The induction of obesity in rodents by means of monosodium glutamate

Abstract

I. Monosodium glutamate (MSG) was administered by various methods to mice and rats of various ages and the incidence of obesity was later measured.2. Newborn mice were injected subcutaneously with 3 mg MSG/g body-weight at I, 2 , 3, 6, 7 and 8 d of age: 16% died before weaning. Of the survivors, 90% or more became markedly obese. Mean carcass lipid content was increased by about I Z O~~ in both sexes at 2-30 weeks of age. In male mice, MSG treatment increased body-weight and epididymal fat pad weight, and greatly decreased adrenaline-stimulated lipolysis in isolated fat cells. Body-weight of females was not increased significantly. Food intake was not increased in either sex from weeks 13 to 15. Blood glucose level was not generally increased by MSG but some of the male mice had abnormally high values.3. Obesity was not detected in the offspring of female mice that had received IOO g MSG/kg diet, either from 3 weeks before mating until weaning, or from the 14th day of pregnancy until weaning.4. Intraperitoneal injection of 10 mg MSG/g body-weight (in two doses) at weaning increased carcass lipid content in female mice by 34% by 23 weeks of age, but female rats were not affected.5. The addition of zo g MSG/I to the drinking-water from weaning onwards did not increase carcass lipid content in female rats or mice.6. The addition of 20 g MSG/kg diet from weaning onwards did not alter body-weight or carcass lipid content in male and female rats by 14 weeks of age.7. The obesity induced in mice by MSG was not associated with hyperphagia, unlike genetic obesity and obesity induced by gold thioglucose (GTG).8. All types of mouse studied, obese and lean, had essentially the same linear relationship between carcass water content and carcass lipid content.9. Although MSG-obese mice could not readily be differentiated from normal mice by the increase in body-weight, which was only about 10% compared to 50-120% for genetic and GTG-induced obesity, the proposed schedule of injections in the newborn was almost I O O~~ reliable in inducing a high extent of adiposity.

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

“…In connection with the development of obesity, the balance between energy supply and expenditure should be taken into consideration. In regard to the energy supply, no hyperphagia was demonstrated in the MSG-treated mice (2,3,20). Hyperplasia of the intestine, noted after 8 weeks of age, suggests a possible acceleration of the absorptive function.…”

“…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.…”

Experimental model to induce obesity in rats

“…Therefore, it is responsible, at least in part, for the increase of glucocorticoids found in these adult rats 16,17 . MSG can be administered subcutaneously or intraperitoneally 18,19 at doses that vary by 2-4 mg/g of body weight of the rat during the neonatal period and for periods ranging by 4-10 doses causing obesity [20][21][22][23][24] . Since MSG is a substance found in several foods consumed daily, it has been targeted by studies on its effects when taken orally.…”

Avaliação do crescimento corporal e dos neurônios mioentéricos de ratos Wistar após tratamento neonatal com glutamato monossódico

“…Saline injection did not result in death of any of the group C animals. The early death of the MSG-injected animals was also reported in another investigation (Bunyan et al, 1976) and is routinely observed in other MSG-treated rats of our laboratory. This is probably due to the injection being made at the cervical region, very close to the developing Central Nervous System, and to the natural fragility of the newborn rats.…”