Insulin status-dependent alterations in lipid/phospholipid composition of rat kidney microsomes and mitochondria

Samir P. Patel, Surendra S. Katyare

Research output: Contribution to journalArticlepeer-review

8 Scopus citations

Abstract

Early and late effects of alloxan-diabetes on lipid/phospholipid composition in rat kidney microsomes and mitochondria were examined. In microsomes, early diabetic state resulted in an increase in contents of total phospholipids (TPL), cholesterol (CHL), with an increase in the lysophospholipids (Lyso), phosphatidylcholine (PC), and phosphatidylinositol (PI) components. The sphingomyelin (SPM), phosphatidylethanolamine (PE), phosphatidylserine (PS), and phosphatidic acid (PA) content decreased. Treatment with insulin had no effect on PC but PE increased and the other components decreased. In the 1-month diabetic group PI, PS, PE, and PA components decreased, whereas Lyso and PC increased. Treatment with insulin had restorative effects on PE, PI, and PS; Lyso was further elevated whereas PA decreased. In mitochondria, at an early stage of diabetes marginally increased CHL content was restored by insulin treatment. Long-term diabetes lowered the TPL and elevated the CHL content. Treatment with insulin partially restored the TPL and CHL content. A diabetic state decreased the proportion of PE and diphosphatidylglycerol (DPC) components but increased the Lyso, SPM, PC, PI, and PS components in the mitochondria. Treatment with insulin had a partial restorative effect. The membrane fluidity of both microsomes and mitochondria decreased in general in the diabetic condition and was not corrected by insulin treatment at a late stage. However, at an early stage, treatment with insulin fluidized both membranes.

Original languageEnglish
Pages (from-to)819-825
Number of pages7
JournalLipids
Volume41
Issue number9
DOIs
StatePublished - Sep 2006

ASJC Scopus subject areas

  • Biochemistry
  • Organic Chemistry
  • Cell Biology

Fingerprint

Dive into the research topics of 'Insulin status-dependent alterations in lipid/phospholipid composition of rat kidney microsomes and mitochondria'. Together they form a unique fingerprint.

Cite this