like growth factor-I (IGF-I) to investigate their roles in the growth of the mice. Two mg/g body weight of MSG was injected into newborn male mice daily for five successive days after birth. Plasma IRI levels were increased on and after 8 weeks of age in MSG-treated mice. There was no significant difference between the plasma T4 levels in MSG-treated mice and those in controls at any age studied. In contrast to this, plasma IGF-I levels in MSG-treated mice were reduced at one week and after. These results suggest that a decreased plasma IGF-I level contributes to the retarded linear growth which develops soon after the administration of MSG, and hyperinsulinemia contributes to the later development of obesity in MSG-treated mice.

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Section: Discussionmentioning

confidence: 99%

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

et al. 1993

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“…Furthermore, it is well known that hyperinsulinemia may induce insulin resistance in experimental models of obesity (3). However, from previous data obtained in oral glucose tolerance tests, MSG-obese mice have been considered not to be resistant to insulin (4). Recently, glucose transporters (GLUT4) have been shown to be decreased in insulin-sensitive tissues of MSG-obese mice (5).…”

mentioning

confidence: 99%

“…One day before the test, the animals were anesthetized with pentobarbital (50 mg/kg body weight) and indwelling catheters were inserted into the right jugular vein for glucose infusion and into the right femoral artery for blood sampling. Glucose (0.75 g/kg body weight) was quickly injected and blood samples for insulin and glucose evaluations were drawn 4,8,12,16,20,24, 28 and 32 min after injection. For euglycemic hyperinsulinemic clamp (8 rats per group) a prime continuous (3.0 mU .…”

mentioning

confidence: 99%

Monosodium glutamate (MSG)-obese rats develop glucose intolerance and insulin resistance to peripheral glucose uptake

Hirata¹,

Andrade²,

Vaskevicius³

et al. 1997

Braz J Med Biol Res

105

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Different levels of insulin sensitivity have been described in several animal models of obesity as well as in humans. Monosodium glutamate (MSG)-obese mice were considered not to be insulin resistant from data obtained in oral glucose tolerance tests. To reevaluate insulin resistance by the intravenous glucose tolerance test (IVGTT) and by the clamp technique, newborn male Wistar rats (N = 20) were injected 5 times, every other day, with 4 g/kg MSG (N = 10) or saline (control; N = 10) during the first 10 days of age. At 3 months, the IVGTT was performed by injecting glucose (0.75 g/kg) through the jugular vein into freely moving rats. During euglycemic clamping plasma insulin levels were increased by infusing 3 mU . kg -1 . min -1 of regular insulin until a steady-state plateau was achieved. The basal blood glucose concentration did not differ between the two experimental groups. After the glucose load, increased values of glycemia (P<0.001) in MSG-obese rats occurred at minute 4 and from minute 16 to minute 32. These results indicate impaired glucose tolerance. Basal plasma insulin levels were 39.9 ± 4 µU/ml in control and 66.4 ± 5.3 µU/ml in MSG-obese rats. The mean post-glucose area increase of insulin was 111% higher in MSG-obese than in control rats. When insulinemia was clamped at 102 or 133 µU/ml in control and MSG rats, respectively, the corresponding glucose infusion rate necessary to maintain euglycemia was 17.3 ± 0.8 mg . kg -1 . min -1 for control rats while 2.1 ± 0.3 mg . kg -1 . min -1 was sufficient for MSG-obese rats. The 2-h integrated area for total glucose metabolized, in mg . min . dl -1 , was 13.7 ± 2.3 vs 3.3 ± 0.5 for control and MSG rats, respectively. These data demonstrate that MSG-obese rats develop insulin resistance to peripheral glucose uptake.

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“…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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Effects of Monosodium Glutamate‐induced Obesity in Mice on Carbohydrate Metabolism in Insulin Secretion

Cited by 39 publications

References 19 publications

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

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

Monosodium glutamate (MSG)-obese rats develop glucose intolerance and insulin resistance to peripheral glucose uptake

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

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