According to Ahme, Muniandy, and Ismail (2010), type 2 diabetes consists of a combination of dysfunctions that are characterized by inadequate secretion and peripheral insulin resistance of insulin. According to Khardori (2013), a combination of genetic factors such as metabolic disorders and environmental conditions contribute to the prevalence of type 2 diabetes. The disease makes a gradual onset with mild symptoms, leading to prolonged periods of hyperglycemia. That makes early diagnosis of the disease difficult, leading to serious conditions because late diagnosis allows for severe diabetic complications and serious negative effects on major parts of the body. At the onset, the pancreas does not secrete enough insulin to keep the level of glucose normal in the blood (Khardori, 2013). When the secretion of beta cells is insufficient, type 2 diabetes develops primarily within the fat tissues, the liver, and muscles of the body. The secretion rate of insulin and its level in the body is controlled by non-enzymatic glycosylation of proteins and causes amino-terminal acid and/or lysine to alter the protein structure and gradually the enzymatic functioning and signaling of the cells (Song, 2008). Altering the lipid mechanism in the presence of insulin enhances fatty acid and triglyceride synthesis and reduces the oxidation of fatty acids and triglyceride hydrolysis (Song, 2008). The absence of insulin lowers the synthesis and conversion of fatty acids into triglycerides and increases lipolysis and the oxidation of fatty acids (Khardori, 2013). Excess glucagon provides inlets for paracrinopathy in which either the insulin-secreting beta cells or glucagon-secreting alpha cells are lost causing hyperglucagonemia and hyperglycemia.
According to Song (2008), type 2 diabetes mellitus occurs in the presence of inadequate secretion and poor resistance of insulin. The concentration of insulin might not be sufficient for glycemic conditions to prevail, which leads to the development of diabetes (Khardori, 2013). At the initial stages, the physical and clinical signs and symptoms include polyuria, frequent urination, hunger (polyphagia), and thirst (polydipsia). Other signs include high levels of fatigue, impotence in men, blurred vision, and slow healing infections (Song, 2008).
A study that used pressure myography to determine the mechanics of vascular morphology in type 2 diabetes revealed the presence and activity of endothelin-1 and angiotensin II as critical elements in vascular remodeling. That provided evidence of attenuation and the reciprocating responses in clinical and experimental diabetes. That leads to a muscular complication because of atherosclerosis which plays a significant role in the morbidity and mortality rates of patients with type 2 diabetes. That leads to cardiovascular complications including acute myocardial infractions and coronary diseases. The early onset of type 2 diabetes is dissimilar to the late onset of the diseases and is characterized by the failure of β-cells (Song, 2008). According to Song (2008), cardiovascular complications are pronounced at the earlier stages of the disease and not at the advanced stages because of higher myocardial infarctions. Song (2008) argues that advanced stages of the disease lead to the development of atherosclerotic vascular which is caused by microvascular complications because of poor glycemic control and development of microalbuminuria and nephropathy (Song, 2008).
In conclusion, type 2 diabetes results from insulin deficiency and a combination of genetic and environmental factors. More studies and detailed clinical trials are required to discover effective methods of managing the disease.
References
Ahme, K. A, Muniandy, S. & Ismail, I. S. (2010). Type 2 Diabetes and Vascular Complications: A pathophysiologic view. Biomedical Research, vol. 21, no. 2, pp. 147-155.
Khardori, R. (2013). Type 2 diabetes mellitus. Web.
Song, S. H. (2008). Early-Onset Type 2 Diabetes Mellitus: A Condition with Elevated Cardiovascular Risk? Web.