What is Diabetes?

(I) Introduction

As mentioned above Type 1 diabetes(T1D) results from pancreatic beta cell destruction. This leads to absolute insulin deficiency. In T1D, the islets of Langerhans become infiltrated with activated T lymphocytes. This leads to a condition called insulitis. After some years, this autoimmune attack on the beta cells leads to sudden depletion of the beta cell population. However, symptoms appear unexpectedly when 80-90% of the beta cells have been destroyed. At this point, the pancreas fails to respond.

This leads to ingestion of glucose and insulin therapy. This therapy is required to restore metabolic control and prevent life-threatening ketoacidosis. Beta cell destruction requires both stimulus from the environment and a genetic determinant that causes the beta cells to be mistakenly identified as “nonself.”

(II) Diagnosis

The onset of T1D is typically during childhood or puberty and symptoms develop suddenly. Individuals with T1D can usually be recognized by the sudden appearance of frequent urination which is known as polyuria, excessive thirst which is known as polydipsia and excessive hunger which is known as polyphagia. They also triggered by physiologic stress such as infection. These symptoms are usually follow by fatigue and weight loss. The diagnosis is confirmed by a FBG ? 126 mg/dl. The normal condition is in between 70-99 mg/dl. However, a FBG of 100-125 md/dl is categorized as an impaired FBG. Individuals with impaired FBG is considered as prediabetic. They are at increased risk developing T2D. When the blood glucose is more than 180mm/dl, the ability of renal sodium dependent glucose transporters to reclaim glucose is impaired. Then, the glucose spills into urine. The loss of glucose is followed by the loss of water. This results in the characteristic polyuria and polydipsia of diabetes.

(III) Metabolic Changes

On the other hand, the metabolic abnormalities of T1D result from a deficiency of insulin that profoundly affects metabolism in three tissues which are the liver, skeletal muscle and white adipose. Firstly, hyperglycemia and ketonemia. The increased level of blood glucose and ketone bodies are the official marks of untreated T1D. Hyperglycemia is caused by increased hepatic production of glucose via gluconeogenesis. It is combined with decreased peripheral utilization. Nevertheless, ketonemia results from increased mobilization of fatty acids from triacylglycerol in adipose tissue. These are combined with accelerated hepatic fatty acid beta oxidation and synthesis of 3-hydroxybutyrate and acetoacetate. Diabetic ketoacidosis is a type of metabolic acidosis. It is caused by an imbalance between ketone body production and use. It is normally occurring in 25-40% for those who are diagnosed as T1D. There are chances to severe if the patient become ill. Usually, the physicians treat the patient with diabetic ketoacidosis by replacing the fluid and electrolytes. Then, they will replace into short-acting insulin to gradually correct the hyperglycemia without triggering hypoglycemia.

(IV) Treatments

Individuals with T1D must rely on exogenous insulin delivered subcutaneously either by periodic injection or by continuous pump-assisted infusion to control the hyperglycemia and ketonemia. There are two types of therapeutic injection regimens are currently used, standard and intensive. What is the difference between standard and intensive treatment? Two or three daily injections of recombinant human insulin is known as standard treatment. The blood glucose levels needed are around 225-275 mg/dl, with the glycated hemoglobin which is known as HbA1c level of 8-9% of the total hemoglobin. On the other hand, the blood glucose level is normal through more frequent injections of insulin is known as intensive treatment. Usually, more than four times per day the patient has to inject the insulin. The blood glucose levels needed are around 150 mg/dl which can achieve with HbA1c of 7% of the total hemoglobin. By the way, the normal values of glucose are not achieved intensively treated patients. However, patients on intensive therapy show a ?50% reduction in the long-term microvascular complications of diabetes compared with patients receiving standard care. This confirms that the complications of diabetes are related to an elevation of plasma glucose.

Furthermore, is about hyperglycemia in T1D. In diabetes, one of the therapeutic goal is to decrease blood glucose levels. This is possible by an effort to minimize the development of long-term complications of the disease. Nevertheless, the appropriate dosage of insulin is difficult to achieve. Excess insulin is the major complication of insulin therapy. This leads to hypoglycemia. This occurs normally more than 90% of patients. In normal individuals, hypoglycemia triggers a discharge secretion of counter regulatory hormones. The hormones are most probably glucagon and epinephrine. These help to promote the hepatic production of glucose. Whereas, T1D patients have to face the deficiency of glucagon secretion. This deficiency happens early in the disease. Even it will appear after four years of diagnosis. So, these patients are living based on the epinephrine secretion. Epinephrine secretes to prevent severe hyperglycemia. However, when the disease is progressing day by day, the T1D patients show diabetic autonomic neuropathy. Other than that, T1D patient might not be able to secrete epinephrine to overcome hyperglycemia. Thus, the glucagon and epinephrine secretion deficiency creates a symptom-free condition. This is called as “hypoglycemia unawareness.” So, T1D patients might be risky to hypoglycemia if they are not treated in an earlier stage. Even sometimes, hypoglycemia can cause by heavy exercises. This is because glucose uptake is higher in muscle during exercising. As the glucose level is higher the insulin level will be lower. So, patients are advised by the physicians to check their blood glucose level before and after heavy exercises. This helps to prevent from hypoglycemia.

