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The ontogenesis of the glucose transporters GLUT-1, GLUT-2, and GLUT-4 and the hexokinases HK-I, HK-II, and HK-IV (glucokinase) was studied in rat tissues. In brown adipose tissue, high levels of GLUT-4 and HK-II were observed during fetal life; both decreased at birth and then increased throughout development. At birth, cold exposure increased GLUT-4 and(More)
Previous studies have shown that glucose increases the glucose transporter (GLUT2) mRNA expression in the liver in vivo and in vitro. Here we report an analysis of the effects of glucose metabolism on GLUT2 gene expression. GLUT2 mRNA accumulation by glucose was not due to stabilization of its transcript but rather was a direct effect on gene transcription.(More)
In vivo studies have shown that insulin resistance in late pregnancy results from a decreased sensitivity of liver and peripheral tissues. In the present study, measurements of the rates of glucose utilization by skeletal muscles (soleus, extensor digitorum longus, epitrochlearis, and diaphragm), white adipose tissue, and brain of virgin and 19-day pregnant(More)
The short term effects of ovine placental lactogen and progesterone have been studied on skeletal muscle glucose metabolism in order to determine their respective roles in pregnancy-induced insulin resistance. The rates of hexose transport, glycogen synthesis, and glycolysis were measured in vitro by incubating stretched soleus, extensor digitorum longus(More)
In diabetes-prone BB rats, 30 to 50% of animals undergo autoimmune destruction of the pancreatic B-cells leading to a short period of glucose intolerance, followed by an abrupt onset of diabetes. We have examined whether the glucose intolerance period and the onset of diabetes are associated with changes in insulin sensitivity, using the euglycaemic(More)
Glucose homoeostasis necessitates the presence in the liver of the high Km glucose transporter GLUT2. In hepatocytes, we and others have demonstrated that glucose stimulates GLUT2 gene expression in vivo and in vitro. This effect is transcriptionally regulated and requires glucose metabolism within the hepatocytes. In this report, we further characterized(More)
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