Endothelins urinary excretion is increased in spontaneously diabetic rats: BB/BB

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.

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Insulin metabolism by liver, muscle, and kidneys from spontaneously diabetic rats

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1986.250.5.e530 ◽

1986 ◽

Vol 250 (5) ◽

pp. E530-E537

Author(s):

R. Rabkin ◽

G. M. Reaven ◽

C. E. Mondon

Keyword(s):

Diabetic Rats ◽

Insulin Clearance ◽

Immunoreactive Insulin ◽

Insulin Metabolism ◽

Complex Process ◽

Consistent Manner ◽

Liver And Kidney ◽

Spontaneously Diabetic Rats ◽

And Control

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)

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Improving Metabolic Control Reverses the Histomorphometric and Biomechanical Abnormalities of an Experimentally Induced Bone Defect in Spontaneously Diabetic Rats

Calcified Tissue International ◽

10.1007/s00223-003-0069-6 ◽

2004 ◽

Vol 74 (6) ◽

pp. 551-560 ◽

Cited By ~ 30

Author(s):

N. Follak ◽

I. Kl�ting ◽

E. Wolf ◽

H. Merk

Keyword(s):

Metabolic Control ◽

Bone Defect ◽

Diabetic Rats ◽

Spontaneously Diabetic Rats ◽

Experimentally Induced

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Urinary excretion of nicotinamide and its metabolites in alloxan-diabetic rats fed on a niacin-free diet.

Agricultural and Biological Chemistry ◽

10.1271/bbb1961.53.3353 ◽

1989 ◽

Vol 53 (12) ◽

pp. 3353-3354 ◽

Cited By ~ 3

Author(s):

Katsumi SHIBATA ◽

Mayumi MORITA ◽

Hiroko MATSUO

Keyword(s):

Urinary Excretion ◽

Diabetic Rats

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THYROXINE METABOLISM IN DIABETIC RATS

Acta Endocrinologica ◽

10.1530/acta.0.0860336 ◽

1977 ◽

Vol 86 (2) ◽

pp. 336-343 ◽

Cited By ~ 6

Author(s):

A. A. Zaninovich ◽

T. J. Brown ◽

R. Boado ◽

N. R. Bromage ◽

A. J. Matty

Keyword(s):

Body Weight ◽

Urinary Excretion ◽

Least Squares Method ◽

Intraperitoneal Administration ◽

Binding Activity ◽

Diabetic Rats ◽

Control Group ◽

Metabolic Clearance ◽

Distribution Space

ABSTRACT The metabolism of thyroxine (T4) was determined in untreated and in insulin-treated diabetic rats. The results were compared with those obtained in a control group. Male Wistar rats weighing approximately 200 g were made diabetic by the intraperitoneal administration of streptozotocin (6.5 mg/100 g body weight) and 17 of those with blood sugar levels above 500 mg/100 ml were studied. In addition, 11 insulin-treated diabetic and 18 control rats were investigated. All the animals were injected intravenously with a tracer dose of [125I]T4 (1 μCi and 0.015 μg). After this blood samples were obtained by cardiac puncture at 16, 24, 40 and 48 h. The 24-h urinary excretion of inorganic 125iodide was also determined. The parameters of T4 metabolism were obtained by the least squares method and by an extrapolation technique. In untreated diabetic rats the fractional T4 turnover was 4.4%h, the distribution space 36.7 ml/100 g body weight, metabolic clearance 1.57 ml/100 g/h and urinary clearance 0.33 ml/100 g/h. The 24-h urinary excretion of 125iodide was 21.3 % of the injected radioactivity. Of these values the distribution space (P < 0.001) and metabolic clearance (P < 0.05) were significantly increased above those in the control animals. In insulin-treated rats all parameters were within normal values. Among these groups the serum T4 concentration was measured in 6 control, 5 untreated diabetic and 6 insulin-treated animals. The untreated diabetic animals had a significantly decreased serum T4 level but this was balanced by an enlarged distribution space so that the final hormone degradation was normal. In addition, the T4 binding activity of serum was assessed by the in vitro red cells uptake of [125I] T4 and by determining the proportion of serum free T4. Both these indices indicated a decrease in serum binding activity in the diabetic animals. The data suggest that the fall in serum T4 levels observed in the untreated diabetic rats was the result of decreased plasma binding of T4 and an increase in distribution space precipitated by lack of insulin.

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