High levels of antioxidant enzymatic defence assure good protection against hypoxic stress in spontaneously diabetic rats

2006 ◽  
Vol 38 (12) ◽  
pp. 2196-2208 ◽  
Author(s):  
A. Bonfigli ◽  
S. Colafarina ◽  
S. Falone ◽  
C. Di Giulio ◽  
C. Di Ilio ◽  
...  
Life Sciences ◽  
1994 ◽  
Vol 56 (1) ◽  
pp. PL13-PL18 ◽  
Author(s):  
E. Morabito ◽  
N. Corsico ◽  
E. Arrigoni Martelli

Pancreas ◽  
1990 ◽  
Vol 5 (5) ◽  
pp. 533-539 ◽  
Author(s):  
César L. A. Gómez Dumm ◽  
Maria C. Semino ◽  
Juan Jose Gagliardino

1983 ◽  
Vol 245 (4) ◽  
pp. E379-E383 ◽  
Author(s):  
T. B. Miller

Isolated perfused hearts from control Bio-Breeding/Worcester (BB/W) rats and spontaneously diabetic BB/W rats were studied to determine whether metabolic abnormalities that are expressed in alloxan-diabetic rats in the regulation of enzymes involved in glycogen metabolism could be observed in this non-chemically induced insulin-deficient rat. Perfusion of hearts from control rats with 10(-8) M insulin for 10 min resulted in activation of glycogen synthase (30% synthase I without insulin to 44% synthase I with insulin). Perfusion of hearts from BB/W diabetic rats demonstrated a lack of acute synthase activation with insulin and a 45% decrease in synthase phosphatase activity. Perfusion of hearts from BB/W diabetic rats with 0.28 microM epinephrine for 1 min resulted in a greater activation of phosphorylase (44% phosphorylase a) than that observed in BB/W control hearts (31% phosphorylase a) perfused under the same conditions. Epinephrine produced similar changes in cyclic AMP accumulation, protein kinase activation, and phosphorylase kinase activation in perfused hearts of BB/W control and diabetic rats. Further, phosphorylase phosphatase activities were not changed by epinephrine or insulin deficiency. These studies further document metabolic abnormalities in the BB/W diabetic rat that are attributable to insulin deficiency in a non-chemically induced model for insulin-dependent diabetes.


1986 ◽  
Vol 250 (5) ◽  
pp. E530-E537
Author(s):  
R. Rabkin ◽  
G. M. Reaven ◽  
C. E. Mondon

The in vivo metabolism of insulin is a complex process in which liver, kidney, and muscle are major participants. In this study we evaluated the effect of spontaneous hyperglycemic nonketoacidotic diabetes (DH) and ketoacidotic diabetes (DKA) on insulin clearance and degradation by these organs. Livers, hindlimbs, and kidneys from nondiabetic controls and DH and DKA Bio-Breed rats were isolated and perfused with artificial media. Liver clearance of immunoreactive insulin (ml/min) was significantly higher in DH rats, 6.0 +/- 0.2, but significantly lower in DKA rats, 3.4 +/- 0.5, compared with controls, 4.6 +/- 0.2. Acidosis alone induced by ammonium chloride loading, did not impair liver insulin clearance (4.8 +/- 0.4 ml/min). Muscle responded differently to the diabetic state in that insulin clearance was not altered by DH and DKA. Renal (organ) clearance of insulin was significantly depressed in the DKA state when compared with controls (0.52 +/- 0.04 and 0.75 +/- 0.07 ml X min-1 X g-1, respectively). This could largely be explained by a lower glomerular filtration rate. Fractional urinary insulin clearance was increased twofold above control values in DH kidneys and fourfold in DKA kidneys, indicating that tubular luminal absorption of insulin was impaired in both states. By contrast contraluminal uptake (peritubular clearance) did not differ significantly from controls. 125I-insulin degrading activity of the 100,000 g supernate fraction from muscle homogenates was similar in the diabetic and control groups. However in liver and kidney, degrading activity did not correspond to whole organ insulin clearance in a consistent manner.(ABSTRACT TRUNCATED AT 250 WORDS)


1998 ◽  
Vol 30 (6) ◽  
pp. 333-339 ◽  
Author(s):  
Yasunori Segawa ◽  
Yutaka Shirao ◽  
Sho-ichi Yamagishi ◽  
Tomomi Higashide ◽  
Miho Kobayashi ◽  
...  

2010 ◽  
Vol 28 ◽  
pp. e292-e293 ◽  
Author(s):  
J Radosinska ◽  
B Bacova ◽  
V Dosenko ◽  
H Lin ◽  
I Imanaga ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document