Effect of fasting and refeeding on duodenal alkaline phosphatase activity in monosodium glutamate obese rats.
In the present work the effects of fasting and refeeding on fat pad weight and alkaline phosphatase activity in the brush border of individual duodenal enterocytes have been evaluated in male Wistar rats with obesity induced by monosodium glutamate (MSG) treatment during the early postnatal period. Neonatal rats were treated subcutaneously with MSG (2 mg/g b.w.) or saline (controls) for 4 days after birth. At 4 months of age, two types of experiments were performed. In the first experiment rats, were submitted to 3 or 6 days lasting food deprivation. In the second experiment the rats were refed for 3 or 6 days ad libitum or restrictedly (60% of pre-fasting intake) after a 6 day-fasting period. Fasting and refeeding influenced the body fat and function of the duodenum in MSG-treated rats differently as compared to the controls. However, alkaline phosphatase activity and the weight of epididymal and retroperitoneal fat depots were significantly increased in MSG obese rats (P<0.001) during all the periods examined. While 3 days of food deprivation resulted in both groups in a similar loss of adipose tissue weight and alkaline phosphatase activity, the decrements of these parameters after 6 days of fasting were lower in obese rats suggesting that their capacity to spare body fat stores was enhanced. After 3 days of ad libitum refeeding, a more marked adaptational increase of food consumption and also a significantly increased alkaline phosphatase activity above the pre-fasting level (P<0.01) was observed in the MSG-treated rats. Consequently, a more rapid body fat restoration was demonstrated in these animals. Refeeding of rats at 60% of the pre-fasting intake level resulted in a significant increase of alkaline phosphatase activity in both the MSG and control group; moreover, as food restriction continued, MSG-treated rats tended to further increase the enzyme activity. Our results revealed that MSG treatment of neonatal rats may significantly change the intestinal functions. Permanently increased alkaline phosphatase activity observed in MSG obese rats during all investigated periods suggests that this functional alteration is probably not a consequence of actual nutritional variation but could be a component of regulatory mechanisms maintaining their obesity at critical values.
Racek
L
L
Institute ofAnimal Physiology, Slovak Academy of Sciences, Kosice, Slovak Republic.
Lenhardt
L
L
Mozes
S
S
D000273:Adipose Tissue / Q000033:anatomy & histology; D000469:Alkaline Phosphatase / Q000378:metabolism*; D000818:Animals; D000831:Animals, Newborn; D004386:Duodenum / Q000166:cytology / Q000201:enzymology*; D004435:Eating / Q000502:physiology*; D020895:Enterocytes / Q000201:enzymology; D005215:Fasting / Q000502:physiology*; D005260:Female; D005503:Food Additives; D008297:Male; D009765:Obesity / Q000139:chemically induced / Q000378:metabolism*; D009929:Organ Size; D051381:Rats; D017208:Rats, Wistar; D012970:Sodium Glutamate
D005503:Food Additives; D000469:Alkaline Phosphatase; D012970:Sodium Glutamate