Insulin treatment improves the spontaneous remission of neonatal streptozotocin diabetes in the rat

Diabetes ◽  
1982 ◽  
Vol 31 (2) ◽  
pp. 165-169 ◽  
Author(s):  
B. Portha ◽  
L. Picon
1996 ◽  
Vol 116 (1) ◽  
pp. 67-71 ◽  
Author(s):  
Süleyman Aydin ◽  
Yusuf Öztürk ◽  
V.Melih Altan ◽  
Nuray Yildizoğlu-Ari ◽  
A.Tanju Özçelikay

1981 ◽  
Vol 241 (2) ◽  
pp. E129-E135 ◽  
Author(s):  
W. D. McCumbee ◽  
H. E. Lebovitz

Diabetes and malnutrition result in decreased somatomedin production and cartilage growth in rats. The growth and metabolism of the Swarm rat chondrosarcoma are dramatically affected by somatomedins. Data presented here show that streptozotocin diabetes and diet restriction inhibit in vivo chondrosarcoma growth. Tumors grown in diabetic rats were significantly smaller than tumors grown in diet-restricted rats showing the same changes in body weight. Insulin treatment increased the rate of tumor growth in diabetic rats. Tumors grown in rigidly controlled diabetic rats were as large as tumors grown in nondiabetic controls. Diet restriction and diabetes reduced the capacity of the serum of the rat to stimulate alpha-amino[14C]isobutyrate uptake and [3H]uridine incorporation into RNA in chondrosarcoma pieces grown in nondiabetic rats. This somatomedin activity of the serum was restored by treating diabetic rats with insulin. There was a significant correlation between the in vitro stimulatory effect of a particular serum pool on chondrosarcoma metabolism and in vivo chondrosarcoma growth in the animals from whom the serum was obtained. These studies demonstrate that the in vivo growth of malignant chondrocytes is similar to that of normal chondrocytes with respect to the role of nutrition and insulin.


1988 ◽  
Vol 249 (2) ◽  
pp. 415-421 ◽  
Author(s):  
Z Jamal ◽  
E D Saggerson

1. Adipocytes were isolated from the interscapular brown fat of male rats maintained at 21 degrees C. These animals were controls, streptozotocin-diabetics or 2-day insulin-treated diabetics. 2. With adipocytes from diabetic animals, maximum rates of noradrenaline-stimulated O2 uptake were decreased by 58%, and the Bmax. of [3H]GDP binding to mitochondria was decreased by 55%. Insulin administration reversed both of these changes. 3. Streptozotocin-diabetes increased basal lipolysis in adipocytes incubated with adenosine deaminase (1 unit/ml), decreased the EC50 (concn. giving 50% of maximum effect) for noradrenaline, but did not change the maximum rate of noradrenaline-stimulated lipolysis. Except for some small differences at very low concentrations (10-100 pM), diabetes or insulin treatment did not alter the sensitivity of noradrenaline-stimulated lipolysis or O2 uptake to the inhibitory effect of N6-phenylisopropyladenosine. It is therefore concluded that the lesion(s) in thermogenesis in diabetes are not attributable to any changes in lipolysis. 4. Blood flow through interscapular brown fat, measured by accumulation of [14C]DDT [14C-labelled 1,1,1-trichloro-2,2-bis-(p-chlorophenyl)ethane] was increased by 2.3-fold 70 min after a single administration of insulin to diabetic rats. This treatment decreased blood flow through epididymal white fat by 58%. 5. Propranolol treatment of diabetic rats muted the ability of insulin treatment to increase the maximum rate of noradrenaline-stimulated O2 uptake, suggesting that this action of insulin may be a secondary one rather than a direct effect of the hormone on the adipocytes.


1987 ◽  
Vol 243 (1) ◽  
pp. 289-292 ◽  
Author(s):  
E D Saggerson ◽  
C A Carpenter

At 2 days after administration of streptozotocin (100 mg/kg), activities in rat epididymal fat-pads of the following enzymes were significantly decreased: fatty acyl-CoA synthetase (FAS), mitochondrial and microsomal forms of glycerolphosphate acyltransferase (GPAT), monoacylglycerolphosphate acyltransferase (MGPAT) and Mg2+-dependent phosphatidate phosphohydrolase (PPH). There were no significant changes in diacylglycerol acyltransferase or Mg2+-independent PPH. Insulin administration to diabetic rats over 2 days restored activities of FAS, both forms of GPAT, MGPAT and Mg2+-dependent PPH. Significant restoration of all five activities was also seen 2 h after a single administration of insulin, but was not observed 45 min after insulin treatment. Insulin significantly increased all five enzyme activities when adipocytes from diabetic rats were incubated for 2 h with a mixture of glucose, lactate, pyruvate and amino acids.


