Pathophysiology, risk factors and etiology of type 2 diabetes.

Pathophysiology, Risk factors, and Etiology of Type 2 Diabetes
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Pathophysiology, Risk Factors, and Etiology of Type 2 Diabetes
Diabetes Type 2 is the most prevalent form of diabetes, accounting for about 90% of all diabetic cases. It is a chronic metabolic disorder marked by elevated blood glucose due to dysregulated sugar metabolism. Diabetes mellitus reflects a constellation of metabolic disorders marked by raised blood sugar owing to malfunctioning in insulin secretion, insulin action, or both. Diabetes is among the most common chronic illnesses. Over 415 million people have diabetes, and an approximated value of more than 193 million persons remained undiagnosed of this metabolic disorder worldwide (Chatterjee, Khunti & Davies, 2017). It comes with unprecedented adverse outcomes in terms of complications and associated socio-economic burden. The chronic hyperglycemia in DM is often leading long-term damage, dysfunction, and failure of multi-organ failure involving the eyes, kidneys, nerves, blood vessels, and heart. This paper will explore diabetes in terms of pathophysiology, aetiology, and risk factors.
Pathophysiology of Diabetes
The DM pathophysiology contributes to a better understanding of the disease process. The pathophysiology of diabetes is associated with body insulin levels and its capacity to utilize insulin. Type 2 DM is marked by peripheral tissue resistance to insulin. Insulin resistance refers to a physiological situation when cells in muscles, fat, and liver don't respond sufficiently to insulin leading to impaired uptake and glucose use for energy. Glucose in the blood must enter cells for its metabolism to occur. However, failure to enter cells due to distance leads to accumulation of glucose in the blood, culmination to what is described as hyperglycemia (Liniarski et al., 2017). Rising blood sugars will entail signaling the pancreas to make more insulin, though even the insulin already release is not working, leading to insulinemia and hyperglycemia at the same time. More often, the insulin-receptive response is impaired, leading to resistance. Genetics, aging, and ethnicity may influence developing insulin sensitivity. However, primary factors that lead to insulin resistance and insensitivity include excess body weight, high-density sugar diet, hyperlipidemia, physical inactivity, and even poor sleep. It must be noted that the precise cause of insulin resistance is poorly understood. Insulin resistance causes the body to release more insulin, leading to increased hunger, elevated blood pressure, and weight gain. The insulin resistance and insensitivity constitute primary contributors to metabolic syndrome, diabetes Type 2 and atherosclerotic cardiovascular disease (Kheradmand et al., 2017; Liniarski et al., 2017). Thus, insulin resistance is marked by glucose intolerance, hyperinsulinaemia, dyslipidemia, abdominal obesity and hypertension. It appears that Insulin resistance is a fundamental abnormality in the pathogenesis of type 2 diabetes and atherosclerotic cardiovascular disease because insulin resistance disrupts the functions of insulin-target organs including adipose tissue which functions in which glucose-metabolism activities such as, lipogenesis, and adipokine secretion (Kheradmand et al., 2017).
Available evidence shows that diabetes mellitus is a spectrum of disorders marked by varying amounts of insulin resistance and β-cell dysfunction. The modifying factors either or leads to hyperglycemia and tends to have independent effects. There is a link between hyperglycemia, physiological and behavioral responses. During hyperglycemia, the brain identifies raised blood sugars and sends impulses to the pancreas and other organs to decrease its effect. In type Type 2 DM, this process of recognizing hyperglycemia and subsequent transfer of signals to effect glucose-reducing physiological action is significantly impaired. The multifunctional physiological system in glucose regulation is marked by two primary pathological defects in type 2 diabetes, including impaired insulin secretion via a dysfunctional pancreatic β-cell and impaired insulin action occasioned by insulin resistance (Baynes, 2015).
Usually, the pancreatic β-cell releases insulin as occasioned by rising blood glucose concentration, which reduces glucose levels. However, this happens less in Type 2 DM, where the released insulin is insufficient or fails to act due to tissue insurance resistance. The failure of insulin production or its ...