Hypothalamic lesion induced by injection of monosodium glutamate in suckling period and subsequent development of obesity

Kazuhiko, Tanaka; Shimada, Morimi; Nakao, Koji; Kusunoki, Tomoichi

doi:10.1016/0014-4886(78)90050-x

Cited by 62 publications

(45 citation statements)

References 19 publications

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“…This ®nding also agrees with the fact that mice neonatally injected with MSG do not become obese until puberty. 4 Decreased body weight in these animals may be associated to decreased growth hormone (GH) levels, which was previously found in 30 day old MSG-treated rats. 38,39 Decreased plasma levels of both NEFA and glycerol as well as decreased adipose tissue lipolysis and HSL activity found in our MSG-treated rats also support such decreased GH levels, since these changes have been reported to occur in GH de®cient conditions in adults.…”

Section: Discussionmentioning

confidence: 82%

“…The incubation was stopped by placing the vials on ice. Aliquots of the media were placed in 10% HClO 4 in the cold and supernatants were neutralized with saturated KHCO 3 to measure glycerol. 23 Other aliquots of the medium were used to measure NEFA.…”

Section: Lipid Carcass Contentmentioning

confidence: 99%

“…Neonatal administration of monosodium glutamate (MSG) to rodents destroys 80 ± 90% of the arcuate nuclei neurons 1,2 and injures other central structures 3 resulting in several neuroendocrine and metabolic abnormalities, including arrested growth and obesity. 3,4 Unlike obesity induced by gold thioglucose or bipiperidyl mustard which are associated with hyperphagia, obesity in neonatal MSG-treated rodents, is not a result of overeating. In mice, MSG obesity is associated with a doubling of metabolic ef®ciency, 5 secondary to the high level of corticosterone.…”

Section: Introductionmentioning

confidence: 99%

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Decreased lipolysis and enhanced glycerol and glucose utilization by adipose tissue prior to development of obesity in monosodium glutamate (MSG) treated-rats

et al. 2001

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OBJECTIVE:To determine the metabolic alterations that lead to the neonatal administration of monosodium glutamate (MSG), which results in arrested growth and obesity. ANIMALS AND DESIGN: Wistar rats were injected 5 times, every other day, with 4 g of MSGakg b.w. or with hyperosmotic saline (controls), within the ®rst 10 days of life, and were studied at the age of 30 days. RESULTS: Body weight was lower, whereas adipocyte lipid content, cell diameter, surface area and volume were higher in MSG rats than in controls. Plasma glucose, insulin, NEFA, glycerol and triglyceride levels, and in vitro production of NEFA by lumbar fat pad pieces incubated under basal conditions or in the presence of epinephrine and epinephrine plus glucose in the media were lower in MSG than in control rats. In the same fat pad pieces, the conversion of 1-14 C-glycerol into fatty acids was always enhanced and its conversion into glyceride glycerol was enhanced when incubations were carried out in the presence of epinephrine or glucose. Both the hormone sensitive lipase activity and mRNA expression were lower in adipose tissue from MSG rats. Besides, the number of insulin receptors, lipid synthesis from U 14 C glucose, 3 H-2-deoxy D-glucose uptake and cellular GLUT4 translocation index were higher in adipocytes from MSG rats than from the controls. CONCLUSION: It is proposed that an enhanced insulin sensitivity in 1 month old MSG rats is responsible for the decreased lipolytic activity and enhanced glucose uptake. In addition, the enhanced lipogenesis and glycerol reutilization seen in their adipose tissue, disturbs the normal balance between fat depots breakdown and accumulation in favor of the latter.

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Section: Discussionmentioning

confidence: 82%

Section: Lipid Carcass Contentmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Decreased lipolysis and enhanced glycerol and glucose utilization by adipose tissue prior to development of obesity in monosodium glutamate (MSG) treated-rats

et al. 2001

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“…MSG treatment in infant animals was reported to produce a few acute toxic effects such as an irreversible neuronal degeneration in the inner retina (12)(13)(14)(15) and hypothalamus (1,3,16), transiently depressed extramedullary hematopoiesis (17), and a slight vacuolar change in the hepatocytes (17). No degenerative change as a result of direct toxicity has yet been described in other organs by light microscopy.…”

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: 97%

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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Animal Models of Obesity

York

2003

International Textbook of Diabetes Mellitus

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Animal models have played an important role in advancing our understanding of the causes and consequences of obesity. The spontaneous single gene mutations led to the discovery of leptin and the melanocortin signaling pathways and were important to the understanding of hypothalamic systems that control energy balance. The use of transgenic and gene targeting technologies has opened a new era of investigation, identifying new genes that regulate the development or prevention of obesity and providing the tools for proof of function of genes. These studies have shown that a wide range of genes expressed primarily in the central nervous system or in adipose tissue are potential targets for the treatment of obesity.

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Hypothalamic lesion induced by injection of monosodium glutamate in suckling period and subsequent development of obesity

Cited by 62 publications

References 19 publications

Decreased lipolysis and enhanced glycerol and glucose utilization by adipose tissue prior to development of obesity in monosodium glutamate (MSG) treated-rats

Decreased lipolysis and enhanced glycerol and glucose utilization by adipose tissue prior to development of obesity in monosodium glutamate (MSG) treated-rats

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

Animal Models of Obesity

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