Insulin deficiency is the main cause of insulin-dependent diabetes pathogeny or type I diabetes. Type I diabetes Mellitus is related to insulin deficiency consecutive to reduction of beta-pancreatic cells population. One of the major causes of diabetes Mellitus is inflammation with autoimmune alteration of Lagerhans islets (insulite). It has a specific and exclusive localisation in islets formed of beta cells, while in islets formed of glucagon producing cells inflammation is missing.
Insulin deficiency produces multiple metabolic disturbances with specific severe lesions of body structure. Glycogen and lipid synthesis disturbances constitute the basic and essential metabolic manifestation of insulin deficiency. These are related with insulin/glucagon index.
The pathogenesis of hyperlipidemia (prevalent on account of the very low density lipoprotein and non-esterified fatty acids) can be explained by the fact that the lipase in the absence of adipocyte insulin remain phosphorylated, inactive, dietary fat are not incorporated into adipocytes, and unwanted fatty acids are converted in the liver to very low density lipoprotein.Increase blood concentration of non-esterified fatty acids (hyperlipidemia transport) is the consequence of intense mobilization of lipids from adipose tissue.