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Aslam o alikum I am Hassam ur Rahman and I am teaching Fsc biology since 2014 .I am always trying to improve myself and provide best lecture to students.i am taking content for the lecture from authentic and relevant sources but human errors are possible . you are requested to please highlight the mistakes.My lectures are equally reliable for Fsc and mdcat students #visiblescience #mdcatbiology #alevelbiology #neetbiology #fscbiology My personal channel, I am sure it will change your life and very beneficial for you https://youtube.com/@hassamurRahman?f... My Facebook page link https://www.facebook.com/hassam.urahm... This lecture is about DIABETES MELLITUS AND ITS GENETIC BASIS Diabetes mellitus is a hereditary disease. It is actually a heterogenous group of disorders which are characterized by elevated blood sugar level. Diabetics are unable to metabolise blood sugar in their body. They pass glucose in their urine. Diabetes is the leading cause of kidney failure, adult blindness, lower limb amputation and heart disease. There are two major types of diabetes: Type I is IDDM or insulin dependent diabetes mellitus. Type II is NIDDM or non insulin dependent diabetes mellitus. Type I is also called Juvenile diabetes because it usually occurs in early age before 40. It arises due to deiciency of pancreatic hormone insulin that normally routes blood glucose to cells for use. Type I is an auto immune disorder. The immune system backires and manufactures auto antibodies against body’s own cells. Sometimes, speciic viral infections activate auto immune response. T - cells of immune system attack pancreas and destroy insulin producing (5 - cells. As a result, pancreas does not produce insulin. Diabetics of type I must receive exogenous (from outside source) insulin to survive. Progress is being made in understanding the genetic basis of this disease. The •insulin gene is located on short arm of chromosome 11. Polymorphism and genetic variations within this locus is responsible for diabetes type I susceptibility. But today, it is no more just a recessive single gene trait, rather it is a multifactorial (polygenic with environmental inluence) inheritance associated with several alleles. Diabetes mellitus type II is non insulin dependent. It accounts for 90% of all diabetic patients. These persons produce some endogenous insulin themselves, but their body cells gradually fail to respond to insulin and cannot take up glucose from blood. They develop a sort of insulin resistance. It occurs among people over the age of 40, and is more common among the obese. Obesity increases insulin resistance. As exercise reduces obesity it indirectly increases insulin sensitivity and improves glucose tolerance. There, deinitely exists a genetic component in the form of an underlying tendency to develop diabetes under certain environmental conditions. About 2% - 5% of type II diabetics get the disease early in life, before 25 years of age. It is called maturity onset diabetes of the young (MODY). MODY can be inherited as an autosomal dominant trait. About 50% of cases of MODY are caused by mutations in glucokinase gene. Glucokinase enzyme usually converts glucose to glucose - 6 - phosphate in pancreas. MODY can also be caused by mutations in any of the four other genes which encode transcription factors involved in pancreatic development and insulin regulation. But these four MODY genes do not play any signiicant role in adult - onset type II.