Next, there are some contraindication for tight control. Firstly, children are not allowed to undergo tight control of blood glucose. It is normally for children below 8 years. This is because it might be risky for the children until hypoglycemia affect the brain development. On the other hand, elderly people are not allowed to undergo tight control of blood glucose. This is because hypoglycemia may lead to stroke and heart attacks. In addition, the major goal of tight control is to prevent complications or problems in years later.

TYPE 2 DIABETES

(I) Introduction

As mentioned above, Type 2 diabetes(T2D) is the most common form of the disease. Usually, T2D develops in stages without any clear symptoms. This disease is commonly detected by regular check-ups or medical screening tests. However, most of the patients with T2D have some symptoms. One of the symptom is polyuria which is known as excessive excretion of urine and another symptoms is polydipsia which is known as excessive thirst and fluid intake. These symptoms can be seen in several weeks’ duration. There is one more symptom which is called as polyphagia. Polyphagia is known as excessive eating. It is a very rare symptom in T2D patients. Moreover, patients with T2D have a combination of insulin resistance and dysfunctional of beta cells. These patients do not require insulin to sustain life. However, according to some physicians’ advice, insulin is required in more than 90% of T2D patients to control hyperglycemia. Plus, it also helps to keep the HbA1c less than 7%.  Based on some observations, the metabolic changes in T2D patients are moderate in type than the T1D patients. This is because although the insulin secretion in T2D patients are poor, it does hold back the ketogenesis and blunts the development of diabetic ketoacidosis. Usually, the diagnosis of the patients is based on the presence of hyperglycemia. The T2D is characterized by hyperglycemia, insulin resistance, impaired insulin secretion and even beta cell failure.

(II) Insulin Resistance

Insulin resistance is known as the decreased ability of target tissues such as the liver, white adipose and skeletal muscle. These help to react or respond accordingly to normal circulating concentration of insulin. For example, insulin resistance is characterized by increased hepatic glucose production, decreased glucose uptake by muscles and adipose tissue and increased adipose lipolysis with production of free fatty acids.

1) Insulin resistance and obesity.

Obesity is the most common cause of insulin resistance. This increases the risk of T2D patients. Most of the people with obesity and insulin resistance do not develop diabetes. Obese individuals can compensate for insulin resistance with elevated level of insulin during the absence of a defect in beta cell. The insulin secretion is two or three times higher in obese people. Thus, the higher insulin concentration compensates for the decreased effect of the hormone. This will produce blood glucose levels similar to those with normal body condition.

2) Insulin resistance and type 2 diabetes

Insulin resistance will not lead to T2D without any external help. Rather, T2D develops in insulin-resistant individuals who also show impaired beta cell function. Moreover, the risk for the development of T2D is usually can be seen in the obese people, the people who are physically inactive or in elderly and a least percentage in pregnant women. The diabetes that develop in pregnant women is known as gestational diabetes. In conclusion, these patients are unable to compensate enough for insulin resistance with increased insulin release.

3) Causes of insulin resistance

Insulin resistance usually increases with weight gain and decreases with weight loss. Plus, the excess adipose tissue is the key in the development of insulin resistance. We all know that the adipose tissue as an energy storage but it is also a secretory tissue. There are changes in the adipose secretions that result in insulin resistance with presence of obesity. These include the secretion of proinflammatory cytokines such as interleukin 6 and tumor necrosis factor-? by activated macrophages. In addition, increased synthesis of leptin, a protein with proinflammatory effects and decreased secretion of adiponectin a protein with anti-inflammatory effects. The net result is chronic, low-grade inflammation. Furthermore, the effect of insulin resistance is increased lipolysis and production of free fatty acid. Free fatty acid decreases the use of glucose which is contributing to the hyperglycemia. It also increases ectopic deposition of triacylglycerol(TAG) in the liver. Free fatty acid also has a proinflammatory effect. The free fatty acid also impair insulin signaling.

(III) Dysfunctional beta cells

The pancreas initially keeps back the beta cell capacity in T2D patients. It results in the insulin levels that differ from above normal to below normal. However, after some time the beta cell becomes even more dysfunctional. Plus, it fails to secrete enough insulin to correct the prevailing hyperglycemia. For example, normally in obese T2D patients the insulin levels are high but not as high as in the obese people who do not have diabetes. So, the normal and natural process of the disease results in a stop the function to control hyperglycemia with endogenous secretion of insulin. The failure of beta cell function may be bringing into the toxic effects of sustained hyperglycemia. Plus, it is elevated free fatty acid and a proinflammatory environment.

(IV) Metabolic changes

The metabolic abnormalities of glucose and triacylglycerol in T2D are mainly result in insulin resistance. It is normally happening in the liver, skeletal muscle and white adipose tissue. Firstly, is about the hyperglycemia. The higher number of hepatic production of glucose which is combined with decreased use of glucose by the muscles and adipose tissues is caused by the hyperglycemia. However, ketonemia is normally in T2D patient is in a very minimal or even sometimes totally absent state. This is because the presence of insulin or even in the presence of insulin resistance it will hold back hepatic ketogenesis.

