Physiological Processes Of Blood Glucose Control, Consequences Of Poorly Controlled Hyperglycaemia, Drugs For Managing Type II Diabetes Mellitus, Insulin Resistance & Use Of HbA1c For Diabetic Patients

Insulin synthesis and release in diabetic and non-diabetic person

1. In a healthy and non-diabetic individual insulin functions by binding to the target tissues and enabling them to uptake glucose present in the blood. In absence of insulin the blood glucose level increases. Therefore, synthesis and release of insulin is as important as its binding to the target tissues (American Diabetes Association 2014). Insulin is produced and secreted by the beta cells of pancreas. This hormone maintains the blood sugar level and prevents development of hyperglycaemia or hypoglycaemia. Insulin keeps the BGL in check by activating the target cell receptors that are used to uptake the glucose from the blood. If insulin is not produced adequately, the glucose metabolized from carbohydrates remains in the blood and elevates the blood glucose levels markedly. Moreover, if insulin is produced, but is unable to act on the target cells it can also lead to increased BGL. In Type II Diabetes the affected person starts to show insulin resistance where the body does not effectively respond to insulin. Therefore the tissues refuse to take up glucose from blood and thereby the blood glucose level increases. If the disease is left untreated, the increasing pressure on the pancreas results in complete abolishment of the insulin producing pancreatic beta cells (Kahn, Cooper and Del Prato 2014). Insulin plays a major role in regulating the glucose level in blood. Insufficient amount of insulin or the inability to respond to the insulin action, develops diabetic symptoms in people. Insulin plays several key roles in the body. One of its major functions include regulation of glucose and fat storage in the body. Multiple tissues in human body relies on insulin to take up glucose from the blood for utilizing that glucose later for energy production. Insulin signals the liver, muscles and adipose tissues to take up glucose from the blood. With the help of insulin hepatic tissues take up glucose and turn it into glycogen.

2. Diabetes can be treated with proper care, but if the BGL is left uncontrolled then it can increase the risk of heart diseases such as myocardial infarction (Courcoulas et al. 2015). People who are suffering from Type II diabetes can develop cardiovascular diseases if their risk factors are not addressed. Increased level of blood glucose triggers the condition of MI as it favors the fatal occurrence of arrhythmia. Acute hyperglycaemia induces ischaemic conditions in heart and thereby results in worse myocardial functions. Increased platelet activation in non-diabetic patients is related with hyperglycaemia. If hyperglycaemia results in increased stress, it amplifies the immune responses and worsens the cardiac functions (Scheen 2015). Acute hyperglycaemia resulting from diabetes, leads to an increase in inflammatory markers, resulting in a detrimental effect in case of MI. Endothelial dysfunction is common with MI and plays a major role in cardiovascular diseases. Increased hyperglycaemia induces the endothelial dysfunction thereby leading to myocardial infarction. Along with this, if the patient is overweight they may tend to have an increased level of unhealthy blood cholesterol (high LDL and low HDL) they can easily develop heart diseases. Such blood lipid imbalances can be caused by insulin resistance which is known as diabetes dyslipidemia. Therefore, obesity and overweight increases the chances of MI in patients with T2DM (Ozougwu et al. 2013). Obesity has strong associations with insulin resistance. Another major risk factor of T2DM associated cardiovascular diseases is lack of physical activity. Mrs. Roberts does not exercise at all and leads an extremely sedentary lifestyle. Regular exercise and thereby maintaining to lose weight in a healthy way can delay the onset of diabetes and helps in effectively manage the disease. Physical activity manages the blood pressure in patients suffering from hypertension and reduces the chances of myocardial infarction.

Consequences of poorly controlled hyperglycaemia in diabetic patients

3. The drug that is used in treating type II diabetes mellitus in the patient Mrs. Emily Roberts is Metformin. Metformin is a hypoglycaemic medication that improves the blood glucose status of the individuals. This drug acts on the glucose utilization rather than the glucose absorption. It has been reported that metformin induces the insulin- induced glucose uptake action of the skeletal muscle cells and the adipose tissues (Zaccardi et al. 2015). In the hyperglycaemic state the action of the drug is enhanced. It acts on the insulin receptors and the glucose transporters, increases the insulin binding capacity of the cells, and stimulates glucose uptake. Metformin also acts as a stimulator for uptake of glucose. It mostly works on the skeletal muscles and increases the glucose transport across the muscle membrane. Metformin reduces the glucose production level of liver cells, decreases the absorption of glucose through the intestines and promotes the insulin sensitivity of target cells by maintaining a normal level of glucose uptake by the peripheral tissues. Therefore, the primary action of Metformin is lessening glucose release from liver, and its secondary action is that it increases the insulin sensitivity and stimulates the absorption of glucose by target cells (Lee et al. 2016). Along with this, researches have proved that Metformin can help the individuals lose weight. Metformin reduces the appetite, and thereby combats the symptom of frequent hunger of the affected persons. Thus, it can lead to weight loss. It has been reported that people who exercise regularly and follow a healthy diet and lifestyle tend to lose the most weight while taking Metformin. The patient is overweight and does not exercise. Therefore, if Metformin can help her lose weight while addressing her hyperglycaemic condition, it will be helpful for her.

