Insulin-Dependent Diabetes Mellitus
How it works
Diabetes Mellitus 1, more specifically known as IDDM is a disorder concerning glucose homeostasis, which needs insulin therapy is generally seen in children. Diabetes is generally classified into 2 types IDDM (Insulin dependent diabetes mellitus) and the other NIDDM (Non-insulin dependent diabetes mellitus). Diabetes simply means an increase of glucose levels in the body as a result of the improper or no production of insulin from ones pancreatic ??-cells. The standard auto-immune response of type 1 diabetes is specific destruction of pancreatic islets (??-cells).
The invasion of the Islets cells by the immune system (leukocytes) simultaneously prevents the production of insulin which causes the onset of Type 1 diabetes (Mathis, Vence, & Benoist, 2001). Resulting hyperglycemia causes somatic cells to be deprived of the glucose for energy. Moreover, a side effect of gluconeogenesis developing a condition called ketoacidosis due to the accumulation of excess fatty acids from fat oxidation can lead the patient with symptoms like frequent urination, thirst, weight loss without trying, numbing of feet or tingling, etc. Treatment is almost impossible, yet clinical management can bring the patient back to normal living by food intake alterations and regular exercise along with intravenous insulin injections to bring the glucose levels within the accepted range.
Studies of inheritance shows IDDM 30-50% similarity among monozygotic twins’ which suggests this disorder to be affected by both environmental factors and involved genes. For, siblings the risk was found to be 6% (Todd,1990). Further studies by Craighead (1978) showed influences by genetic and environmental factors in IDDM. Since, any genetic disorder shows a direct connection to the basis of genetics when it comes to the critical form. Research by Todd had discovered that the correlation of IDDM to genetics is less direct to INDDM. The similarity in INDDM was 100% for identical twins where the onset of diabetes was diagnosed following 45 years of age, which included individuals having at least one diabetic parent. IDDM gives support to the multifactorial hypotheses. Nilsson in 1964 stated, the distinguishing features of dominant and recessive inheritance for high gene frequency. The gene frequency for autosomal recessive inheritance was accounted to be 0.30 and the gene frequency of 0.05 was considered for the dominant hypothesis. The molecular genetics, which is the study of the chemical nature of genes and how they operate at a molecular level; behind this disorder was explained by Todd (1987). Studying the DNA sequences for diabetics, and that alleles of a certain type had confirmed susceptibility and resistance to the disease. His results showed alleles both susceptible to IDDM and resistive against the insulin production via ??-cells.
There is instability between the onset symptoms of IDDM for children and adults. Childrens seen to have more acute problems of polydipsia, polyuria and ketonemia while for adults it being a more gradual onset, yet decoyed towards a type 2 diabetes diagnosis (Chiang, Kirkman, & Peters, 2014). Further, clinical clues related to the environmental factors based on the multifactorial hypotheses suggest, a lean person to be more susceptible to have type 1 diabetes with a distant relative having a positive history of type 1 diabetes. Contributing factors, like obesity and unhealthier lifestyle supported the diagnosis of type 2 diabetes, for an individual with family history showing type 2 diabetes. Obesity wasn’t completely responsible for the development of type 2 diabetes even though its overproduction in an obese person which brings us to the conclusion that phenotypic type 2 diabetics, showed the initial islet autoimmunity confirming type 1 diabetes. Thus, leaner individual having potential phenotypic type 2 diabetes are more likely to be diagnosed with type 1 diabetes. Generally, for these patients the noninsulin-based treatments used for treating type 2 diabetes is infective and IDDM is considered to be expressed.
Family history plays an important role in early prevention or diagnosis for example, the risk for type 1 diabetes in U.S is ~0.3%, but for those with first degree relative with diabetes the risk is bumped up to ~5% which is an increase of 15 folds (Chiang, Kirkman, & Peters, 2014). The standard testing procedure to keep the glucose levels in check is called the A1C test with reflects the range of one’s glycemic levels. Insulin therapy including 3-4 injections depending on the meal intake per day given subcutaneously or an alternative to that is using insulin pump therapy both uses r-DNA human insulin for better outcomes.
Genetics techniques of recombination is highly useful in this therapy to produce an insulin suitable for human rather than using animal insulin. Diabetes type 2 considered as a less critical or mild from compared to type 1 because the of no treatment possibilities currently. Yet many ongoing researches based solely on the purpose of regenerating or transplanting islets cells is under way. Pancreas transplants are now considered the only successful therapy which comes with its own risks of finding a compatible pancreas donor. Since, the blood type of the patient must match with the donors to prevent any post operational complication with the functioning or the acceptability by body’s own immune system (antibodies). Islet transplantation is mostly on experimental trials working on cell transplantation and preventing it from the autoimmune destruction. Methods involving pluripotent stem cell treatment, or regeneration of the pancreas itself is considered.
IDDM in united states is more frequent to the children about 20 times more than that of the china. Population genetics which is the study of genetic variation within and among populations; further reviewed by Bao et al. (1989), that it was due to a difference in the allele frequency which points towards the location of aspartic acid in 57 position of the beta chain. Concluding that its presence is responsible to protect against IDDM, which in case of an uncharged amino acid would have resulted in increased susceptibility at the same position. Since, autoimmunity caused by the defective T-cell response in a type 1 diabetic patient (T1D) is mainly focused on a series of signals it could be altered to correct or suppress the autoimmunity. Examinations on the micro RNA particularly miRNA181a by Serr and colleagues showed it can be used to suppress the immune response in T1D. Further studies specify the dampening of T cell induction by production of a nuclear factor of activated T cells 5 (NFAT5) which chemically impairs the immune balance to bring it back to normal (Serr, Scherm, Zahm, Schug, & Flynn, 2018).