ABSTRACT
Diabetic retinopathy (DR) is a major microvascular complication of diabetes. It is the most common cause of blindness in the working-age population in developed countries. We wanted to analyse the correlation between risk factors of blindness like duration of diabetes, dyslipidaemia, hypertension, HbA1c with severity of diabetic retinopathy in order to design appropriate strategies for prevention and treatment of diabetic retinopathy.METHODSThis was a retrospective study of all diabetic patients with diabetic retinopathy who presented to the eye OPD at KS Hegde Medical Academy from April 1st 2018 to March 31st 2019 that fulfilled the inclusion criteria. A dilated fundus examination was done to note the grade of diabetic retinopathy. The demographic data along with the duration of diabetes, HbA1c values, Cholesterol levels and Blood pressure were documented and correlated with the severity of diabetic retinopathy.RESULTSThe study included 92 patients, of which 63 were males and 29 were females with a mean age of 54.5±2.8 years. We found that there was statistically significant association between the duration of diabetes and HbA1c levels with severity of diabetic retinopathy (p= 0.022 and 0.034 association), whereas there was no statistically significant correlation between blood pressure and cholesterol levels with severity of diabetic retinopathy (p= 0.52 and 0.456 respectively)CONCLUSIONSDiabetic retinopathy showed a male preponderance, with risk factors like duration of diabetes and HbA1c levels having a significant association with the severity of diabetic retinopathy. Therefore, it is essential to have a good systemic control of diabetes with diet and suitable medications. Diabetic retinopathy is a preventable cause of blindness when diagnosed early and screening of diabetic retinopathy must be done in all diabetics to prevent the progression of the disease.
ABSTRACT
Objective To analyze the effects of acute depletion of liver-specific insulin signaling on secretion of apolipoprotein B (apoB) and triglyceride (TG).Methods Based on Cre-LoxP principle,a promoter of hepatic tissue specific albumin gene was inserted into upstream of the cre recombinase gene.Albumin-Cre adenovirus (Ad-CRE) and GFP adenovirus (Ad-GFP) were amplified in 293A cells and purified before intravenous administration to mice.After adenovirus infection for 2 days,4 days and 6 days,blood samples from mice were collected and hepatic tissues were frozen.The secretion rates of hepatic newly synthesized apoB and very low density lipoprotein (VLDL)-TG were determined by injection of Triton WR-1339.The levels of plasma cholesterol (TC) and TG were measured.The expressions of insulin receptor and other lipoprotein metabolism related proteins in hepatic tissues were analyzed by Western blot.Results After 2 d,4 d and 6 d of the Ad-CRE injection into mice,insulin receptor expression was reduced by 30.50％ (P＜0.05),60.12％ (P＜ 0.01) and 99.54％ (P＜0.001),and VLDL-TG secretion rate was decreased by 20.43％ (P＜0.05),33.63％ (P＜0.05) and 44.21％ (P＜0.01),respectively.Expressions of sterol regulatory binding proteins 1,fatty acid synthase,and the related proteins of VLDL-formation were decreased,but there were no changes in hepatic secretion of apoB100 and hepatic lipids.The hepatic secretion of apoB48 was increased by 35.07％ (P＜0.05) 6 d after Ad-CRE injection.Conclusions Acute depletion of hepatic insulin receptor might reduce VLDL-TG secretion in manner of time-dependent,and increase the assembly and secretion of smaller apoB-containing lipoproteins in mice liver,which is probably associated with decreased lipogenesis.
ABSTRACT
Objective The processes responsible for the uptake of very low density lipoprotein(VLDL) by monocyte macrophage cells were investigated. Methods The effects of VLDL concentration, apoE ligand activity and scavenger receptor A (SRA) on the binding of 125 I VLDL to monocyte macrophages were analysed. The influence of VLDL on SRA mRNA and protein expression and VLDL receptor gene translation was probed. Results (1) The differentiated monocyte macrophages induced 125 I VLDL uptake by dose dependent pathway( r =0 71, P