Next is about the dyslipidemia. As mentioned before, the free fatty acids are converted into triacylglycerol in the liver. This process is packaged and secreted in very low density lipoprotein(VLDL). The dietary triacylglycerol rich chylomicrons are synthesized and secreted by the intestinal mucosal cells following a meal. This is because the lipoprotein triacylglycerol degradation catalyzed by lipoprotein lipase in adipose tissue is low in diabetes. Plus, the plasma chylomicron and VLDL levels are elevated. This will be resulting in hypetriacylglycerolemia. The low levels of high density lipoproteins are in combination with T2D are more likely will resulting in increased degradation

(V) Treatment

The main aim or objective in treating the T2D patient is to maintain the blood glucose concentrations within the normal limits and to prevent the development of long term complications. There are few treatments are provided to the T2D patients such as weight reduction, exercise and diet plans. These are to help to correct the hyperglycemia of the T2D patients. There are also other methods to treat the T2D patients. By providing metformin which functions to decrease the hepatic gluconeogenesis, sulfonylureas which helps to increase insulin secretion, thiazolidinedione which helps to decrease free fatty acid levels and increase peripheral insulin sensitivity, ?-glucosidase inhibitors to decrease the absorption of dietary carbohydrates and SGLT inhibitors to decrease renal reabsorption of glucose or insulin therapy may be required to achieve satisfactory plasma glucose levels.

CHRONIC EFFECTS OF DIABETES

As mentioned above, the therapies may reduce the hyperglycemia of diabetes but it fails to get back into a normal stage. The long standing elevation of blood glucose is combined with the chronic complications of diabetes. For example, cardiovascular disease, retinopathy, nephropathy and neuropathy.

The cardiovascular disease is also known as the coronary artery disease. The risk of cardiovascular disease is two to four times higher in a diabetic patient compared to non-diabetic patient. In addition to cardiovascular disease, diabetes patients are also more prone to develop disease of the heart muscle which is known as cardiomyopathy. They are also may lead to risk for sudden cardiac death.

Furthermore, retinopathy is a common complication of diabetes which may lead to serious threat to vision. This disease can be seen in both T1D and T2D patients. Retinopathy affects the small vessels of the retina due to long term uncontrolled hyperglycemia.

Next is about nephropathy. Nephropathy is clinically defined as presence of persistent proteinuria of ? 500 mg/day in a diabetic patient. Nephropathy is the leading cause of chronic renal failure and end stage renal disease. This is due to the increasing level of T2D, longer lifespan of diabetic patients and improved therapeutic options which may lead the patient to live long enough to develop chronic complications including nephropathy.

Finally, it is about neuropathy. Neuropathy is a different condition that lead to peripheral nerve dysfunction. It is most common and most troublesome of all diabetic complications. Neuropathy is defined as presence of symptoms or signs of peripheral nerve dysfunction in people with diabetes after exclusion of other causes.

MANAGEMENT OF DIABETES

What is management? Management is nothing but organizing, planning and controlling things which are important for our daily living. Thus, there are some opinions that are usually given by the physicians to the diabetic patients. First is diet plan. A diabetic diet not to be a complete deviation from the normal diet. The nutritional requirements of a diabetic patients are the same as in non-diabetic people. But the nutrient intake would be different based on the age, gender, weight, height, physical activity, physiological needs and so on. The main goals for diabetic diet are to maintain near normal blood glucose levels and optimum serum lipid levels and also to improve overall health through optimal nutrition.

Next is about exercise. Exercise plays an important role in the therapy for the diabetic patients. An exercise prescription needs to modified to each person’s capability and capacity. The advantages of exercise are to increase the insulin sensitivity. Thus, it helps to reduce the blood glucose level and also to reduce the dosage of medications. It lowers the blood pressure as well. Plus, it helps to correct dyslipidemia and strengthen the heart and circulatory system. It can reduce the body fat and increase muscle tone. It relieves tension, stress and helps the patient to feel relaxed and even it increases the metabolic rate as well.

Finally, stress reduction. Stress is a reaction factor that may be physical, mental or emotional. There are few signs or symptoms of stress such as fatigue, irritability, low self-esteem, alcohol and drug abuse, high blood pressure, change in sleep, insomnia and even more. Based on physicians’ statement, stress can affect diabetes. It makes the blood glucose levels unable to control. Studies have shown that in both T1D and T2D individuals, severe stress may worsen overall control of disease. Plus, it may lead to rise in blood sugar levels. In addition, stress can easily modify the balance of medicine, diet and exercise. According some researchers, the best ways to cope with stress are by meditation, exercise, take control of sleep, think positive, learn to solve problems and learn to manage the emotions.

In conclusion, diabetes mellitus a heterogeneous group of syndrome characterized by an elevation of fasting blood glucose that is caused by a relative or absolute deficiency of insulin.

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