Brown adipose tissue (BAT) has an important role in the thermogenesis of newborn mammals and cold-acclimated rodents. Heat production within the tissue is regulated by the sympathetic nervous system (SNS) via norepinephrine (NE) release. As only little is known of the progressive role of SNS during the developmental period, NE content and turnover were determined in BAT of infant rats 1-33 days of age. The dams and the pups were kept at either 28 or 16 degrees C. It was observed that the NE level in the tissue and the mediator turnover had an almost parallel evolution during the experimental period. In the first week of life, level and turnover of NE were higher in the 28 degrees C group than in the 16 degrees C group. During the second week, the level remained constant in rats kept at 28 degrees C, but the NE turnover slightly decreased. In contrast, a large increase of both parameters was observed in rats kept at 16 degrees C. Then a decrease occurred in both groups until weaning. Subsequently the values remained almost constant. It must be noted that, from the end of the first week, NE content and turnover were always significantly higher in the 16 degrees C group than in the 28 degrees C group. At the end of the first month, the level was 50% higher in cold-acclimated rats and turnover was four times as high as in controls.(ABSTRACT TRUNCATED AT 250 WORDS)
Serum gastrin concentrations were examined following atropinization in 30 patients with liver cirrhosis and in 30 control subjects either basally or after oral glycine load. Basal gastrinaemia and post-glycine serum increases above basal levels were found to be significantly greater in the cirrhotic group (48.56 ± 9.97 and 72.85 ± 10.88 pg/ml, respectively) than in the control group (32.36 ± 6.67 and 53.43 ± 9.67 pg/ml, respectively) (ρ < 0.001). Furthermore, the post-glycine serum gastrin rise appeared to be more prolonged in the cirrhotic group than in the control subjects. The serum gastrin changes in cirrhotics did not appear to be caused by gastric hypoacidity. There was no correlation in cirrhotic patients between the magnitude of the post-glycine serum gastrin rise and the severity of liver insufficiency.
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