Report in Biochemistry (Diabetes Mellitus) Submitted To: Mr. Francis Panaguiton Submitted By: Jeannie Alcazar Stephanie Bernas Jhessel Comparacion Erick Dave Crispo Maude Diaz Reinalyn Jane Diaz Krystal May Manalo Lea Opina I. Brief History of Diabetes Mellitus Diabetes mellitus originated from the Greek word Diabetes means siphon, which refers to a pass-through and the Latin word Mellitus, which indicates sweet or sugary. It simply implies a surfeit sugar found in the blood and urine. In the 6th century, Ayurveda physicians first perceived the sugary taste of urine called the condition madhumeha ("honey urine"). Frederick Banting and Charles Best, 1924 In Traditional Chinese Medicine, the condition was prescribed as xiāo kě, or a malady characterized by extreme thirst and appetite, frequent micturition, and unexplained weight loss. In the early accounts of Avicenna and the Medieval Islamic World, diabetes was described as a disease of the kidneys. In 1674, Thomas Willis implied that diabetes could be a disease in the blood. Johann Peter Frank is attributed with identifying Diabetes Mellitus and Diabetes Insipidus in 1794. In 1889, Joseph von Mering and Oskar Minkowski made a discovery that the pancreas is causing the condition. At the beginning of the 20th century, physicians hypothesized that the Islets of Langerhans secrete a substance called insulin that breaks down carbohydrates. Frederick Banting, J.J.R. Macleod, Charles Best, and James Collip made a discovery and refinement of insulin for clinical use. The patent for insulin was assigned to the University of Toronto in 1923 to keep treatment accessible. II. What is Diabetes Mellitus? Diabetes Mellitus describes as cellular starvation amid plenty. The insufficiency may occur because the pancreatic beta cells do not secrete insulin properly, or the peripheral cell receptors are resistant to the insulin binding or transfer across the cell membrane. It is a complex chronic disease characterized by the non-utilization of carbohydrates, proteins, and fat metabolism. It is either an endocrine or hormonal disease because of its central feature of hyperglycemia. It results from a deficit in the production or utilization of insulin. The pancreatic hormone insulin has an important metabolic role. It decreases blood glucose levels, suppresses fat metabolism, and promotes protein synthesis. Glucagon is a counter regulatory hormone that raises blood glucose levels. It is also responsible Page 2 for using stored fuels and produces new glucose from glycogen and amino acid released into the blood. III. What are the problems occurred in Diabetes Mellitus? A. Insulin Dependent (IDDM), Type 1, is an insulin deficiency caused by islet cell loss. It happens when a type 4 hypersensitivity response or the T cells attack the pancreas. There's a phenomenon called the genetic abnormality that causes a loss of self-tolerance among T cells, and it targets the beta-cell antigens. Losing betacell means less insulin, and glucose piles on the blood because it can't enter the body's cells. 10% of the general population has IDDM Type 1, and it is commonly associated with onset in childhood, adolescence, or young adulthood. It often affects small blood vessels in eyes and kidneys. B. Non-Insulin-Dependent (IDDM), Type 2, occurs when the cells have insulin resistance. The body secretes normal or low amounts of insulin in the blood, and the blood glucose rises higher than usual. The beta-cell defect may worsen as the course of NIDDM progresses from the low levels of insulin. 90% of the general population has NIDDM Type 2, and it is commonly associated with onset after 40 years of age. It often affects large blood vessels and nerves. C. Gestational Diabetes (GDM) is glucose intolerance commonly associated with the onset during childbirth, particularly in the latter half of pregnancy, related to the placental hormones resisting insulin. Gestational Diabetes can be either IDDM or NIDDM if the glucose tolerance remains impaired. IV. What is the Enzyme lacking in Diabetes Mellitus and what happens if the Enzyme cannot take place? The G6PD gene provides instructions for making an enzyme called Glucose-6phosphate dehydrogenase, which plays a crucial part in red blood cells. This enzyme defends red blood cells from damage and premature destruction. A deficiency of Glucose-6-Phosphate Dehydrogenase (G6PD) increases the risk of impaired glucose tolerance and diabetes. G6PD deficiency promotes oxidative stress and decreased betacell insulin secretion. Page 3 V. Signs and Symptoms of Diabetes Mellitus IDDM TYPE 1 NDDM TYPE 2 GDM Polyuria Usually Asymptomatic Extreme Fatigue Polydipsia Polyuria Blurring of vision Polyphagia Polydipsia Polyuria Glycosuria Polyphagia Polydipsia Weight loss Glycosuria Nausea Anorexia, nausea, and Weight gain vomiting Blurring of vision Increase susceptibility to infection Delayed wound healing VI. Diagnosis Test A. Blood Test for Diabetes Mellitus 1. Fasting Glucose Test measures your blood sugar through fasting or not eating or drinking (except water) for a certain period before the actual monitoring. To screen for diabetes in patients recently admitted to hospitals care centers. It is part of annual screening in primary care. 2. Random Glucose Test refers to the sample of blood is taken at any time. The Normal Blood Glucose Level should be 99 milligrams per deciliter or below. 3. Hemoglobin A1C Test measures the amount of glycosylation of normal hemoglobin A, and it correlates with the average blood glucose levels over the past 2 to 3 months. 4. Glucose Tolerance Test measures your blood sugar before and after drinking a sweetened liquid called Glucola. B. Methods/ Gadgets used for testing Self-Monitoring of Blood Glucose (SMBG) One Touch II Blood Glucose Monitor Glucometer M+ Blood Glucose Monitor Page 4 VII. Intervention and Treatment for Diabetes Mellitus A. Primary Prevention a. Advice the patient to attend nutrition counseling and healthy public policies focused on food, diet, and physical activities. b. Cut down sugar and refined carbs from the patient’s diet. c. Drink an adequate amount of water daily d. Exercise regularly e. Avoid cigarette smoking f. Use Dietary patterns to avoid obesity g. Normal Blood Glucose Level and the ideal weight should be maintained or achieved. h. Educate the patient about the signs and symptoms of Diabetes Mellitus and when to seek medical assistance if such disease occurs. B. Secondary Prevention a. Perform health care skills precisely. (Insulin administration, test monitoring and interpretation of results, foot care, diet manipulation, etc.) b. Proper screening of blood glucose level c. Constantly monitor the blood sugar, urine (for any protein or ketones), blood pressure, and weight. d. Instruct the patient to have an annual eye and kidney exam. e. Examine the feet for any unusual blood circulation, loss sensation, and skin integrity. C. Tertiary Prevention a. Monitor and administer Insulin and OHA therapy as ordered by the physician. b. Monitor signs for complications like atherosclerosis and microangiopathy, and renal failure. c. Ensure compliance to medication regimens, monitor changes, and assist them in maintaining self-sufficiency in daily life. d. Prevent the occurrence of further complexities through proper medication. VIII. Reference Cited https://www.news-medical.net/health/History-of-Diabetes.aspx https://www3.paho.org/hq/index.php?option=com_content&view=article&id =6721:2012-interventions-prevention-management-diabetes-obesity https://www.mayoclinic.org/diseases-conditions/diabetes/diagnosistreatment/drc-20371451 https://en.wikipedia.org/wiki/History_of_diabetes Page 5