Inhibition of carnitine palmitoyltransferase 1 by phenylalkyloxiranecarboxylic acid and its influence on lipolysis and glucose metabolism in isolated, perfused hearts of streptozotocin-diabetic rats

Hepatic carnitine palmitoyltransferase (CPT) turnover was studied in control and in non-ketotic hyperglycaemic streptozotocin-diabetic rats. The degradation constant (kd) and half-life (t1/2) did not appear to be altered by mild diabetes. The hepatic CPT (micrograms/g of liver) was not increased by the mild, non-ketotic, diabetes. However, the total hepatic CPT (micrograms/liver) was 37% greater in the diabetic animals, owing to the increased liver weight. This resulted from a 40% increase in the synthesis constant (ks). Hepatic CPT activity (total detergent-solubilized) and translation rates were measured in fed, starved (48 h), non-ketotic diabetic, ketotic diabetic and diethylhexyl phthalate (DEHP)-treated rats. CPT activity (m units/mg of mitochondrial protein) was not significantly increased with non-ketotic diabetes (44% increase, but non-significant), but was increased approx. 2-fold with starvation and ketotic diabetes, and 3.5-fold with DEHP treatment. CPT expressed as units/liver was increased non-significantly (23%) in non-ketotic and starved rats, similar to the turnover study, but was significantly increased with ketotic diabetes and with DEHP treatment. mRNA-translation activity for CPT was elevated in all states to a somewhat greater extent than was activity. It was concluded that protein synthesis as a product of increased CPT-mRNA translation activity is a major means of long-term regulation.

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The role of endogenous catecholamines and prostaglandins in the maintenance of coronary flow in isolated, perfused hearts of control, fasted and streptozotocin-diabetic rats

Journal of Molecular and Cellular Cardiology ◽

10.1016/s0022-2828(77)80333-7 ◽

1977 ◽

Vol 9 (9) ◽

pp. 53-53

Author(s):

H STAM ◽

W HULSMANN

Keyword(s):

Coronary Flow ◽

Diabetic Rats ◽

Endogenous Catecholamines ◽

Streptozotocin Diabetic Rats ◽

Perfused Hearts

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Pulsatile intravenous insulin replacement in streptozotocin-diabetic rats is more efficient than continuous delivery: effects on glycaemic control, insulin-mediated glucose metabolism and lipolysis

Diabetologia ◽

10.1007/bf00400670 ◽

1996 ◽

Vol 39 (4) ◽

pp. 391-400 ◽

Cited By ~ 26

Author(s):

S. J. Koopmans ◽

H. C. M. Sips ◽

H. M. J. Krans ◽

J. K. Radder

Keyword(s):

Glucose Metabolism ◽

Glycaemic Control ◽

Diabetic Rats ◽

Intravenous Insulin ◽

Continuous Delivery ◽

Streptozotocin Diabetic Rats ◽

Insulin Replacement

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Insulin binding and glucose metabolism in adipocytes of streptozotocin-diabetic rats.

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1978.235.2.e175 ◽

1978 ◽

Vol 235 (2) ◽

pp. E175

Author(s):

M Kasuga ◽

Y Akanuma ◽

Y Iwamoto ◽

K Kosaka

Keyword(s):

Glucose Metabolism ◽

Glucose Transport ◽

Glucose Oxidation ◽

Insulin Receptors ◽

Insulin Binding ◽

Diabetic Rats ◽

Glucose Transport System ◽

Streptozotocin Diabetic Rats ◽

Intracellular Glucose ◽

Insulin Insensitivity

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.

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