Morphological and cell proliferative study on the growth of visceral organs in monosodium L-glutamate-treated obese mice.
The 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, 2 mg/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 hypoplastic. Moreover, it seems that hypertrophy and hyperplasia of the intestine suggest a possible acceleration of the absorptive function.
D000818:Animals; D001835:Body Weight; D002455:Cell Division; D005971:Glutamates / Q000494:pharmacology; D007031:Hypothalamus / Q000187:drug effects; D007421:Intestine, Small / Q000473:pathology; D008099:Liver / Q000473:pathology; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D008940:Mitotic Index; D009206:Myocardium / Q000473:pathology; D009765:Obesity / Q000139:chemically induced / Q000473:pathology*; D009929:Organ Size; D012970:Sodium Glutamate / Q000494:pharmacology
D005971:Glutamates; D012970:Sodium Glutamate