Impaired phosphoinositide metabolism in glucose-incompetent islets of neonatally streptozotocin-diabetic rats

The American Journal of Physiology
L MorinB Portha

Abstract

The effects of nutrient and neurotransmitter stimuli on insulin release, loss of phosphoinositides (PI), and production of inositol phosphates (InsP) were investigated in islets from neonatally streptozotocin-injected (nSTZ) rats. In islets from nSTZ rats, insulin secretory responses to 16.7 mM D-glucose and 10.0 mM D-glyceraldehyde were reduced compared with controls. Contents in phosphatidylinositol 4-monophosphate [PtdIns(4)P] and phosphatidylinositol 4,5-bisphosphate [PtdIns(4,5)P2], but not in phosphatidylinositol, were diminished. Glucose effects on breakdown of PtdIns(4)P and PtdIns(4,5)P2 and on total InsP accumulation were both reduced. D-Glucose was unable to increase the levels of both inositol trisphosphate isomers, Ins(1,3,4)P3 and Ins(1,4,5)P3. Glyceraldehyde also failed to promote InsP formation. By contrast, the ability of 1.0 mM carbachol or 300 nM cholecystokinin to stimulate insulin secretion and InsP generation was still observed. Thus a disturbed coupling between nutrient recognition and activation of phospholipase C, possibly together with a shortage of available polyphosphoinositides, could be responsible for the altered islet PI turnover in the nSTZ rats. It is proposed that such defects may contribute t...Continue Reading

References

Apr 1, 1990·Diabetes·A KhanS Efendić
Sep 1, 1990·Proceedings of the National Academy of Sciences of the United States of America·B ThorensS Bonner-Weir
Nov 1, 1989·Endocrinology·W S ZawalichH Rasmussen
Oct 1, 1987·Physiological Reviews·M Prentki, F M Matschinsky
Oct 15, 1984·Experientia·L BestW J Malaisse

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