Changes of Apoproteins in Diabetes Mellitus in South West Region of India

Abstract: Diabetes Mellitus (DM) is a group of metabolic diseases characterized by an elevated blood glucose level – resulting from defects in insulin secretion, in insulin action or both. Diabetes Mellitus is not a pathogenic entity but a group of etiologically different metabolic defects that share the phenotype of hyperglycaemia. Several distinct types of DM exist and are caused by complex interaction of genetic factors and life style choices. Depending on the etiology of DM, factors contributing to hyperglycaemia may include reduced insulin secretion, decreased glucose utilization and increased glucose production. Hyper-lipidaemia as a metabolic abnormality is frequently associated with diabetes. Lp (a) is a cholesterol-ester rich complex composed of an LDL-like particle to which is attached a large, highly glycosylated protein. Lp (a) has two alleles, 11 phenotypes and 19 genotypes, depending on the number of repetitive domains. The smaller isoforms are associated with higher Lp (a) concentrations. Lp (a), when present, is attached to apo B by a disulphide bond. It has significant homology with plasminogen. So, it interferes with plasminogen activation and impairs fibrinolysis. This leads to unopposed intravascular thrombosis and possible myocardial infarction. Present study involves the role of Lp(a) in causing hyper-lipidaemia in Diabetes leading coronary heart disease. Materials and Methods: The subjects for the present study were selected from the diabetic clinic of Calicut Medical College hospital, Calicut, India. Only type 2 diabetic patients who were on oral hypoglycaemic agents were included in the study. These subjects had no previous history of renal, liver or heart diseases. The test group contained 615 diabetic patients. The control group consisted of clinically normal 420 subjects. Measurements of Lipid profiles, Apolipoprotein A and B were done authentic methods. Results: Mean serum levels of Lipoprotein (a) values were significantly lower in diabetic patients. The mean lipoprotein (a) values were 69.20 ± 2.4 (p<0.001), 71.84 ± 1.8 (p<0.001), 64.38 ± 2.1 (p<0.001), 18.16 ± 0.32mg/dl in the test groups 3, 2, 1 and the control group respectively. The serum level of lipoprotein (a) was found to be higher in all the test groups irrespective of whether these diabetics were well controlled or poorly controlled. The mean values of serum apolipoprotein B were increased in test group 3, test group 2 and test group 1 categories when compared to the control group (non-diabetic healthy group). Conclusion: The estimation of apolipoprotein B and Lipoprotein (a) revealed significant elevation in both of these parameters. Apolipoprotein B was inversely proportional to glycaemic control. Lipoprotein (a) was significantly elevated in all the groups of patients irrespective of the glycaemic status. This abstract was presented at the American Physiology Summit 2025 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.