Kininogen and prekallikrein increases in the blood of streptozotocin-diabetic rats are normalized by insulin in vivo and in vitro

Diabetic encephalopathy is one of the complications of diabetes. Cognitive dysfunction is the main consequence. Previous findings from neuroanatomical andin vitroelectrophysiological studies showed that the structure and function of the hippocampus is impaired in diabetes, which may underlie the cognitive dysfunction induced by diabetes. However the study of electrophysiological abnormality of hippocampal neurons in intact networks is sparse. In the current study, we recorded the spontaneous firing of neurons in hippocampal CA1 area in anesthetized streptozotozin (STZ)-diabetic and age-matched control rats. Profound reduction in burst activity was found in diabetic rats. Compared to control rats, the intra-burst inter-spike intervals were prolonged significantly in diabetic rats, while the burst ratio and the mean number of spikes within a burst decreased significantly. Treatment with APP 17-mer peptide retarded the effects of diabetes on these parameters. In addition, the average PLV of diabetic rats was lower than that of control rats. These findings providein vivoelectrophysiological evidence for the impairment of hippocampal function in STZ-diabetic rats, and may have some implications in the mechanisms associated with cognitive deficits in diabetes.

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Hypothalamic osmoregulation for vasopressin release in streptozotocin-diabetic rats in vivo and in vitro

Brain Research ◽

10.1016/0006-8993(92)90372-g ◽

1992 ◽

Vol 569 (1) ◽

pp. 86-92 ◽

Cited By ~ 3

Author(s):

Takao Akaishi ◽

Shinji Homma

Keyword(s):

Diabetic Rats ◽

Vasopressin Release ◽

Streptozotocin Diabetic Rats

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Catecholamine activation of pyruvate dehydrogenase in white adipose tissue of the rat in vivo

Biochemical Journal ◽

10.1042/bj2410415 ◽

1987 ◽

Vol 241 (2) ◽

pp. 415-419 ◽

Cited By ~ 6

Author(s):

E Kilgour ◽

R G Vernon

Keyword(s):

Adipose Tissue ◽

White Adipose Tissue ◽

Pyruvate Dehydrogenase ◽

Serum Insulin ◽

Diabetic Rats ◽

Maximum Effect ◽

White Adipocytes ◽

Streptozotocin Diabetic Rats

Intraperitoneal injections of noradrenaline or adrenaline into rats increased the proportion of pyruvate dehydrogenase in the active state in white adipose tissue; this effect of catecholamines was also apparent in streptozotocin-diabetic rats, showing that it was not due to an increase in serum insulin concentration. The catecholamine-induced increase in pyruvate dehydrogenase of white adipose tissue in vivo was completely blocked by prior injection of either the beta-antagonist propranolol or the alpha 1-antagonist prazosin. Cervical dislocation of conscious rats increased pyruvate dehydrogenase activity of white adipose tissue, which was prevented by prior injection of propranolol. Adrenaline (30 nM) activated pyruvate dehydrogenase in white adipocytes in vitro; the maximum effect of adrenaline required activation of both alpha 1- and beta-receptors. The results show that catecholamines activate pyruvate dehydrogenase of white adipose tissue both in vivo and in vitro and that this effect is mediated by a combination of alpha 1- and beta-adrenergic receptors.

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Normal Ca2+ extrusion by the Ca2+ pump of intact red blood cells exposed to high glucose concentrations

AJP Cell Physiology ◽

10.1152/ajpcell.2001.280.6.c1449 ◽

2001 ◽

Vol 280 (6) ◽

pp. C1449-C1454 ◽

Cited By ~ 10

Author(s):

Julia E. Raftos ◽

Amanda Edgley ◽

Robert M. Bookchin ◽

Zipora Etzion ◽

Virgilio L. Lew ◽

...

Keyword(s):

High Glucose ◽

Diabetic Rats ◽

Maximal Velocity ◽

Glucose Levels ◽

Normal Human ◽

Streptozotocin Diabetic Rats ◽

The Mean ◽

Human Rbcs

The ATPase activity of the plasma membrane Ca2+ pump (PMCA) has been reported to be inhibited by exposure of red blood cell (RBC) PMCA preparations to high glucose concentrations. It has been claimed that this effect could have potential pathophysiological relevance in diabetes. To ascertain whether high glucose levels also affect PMCA transport function in intact RBCs, Ca2+extrusion by the Ca2+-saturated pump [PMCA maximal velocity ( V max)] was measured in human and rat RBCs exposed to high glucose in vivo or in vitro. Preincubation of normal human RBCs in 30–100 mM glucose for up to 6 h had no effect on PMCA V max. The mean V max of RBCs from 15 diabetic subjects of 12.9 ± 0.7 mmol · 340 g Hb−1 · h−1 was not significantly different from that of controls (14.3 ± 0.5 mmol · 340 g Hb−1 · h−1). Similarly, the PMCA V max of RBCs from 11 streptozotocin-diabetic rats was not affected by plasma glucose levels more than three times normal for 6–8 wk. Thus exposure to high glucose concentrations does not affect the ability of intact RBCs to extrude Ca2+.

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