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1.
Kingston; s.n; 1986. 77 p. tab.
Tese em Inglês | MedCarib | ID: med-13656

RESUMO

The erythrocytes of malnourished animals bound less insulin than controls (6.4 percent vs. 17 percent respectively, p<0.01 at 10 days post weaning pw). In the later stages of malnutrition (20 days pw) insulin binding was significantly less than in the early stage (5 days pw).(2.7 percent vs. 14.7percent, p<0.01 respectively). The decreased binding was also reflected in decreased receptor affinity in the malnourished compared to the control (0.54 K x 10 8/M vs. 1.4 K x 10 8/M, p<0.01 at 10 days pw). There was no significant difference between the number of receptors in malnourished and control states. The malnourished animals became insulin resistant, as suggested by a diminished glucose tolerance and a lowered insulin to glcose ratio. Insulin release was also impaired with the malnourished having a lowered plasma insulin concentration compared to the control of the same age (8 æU/ml vs. 15.3 æU/ml, p<0.05; 10 days pw). As physiological development proceeded from zero to twenty days post-weaning, the total binding (Bo) and the affinity decreased in both the malnourished and the control. This decrease was steeper in the malnourished than the control suggesting that the effects of the age on insulin receptor characteristics are exacerbated by malnutrition. In the control but not in the malnourished, the number of receptors decreased as development proceeded. In the control animals, the plasma insulin levels increased with age from 8.1 æU/ml at weaning to 27.5 æU/ml (p<0.05). While the increase in plasma insulin values shown by the malnourished was not statistically different (10.34 æU/ml, 20 days pw). There was an inverse relationship between plasma insulin levels and insulin binding as the control animals increased in age (AU)


Assuntos
Ratos , Desnutrição Proteico-Calórica , Eritrócitos , Fatores Etários , Teste de Tolerância a Glucose , Receptor de Insulina/metabolismo , Fracionamento Celular
2.
Biochem J ; 123(1): 35-9, 1971.
Artigo em Inglês | MedCarib | ID: med-12143

RESUMO

A method for the assay of phosphoenolpyruvate carboxykinase is presented, based on the enzymic determination of the phosphoenolpyruvate produced by the enzyme reaction. The subcellular distribution of phosphoenolpyruvate carboxykinase in the kidney of several animal species resembled the distribution in the liver. The rise in enzyme activity in the kidney cortex of rats made acidotic by feeding with ammonium chloride was not prevented by the administration of ethionine or actinomycin. The possibility is suggested that in the kidney acidosis causes activation of an inactive form of the enzyme already present. (AU)


Assuntos
Humanos , Cães , Cobaias , Coelhos , Ratos , 21003 , Acidose/enzimologia , Carboxiliases/análise , Rim/enzimologia , Acidose/induzido quimicamente , Cloreto de Amônio , Fracionamento Celular , Citoplasma/enzimologia , Dactinomicina/farmacocinética , Ativação Enzimática , Etionina/farmacocinética , Rim/efeitos dos fármacos , Mitocôndrias/enzimologia , Fosfoenolpiruvato/metabolismo , Ultracentrifugação
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