4a. Abdominal adiposity is classified as a condition that results in excessive fat deposition in the abdominal region. Abdominal adiposity poses a greater implication for diabetes. Abdominal adiposity has a greater chance of developing diabetes and other metabolic syndromes rather than obesity. The excessive fat deposition in the abdominal cavity of individuals is classified as visceral adiposity or subcutaneous adiposity according to the place of fat deposition. Women are more prone to abdominal adiposity than men (Singh et al. 2013). However, the differences in the sexes of the individuals do not affect the degree of adiposity. There are three measures of adiposity such as BMI, percent fat and the waist circumference of the individuals. These are the best predictors of insulin sensitivity. If adiposity is controlled in aged patients, insulin sensitivity tends not to get affected by the patient’s age. Contribution of abdominal adiposity to increasing the risks of diabetes has also been reported.

4b.  Haemoglobin A1c test or the glycated hemoglobin test is used to assess the blood glucose level of a patient over the past 2-3 months. This test helps determine the average blood glucose levels in the patients who are suffering from diabetes (Kautzky-Willer, Harreiter and Pacini 2016). Sometimes the test is also used for diagnosis of diabetes. This test is based on the fact that when glucose levels increase in blood, the glucose binds to the red blood cells present in the blood. With the help of this test the amount of glucose bound to RBCs can be measured. If the BGL has increased in the patient over the last few days the result of the HbA1c test will be higher. In case of the non-diabetic patients, the normal range of HbA1c test ranges between 4-5.6% (Scirica et al. 2013). If the percentage gets higher than 6.5% it means that the individual is suffering from diabetes.

References:

American Diabetes Association, 2014. Diagnosis and classification of diabetes mellitus. Diabetes care, 37(Supplement 1), pp.S81-S90.

Courcoulas, A.P., Belle, S.H., Neiberg, R.H., Pierson, S.K., Eagleton, J.K., Kalarchian, M.A., DeLany, J.P., Lang, W. and Jakicic, J.M., 2015. Three-year outcomes of bariatric surgery vs lifestyle intervention for type 2 diabetes mellitus treatment: a randomized clinical trial. JAMA surgery, 150(10), pp.931-940.

Kahn, S.E., Cooper, M.E. and Del Prato, S., 2014. Pathophysiology and treatment of type 2 diabetes: perspectives on the past, present, and future. The Lancet, 383(9922), pp.1068-1083.

Kautzky-Willer, A., Harreiter, J. and Pacini, G., 2016. Sex and gender differences in risk, pathophysiology and complications of type 2 diabetes mellitus. Endocrine reviews, 37(3), pp.278-316.

Lee, A.L., Chen, B.C., Mou, C.H., Sun, M.F. and Yen, H.R., 2016. Association of traditional Chinese medicine therapy and the risk of vascular complications in patients with type II diabetes mellitus: a nationwide, retrospective, Taiwanese-registry, cohort study. Medicine, 95(3).

Ozougwu, J.C., Obimba, K.C., Belonwu, C.D. and Unakalamba, C.B., 2013. The pathogenesis and pathophysiology of type 1 and type 2 diabetes mellitus. Journal of Physiology and Pathophysiology, 4(4), pp.46-57.

Scheen, A.J., 2015. Pharmacodynamics, efficacy and safety of sodium–glucose co-transporter type 2 (SGLT2) inhibitors for the treatment of type 2 diabetes mellitus. Drugs, 75(1), pp.33-59.

Scirica, B.M., Bhatt, D.L., Braunwald, E., Steg, P.G., Davidson, J., Hirshberg, B., Ohman, P., Frederich, R., Wiviott, S.D., Hoffman, E.B. and Cavender, M.A., 2013. Saxagliptin and cardiovascular outcomes in patients with type 2 diabetes mellitus. New England Journal of Medicine, 369(14), pp.1317-1326.

Singh, S., Chang, H.Y., Richards, T.M., Weiner, J.P., Clark, J.M. and Segal, J.B., 2013. Glucagonlike peptide 1–based therapies and risk of hospitalization for acute pancreatitis in type 2 diabetes mellitus: a population-based matched case-control study. JAMA internal medicine, 173(7), pp.534-539.

Zaccardi, F., Webb, D.R., Yates, T. and Davies, M.J., 2015. Pathophysiology of type 1 and type 2 diabetes mellitus: a 90-year perspective. Postgraduate medical journal, pp.postgradmedj-2015.