scholarly journals The Importance of the Liver in Insulin Replacement Therapy in Insulin-Deficient Diabetes

Diabetes ◽  
2014 ◽  
Vol 63 (5) ◽  
pp. 1445-1447 ◽  
Author(s):  
W. Blair Geho
Keyword(s):  
Replacement Therapy ◽  
Insulin Replacement

Downregulation of the renin-angiotensin system in streptozotocin-diabetic rats

1992 ◽  
Vol 262 (1) ◽  
pp. E105-E109 ◽  
Author(s):  
L. A. Cassis
Keyword(s):  
Adipose Tissue ◽  
Replacement Therapy ◽  
White Adipose Tissue ◽  
Plasma Concentrations ◽  
Renin Angiotensin System ◽  
Diabetic Rats ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Brown Adipose ◽  
Insulin Replacement

To determine if insulin has the ability to regulate components of the renin-angiotensin system, renin and angiotensinogen mRNA and plasma concentrations were determined in 4-wk streptozotocin (STZ)-diabetic rats. In another group of STZ-diabetic rats, replacement insulin therapy was given over the 4-wk period, and the above parameters were examined. In STZ-diabetic rats, there was a significant regression of white adipose tissue that was accompanied by an increase in the yield of RNA obtained. Changes in white adipose tissue were reversed by insulin replacement therapy in STZ-diabetic rats. There were no changes in brown adipose tissue weight or RNA yield in STZ-diabetic rats. Plasma renin activity (PRA) was significantly decreased in STZ-diabetic rats; however, plasma angiotensinogen concentration was not significantly affected by diabetes. PRA was restored to control levels in STZ-diabetic rats with insulin replacement. Kidney renin mRNA as well as liver, epididymal, and interscapular fat angiotensinogen mRNA were significantly decreased in STZ-diabetic rats. Renin and angiotensinogen mRNA were not significantly different from control in all tissues examined in STZ-diabetic rats with insulin replacement therapy. Results from this study suggest a downregulation of the renin-angiotensin system in 4-wk STZ-diabetic rats at the level of mRNA expression that is restored by replacement therapy with insulin; therefore, insulin may directly or indirectly regulate the renin-angiotensin system.

Decreased cardiac output at the onset of diabetes: renal mechanisms and peripheral vasoconstriction

2000 ◽  
Vol 278 (5) ◽  
pp. E917-E924 ◽  
Author(s):  
Michael W. Brands ◽  
Sharyn M. Fitzgerald ◽  
William H. Hewitt ◽  
Allison E. Hailman
Keyword(s):  
Blood Flow ◽  
Type 1 Diabetes ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Replacement Therapy ◽  
Sodium Intake ◽  
Sodium Balance ◽  
Insulin Replacement

Recently we reported that hindquarter blood flow, measured 24 h/day, decreased progressively over the first 6 days of type 1 diabetes in rats. That response, coupled with the tendency of mean arterial pressure to increase, suggested a vasoconstrictor response. The purpose of this study was to measure the changes in cardiac output together with the renal hemodynamic and excretory responses to allow integrative determination of whether vasoconstriction likely accompanies the onset of type 1 diabetes. Rats were instrumented with a Transonic flow probe on the ascending aorta and with artery and vein catheters, and cardiac output and mean arterial pressure were measured continuously, 24 h/day, throughout the study. The induction of diabetes, by withdrawing intravenous insulin-replacement therapy in streptozotocin-treated rats, caused a progressive decrease in cardiac output that was 85 ± 5% of control levels by day 7. This was associated with significant increases in glomerular filtration rate, renal blood flow, and microalbuminuria as well as urinary fluid and sodium losses, with a negative cumulative sodium balance averaging 15.7 ± 1.6 meq by day 7. Restoring insulin-replacement therapy reversed the renal excretory responses but did not correct the negative sodium balance, yet cardiac output returned rapidly to control values. Increasing sodium intake during the diabetic and recovery periods also did not significantly affect the cardiac output response during any period. These results indicate that cardiac output decreases significantly at the onset of type 1 diabetes without glycemic control, and although volume loss may contribute to this response, there also is a component that is not volume or sodium dependent. We suggest this may be due to vasoconstriction, but to what extent local blood flow autoregulation or active vasoconstriction may have mediated that response is not known.

Engineering of a Glucose-Responsive Surrogate Cell for Insulin Replacement Therapy of Experimental Insulin-Dependent Diabetes

2000 ◽  
Vol 11 (3) ◽  
pp. 403-414 ◽  
Author(s):  
Markus Tiedge ◽  
Matthias Elsner ◽  
Neville Hugo McClenaghan ◽  
Hans-Jurgen Hedrich ◽  
Dietrich Grube ◽  
...  
Keyword(s):  
Replacement Therapy ◽  
Insulin Dependent Diabetes ◽  
Insulin Dependent ◽  
Insulin Replacement

scholarly journals Histological Study on The effect of Diabetes and Insulin Replacement Therapy on The prostate of Albino Rats

2021 ◽  
Vol 2 (2) ◽  
pp. 203-226
Author(s):  
Mohammed Ahmed Abd-El Hafez ◽  
Safinaz Salah El-Din Sayed ◽  
Dalia Hussein Abd El Azize ◽  
Amira Shaban Gaeidy Rashwan
Keyword(s):  
Replacement Therapy ◽  
Histological Study ◽  
Albino Rats ◽  
Insulin Replacement

529-P: Insulin Replacement Therapy Does Not Fully Prevent Peripheral Neuropathy in Type 1 Diabetic Mice

Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 529-P
Author(s):  
STEPHANIE EID ◽  
LUCY M. HINDER ◽  
JOHN M. HAYES ◽  
FAYE MENDELSON ◽  
EVA L. FELDMAN
Keyword(s):  
Peripheral Neuropathy ◽  
Replacement Therapy ◽  
Diabetic Mice ◽  
Insulin Replacement
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