Decreased TC, LDL C and TG levels and increased HDL C was observe

Decreased TC, LDL C and TG levels and increased HDL C was observed following short term CSII in the reported study. Similar results were found in another study evaluating the long term effects of CSII on dyslipidemia in type 2 diabetics without previous history of major cardiovascular disease. We have observed an approximately 17% significant decrease in mean blood glucose selleck chemical Regorafenib Inhibitors,Modulators,Libraries levels 48 h after the ini tiation of insulin analog therapy. According to AACE, insulin therapy should target HbA1c levels of 6. 5% or less for most adults. The estimated average glucose level which corresponds to 7% HbA1c level is reported to be 154 mgdl. Although the achieved reduction in mean blood glucose levels in our study was above the reported tar get, we still observed an improvement in lipid parameters as shown in Table 2.

Thus, insulin analog initiation Inhibitors,Modulators,Libraries therapy Inhibitors,Modulators,Libraries has shown beneficial effects on lipo protein profile in a very short period of time. We Inhibitors,Modulators,Libraries have seen a significant increase in LDL 1 fraction and a significant decrease in LDL 2, LDL 3 and LDL 4 fractions after treatment with insulin analogs. Our findings are in agreement with a previous study that has shown that insulin therapy independently of variations in blood glu cose control induces an improvement in LDL subfraction distribution with a shift toward a decrease in small dense LDL in type 2 diabetic patients. We have observed that insulin analog initiation ther apy caused a significant increase in HDL large, HDL intermediate and a significant reduction in HDL small subfractions.

Our data is in agreement with a previous study which has reported that Inhibitors,Modulators,Libraries intensive insulin therapy is associated with increased large buoyant HDL subspe cies in type 2 diabetic patients. The observed in crease in both LDL 1 and large HDL fractions following insulin therapy may be attributed to the reduction in circulating triglycerides. CETP mediates the transfer of TG from VLDL to HDL andor LDL in exchange for cholesteryl ester. It is important to note that CETP does not drive triglycerides or cholesterol esters in one direction or another but is simply a shuttle pro tein for whatever lipids are available. It is likely that the reduction in circulating triglycerides reduced the ex change of triglycerides in VLDL for cholesterol esters in HDL and LDL, thus, returning them to their normal composition of more large particles and fewer small particle. Our finding of increased CETP activity is in agreement with previous studies which have also shown that insulin treatment increased CETP activity and im proved postprandial lipemia. We have observed that insulin treatment significantly decreased ApoB levels. ApoB reference 4 can be degraded in response to decreased VLDL secretion following insulin therapy.

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