Diabetes is a condition of high levels of sugar in the blood. It is a metabolic disorder characterized by insulin deficiency that leads to impaired utilization of glucose, which induces hyperglycemia. Hyperglycemia is a condition of high blood sugar while hypoglycemia is a condition of low blood sugar. Insulin is a hormone produced in pancreatic cells and it is released in blood in response to high sugar. There are two types of diabetes, type 1 insulin-dependent diabetes mellitus, and type 2, noninsulin-dependent diabetes mellitus. Type 1 is associated with the inability of the pancreatic Beta cells to produce insulin (Leonid, 2002).
In type 2 diabetes disorder, the body can not utilize the insulin produced by the pancreas properly and sometimes the body does not produce enough insulin. It occurs in people over forty-five years, mostly overweight, and without treatment, it results in too much sugar in the blood. Type 2 diabetes is insulin resistance, meaning the hormone does not bind to its receptors due to impairment thus insulin does not move glucose to cells. This leads to the accumulation of sugar in the blood. Type 2 diabetes is caused by several environmental factors such as hypertension, high levels of cholesterol, obesity but the most common cause is due to age and gene mutation. A human being with homozygous transcription factor-7 like gene 2 has impaired glucose tolerance (IGT) to diabetes mellitus, thus they have decreased insulin secretion and not insulin resistance (Valentine, Biermann & Toohey, 1998).
Pathogenesis of type 2 diabetes is a complex of multi-factorial disorders caused by genetic factors and obesity. Unlike type I diabetes, noninsulin-dependent diabetes mellitus is not linked to class-II antigen or major histocompatibility (MCH) molecules, thus there is no involvement of autoimmune mechanism. The effects of western lifestyle or obesity play a great role in the development of clinical symptoms of type 2 diabetes. Obesity decreases the number of insulin receptors in the insulin target cells throughout the body thus making the amount of insulin that is available less effective in promoting its usual metabolic effects (Leonid, 2002).
The pathogenesis mechanism of type 2 diabetes is due to impairment of pancreas Beta cells and insulin resistance. Impairment of pancreas Beta cells results in pancreatic genetic disorder where pancreatic Beta 2-adrenergic receptor genes become mutated. Inheritance of these mutated genes puts one at a high risk of having diabetes mellitus. During protein synthesis, wrong nucleotide transcription leads to a change of genes regulation, men with these genes easily develop noninsulin-dependent diabetes mellitus. Lifestyle in a family can also be inherited, for example, poor eating habits like overeating, lack of exercise increase the high risk of development of diabetes mellitus in the family (Valentine, Biermann & Toohey, 1998).
People at age above forty-five years with a poor metabolic profile such as high blood pressure, obesity, low glucose in the blood, poor glycemic control, or low levels of high-density lipoprotein have a high chance of type 2 diabetes. Early-onset diabetes occurs in ages less than thirty-five years can also be caused by a poor metabolic profile. Children born by a parent with early-onset diabetes are at high risk of developing the disease at an earlier age. Thus the age and metabolic factors are the main causes of onset diabetes. Families with traces of noninsulin-dependent diabetes mellitus increase the risk of the development of diabetes to the first-degree generation. Inheritance of the mutated gene of the islet of Langerhans responsible for insulin production also increases the risk of development of non-insulin-dependent diabetes (NIDDM). Type 2 diabetes is managed by taking précised balanced diet and observing healthy exercise (Leonid, 2002).
Reference list
Leonid, P. (2002). Principles of diabetes mellitus. California: Sage publication.
Valentine, V. Biermann, J & Toohey, B. (1998). Diabetes type 2 and what to do. USA: Lowell House.