Glucose metabolism in jejunal mucosa of fed, fasted, and streptozotocin-diabetic rats

1974 ◽  
Vol 226 (1) ◽  
pp. 226-229 ◽  
Author(s):  
JW Anderson
2014 ◽  
Vol 737 ◽  
pp. 91-96 ◽  
Author(s):  
Michael Feigh ◽  
Sara T. Hjuler ◽  
Kim V. Andreassen ◽  
Sofie Gydesen ◽  
Ida Ottosen ◽  
...  

1986 ◽  
Vol 18 (06) ◽  
pp. 361-364 ◽  
Author(s):  
Y. Okuda ◽  
K. Kawai ◽  
Y. Chiba ◽  
Y. Koide ◽  
K. Yamashita

1981 ◽  
Vol 241 (3) ◽  
pp. E238-E245 ◽  
Author(s):  
M. A. McNurlan ◽  
P. J. Garlick

Protein synthesis (as a percent of the protein pool synthesized per day) has been measured in liver and small intestine of young male rats from the incorporation of 100 mumol [1–14C]leucine/100 g body wt into protein over 10 min. Dietary protein deprivation for 8 days depressed protein synthesis in liver (30%), jejunal mucosa (20%), and jejunal serosa (25%). In serosa, reduced levels of RNA relative to protein could account for altered synthesis; in liver and mucosa, the amount of protein synthesized per unit RNA was reduced. In liver of streptozotocin-diabetic rats protein synthesis was depressed 45%, whereas it was maintained in jejunal mucosa and serosa. Depressed synthesis in liver was accompanied by both a loss of RNA relative to protein and a reduction in the protein synthesized per RNA.


1978 ◽  
Vol 235 (2) ◽  
pp. E175
Author(s):  
M Kasuga ◽  
Y Akanuma ◽  
Y Iwamoto ◽  
K Kosaka

To investigate the mechanism of the cellular insulin insensitivity of diabetic rats, insulin binding, glucose transport, and glucose oxidation were studied in adipocytes from streptozotocin-diabetic rats. Increased insulin binding was found in cells from diabetic rats, and this was due to an increased number of insulin receptors rather than a change in receptor affinity. Basal and insulin-stimulated glucose oxidation was decreased in adipocytes from diabetic rats when the data are expressed in absolute terms or as percent increased above basal. Although the absolute rate of basal and insulin-stimulated glucose transport was decreased in adipocytes from diabetic rats, the percent increase above basal of insulin-stimulated glucose transport was not decreased. In conclusion, although the cellular insulin insensitivity exists in adipocytes from diabetic rats, the number of insulin receptors was increased, coupling between insulin receptors and the glucose transport system is intact in adipocytes from diabetic rats, and a defect in intracellular glucose metabolism rather than glucose transport plays a major role in the insulin insensitivity of adipocytes from diabetic rats.


2007 ◽  
Vol 572 (2-3) ◽  
pp. 213-219 ◽  
Author(s):  
Yanfen Niu ◽  
Weiping Liu ◽  
Changfu Tian ◽  
Mingjin Xie ◽  
Lihui Gao ◽  
...  

1992 ◽  
Vol 70 (11) ◽  
pp. 1468-1472 ◽  
Author(s):  
Soter Dai ◽  
Heather Fraser ◽  
John H. McNeill

A previous study in our laboratory showed that streptozotocin (STZ) induced diabetic, deoxycorticosterone acetate (DOCA) induced hypertensive rats exhibited significantly lower levels of plasma glucose than did normotensive diabetic animals. The present experiments further investigate the effects of DOCA treatment on fasting levels of plasma glucose and insulin and on their changes after oral glucose challenge in nondiabetic and STZ-diabetic rats. It was found that, in nondiabetic rats, DOCA-induced hypertension was associated with normal glucose levels and glucose tolerance but with significantly lower levels of plasma insulin. DOCA-treated diabetic animals showed significantly lower levels of plasma glucose, but their plasma insulin concentrations were not significantly different from those of the DOCA vehicle treated diabetic rats. DOCA-treated diabetic rats also had significantly higher plasma levels of cholesterol and triglycerides. It is suggested that DOCA may have a direct or indirect action on the assimilation, production, or utilization of glucose, perhaps leading to an improvement in insulin sensitivity and subsequently a decrease in insulin secretion.Key words: glucose metabolism, insulin, deoxycorticosterone acetate, streptozotocin.


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