Increased hyperglycemia with altered serum lipid composition in diabetes mellitus causes glycation of membrane enzymes this along with oxidative stress leads to decrease in activity of Na + K + -ATPase and other changes in erythrocyte membrane. Significant findings of the study: As the lipid level increases there is increased lipid peroxidation and the membrane composition gets altered.

Background: In Diabetes mellitus there is decreased number of pump units on the erythrocyte membrane, altered lipid-protein interaction, depleted membrane anionic charge and enzyme glycation and peroxidation which account for many abnormal complications. Method: Diabetes subjects with and without dyslipidemia were selected along with healthy control then we correlate the changes in serum and erythrocyte membrane. Result: The lipid composition of membrane is significantly increased with cholesterol:phospholipid ratio and Na + K +-ATPase of membrane was decreased when compared to control. Conclusion: Lipid composition disturbances along with increased hyperglycemia which causes glycation of enzymes and oxidative stress causes the decrease in activity of Na + K +-ATPase and other changes in erythrocyte membrane. Serum Components Control (Group-I) Group-II Group-III

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Summary: Polymorphism of Insulin Receptor Substrate-1, especially the GGG→AGG (Gly-Arg) substitution at codon 972, is one of the major factors leading to the development of type 2 diabetes mellitus. This defect in IRS-1 causes insulin resistance along with many other consequences. It generally impairs insulin signalling via the phosphadylinositol-3 (PI3)-Kinase pathway. In this study, the heterozygous Gly→Arg substitution at codon 972 of the IRS-1 gene was found in 2 of the 43 control Indian subjects, which is higher than normal when compared with the other popu lation. The prevalence of the codon 972 GGG→AGG sub stitutions was found to be around 4.6%, which may be due to a predisposition factor. In diabetic subjects, on the other hand, 5 out of 43 showed substitution at codon 972, with a percent prevalence of 14%, establishing the role of the polymorphism of IRS-1 codon in the prevalence of diabetes mellitus. Keywords: insulin, diabetes, polymorphismKratak sadr`aj: Polimorfizam supstrata insulinskog recep tora 1, posebno supstitucija GGG→AGG (glicinarginin) u 972. kodonu, jedan je od glavnih faktora koji dovode do razvoja dijabetes melitusa tipa 2. Ovaj defekt u IRS-1 izaziva insulinsku rezistenciju kao i brojne druge posledice. U najve}em broju slu~ajeva o{te}uje insulinsku signalizaciju preko putanje fosfadilinositol-3 (PI3)-kinaza. U ovoj studiji, heterozigotna supstitucija glicin arginin u 972. kodonu gena IRS-1 prona|ena je kod 2 od 43 kontrolna subjekta indijske nacionalnosti, {to je vi{e od normalnog nivoa u pore|enju s drugom populacijom. Utvr |eno je da je pre valenca supstitucija GGG→AGG u 972. kodonu oko 4,6%, {to mo`e biti posledica faktora predispozicije. S druge stra ne, 5 od 43 subjekata sa dijabetesom imalo je supstituciju u 972. kodonu, uz prevalencu od 14%, {to ukazuje na to da polimorfizam kodona u IRS-1 ima ulogu u prevalenciji dijabetes melitusa.Klju~ne re~i: insulin, dijabetes, polimorfizam phatidyl-inositol (PI) 3-kinase pathway, and the Ras/MAP kinase pathway. The IRS/PI 3-K pathway leads to the activation of a cascade of PI-dependent kinases. These include PDK1, PKC isoforms and the serine/threonine kinase AKT. AKT phosphorylates gly cogen synthase kinase 3 (GSK3), cGMP-inhi bitable phosphodiesterase and FKHR transcription factors, leading to the stimulation of glycogen synthesis and inhibition of lipolysis and gene expression, respecti vely. There is also evidence linking the activation of AKT to the stimulation of glucose transport. The Ras/MAP kinase pathway can be activated by insulin through the formation of complexes between the exchange factor SOS and GRB2. GRB2 can be activated by IRS or SHC, which are direct substrates of the IR kinase. It appears that the acute metabolic effects of insulin require activation of the IRS/PI 3-K