1952 ◽  
Vol 98 (411) ◽  
pp. 287-293 ◽  
Author(s):  
F. Mackenzie Shattock ◽  
Lorna P. Micklem

Somatic disturbances in schizophrenia include metabolic, circulatory and endocrine changes frequently associated with disorders of the pituitary gland and adrenal cortex. Depression of the metabolic rate is often severe (Hoskins, 1932), the systolic blood-pressure is sometimes as low as 80 mm. Hg (Hoskins, 1934; Rheingold, 1939; Shattock, 1950), and the pulse pressure only a few millimetres. Peripheral vascular deficiency and atrophy of the tissues (Bleuler, 1920; Mapother, 1924; Minski, 1937; Shattock, 1950), asthenia and various cutaneous changes are common; amenorrhoea is almost the rule.It is remarkable that these disturbances are reversible, and that they are relieved or greatly alleviated during mental remission. Physical health is restored during a spontaneous remission, and a gradual improvement can be observed during a course of insulin comas. Sometimes a dramatic recovery follows electroconvulsion when this initiates a mental remission; somatic improvement is then rapid and the vascular deficiency may be relieved within a few hours (Shattock, 1950). Unfortunately these remissions are often brief, and as relapses become more frequent after repeated treatment, physical and mental deterioration may be noticeable a few days after the initial improvement. The point of interest is a concordance of physical and mental changes, and not the therapeutic value of E.C.T. used as an adjunct to insulin treatment or as a means of moderating extreme restlessness in chronic patients.


1981 ◽  
Vol 98 (3) ◽  
pp. 432-436 ◽  
Author(s):  
T. T. Andreassen ◽  
K. Seyer-Hansen ◽  
H. Oxlund

Abstract. The biomechanical properties of skin and aorta were studied in rats with experimental (streptozotocin) diabetes. After 30 days of diabetes the collagen content of the skin was diminished by 30%. By biomechanical testing collagen from diabetic rats was found to exhibit increased stiffness and strength: maximal stiffness was increased by 20% and the strain at maximum stress was decreased by 10%. Insulin treatment prevented all changes. No differences were found between aortic specimens from diabetic and normal rats.


1980 ◽  
Vol 239 (3) ◽  
pp. E215-E222 ◽  
Author(s):  
M. E. May ◽  
V. J. Mancusi ◽  
R. P. Aftring ◽  
M. G. Buse

Oxidative decarboxylation is the first irreversible step in the degradation of leucine. The effect of streptozotocin diabetes on this reaction was studied in cell-free rat liver preparations, using [1-14C]alpha-ketoisocaproate as substrate. Diabetes increased the branched-chain ketoacid dehydrogenase (BCKD) activity (per g liver or per mg protein) of homogenates, but the ratios of homogenate BCKD activity to other mitochondrial markers remained unchanged. A cytosolic branched-chain ketoacid decarboxylase activity (15-22% of homogenate activity), which did not require NAD, CoA, or NADP, was also increased in diabetics. Insulin treatment of diabetics normalized enzyme activity in all fractions. The apparent Km of BCKD in homogenates was 43-45 microM; diabetes increased the apparent Vmax from 165 nmol x min-1 x g tissue-1 to 260 nmol x min-1 x g-1. In contrast, the Km for cytosolic alpha-ketoisocaproate decarboxylation was 270 microM in controls, and diabetes resulted in both a lower Km (210 microM) and a higher Vmax. Adrenalectomy did not affect activity in homogenates from controls, but partially reversed the diabetes-associated increase. Glucagon pretreatment of controls did not affect activity. In summary, distinct mitochondrial and cytosolic enzymes decarboxylate alpha-ketoisocaproate in liver. The increased hepatic capacity of diabetic rats to degrade the carbon skeleton of leucine is attributed mainly to a relative increase in mitochondrial mass.


Sign in / Sign up

Export Citation Format

Share Document