Renal Phospholipid Metabolism in Streptozotocin-lnduced Diabetic Rats

Abstract

The effect of acute and chronic streptozotocin-induced diabetes on phospholipid metabolism in papillary, medullary and cortical slices was studied. No changes were observed in either the phospholipid content or composition in the papilla, medulla and cortex from acute and chronic diabetic rats. With reference to (U-¹⁴C)glycerol incorporation in the papilla from chronic diabetic rats, it increased in PtdCho, Ptdlns and PtdEtn. In the medulla, the incorporation to PtdCho decreased in the acute diabetic state, while in the chronic diabetic state the incorporation to PtdCho and Ptdlns decreased. No changes were observed in cortical phospholipids from diabetic rats. As regards ³²P-sodium orthophosphate incorporation to phospholipids, while it increased in PtdCho, Ptdlns and PtdEtn in the papilla from acute and chronic diabetic rats, in the medulla from both groups, the incorporation in PtdCho and Ptdlns decreased, and in the cortex from acute diabetic rats it decreased only in Ptdlns. Even though no changes were detected in phospholipid composition, alterations in phospholipid metabolism were induced by experimental diabetes.

Environmental hyperosmolality regulates phospholipid biosynthesis in the renal epithelial cell line MDCK

“…For propidium iodide staining, the fi xed cells were washed once with PBS and from our laboratory demonstrated that the inner renal medulla has the most-active phospholipid synthesis and membrane turnover of all kidney zones ( 24 ). We have demonstrated that the ability of the inner renal medulla to renew the phospholipidic constituents of cell membranes is a defense mechanism against diverse injuries (25)(26)(27). We have speculated that such an active phospholipid metabolism in renal medullary cells is a consequence of the high interstitial osmolality, but we did not confi rm this hypothesis.…”

High Glucose Concentrations Stimulate Renal Papillary Phosphatidylcholine Biosynthesis

“…For the present study, 25 m M glucose, five times the physiological value, was used as a high extracellular glucose concentration, since it was the highest plasma glucose concentration reached by the experimental diabetes model used [6]. This glucose value also simulates the hyperglycemic condition that can occur in a situation of decompensated diabetes, and is consistent with the possibility that hyperglycemia per se may mediate the modifications in papillary PtdCho biosynthesis observed in diabetic rats.…”

“…Glycerol-3-phosphate is not only an intermediate in the metabolism of glucose to lactate, but also acts as a precursor in phospholipid biosynthesis. Taking into account that glucose enters the papillary cells by an insulin-independent mechanism, the papillary increase in phospholipid de novo synthesis might be a consequence of the rise in intracellular glucose, which could induce an increase in the final products of the synthesis – such as phospholipids – by exacerbation of such a pathway [6]. …”

“…The diabetic condition was confirmed by the presence of glycosuria, ketonuria (only in the acute state), glucose plasma levels ranging from 400 to 480 mg/dl at the time of decapitation, and a marked weight loss [6]. All these parameters could be restored to normal values by insulin treatment.…”

“…We have previously shown that only the papilla – the most active zone of the kidney with regard to phospholipid metabolism [5]– increases its phospholipid de novo biosynthesis in the diabetic state [6]. …”