Homeostasis and Chronic Disease: Diabetes

Introduction

Diabetes is a chronic clinical condition that occurs whenever there is failure or disturbance in insulin hormone production and thus the blood sugar regulation in the body, which is also known as blood sugar homeostasis. The progressive disease clinically manifests itself when there is improper body production or utilization in insulin, which is a physiological hormone that converts simple sugars, starch and other carbohydrate foods into glycogen the energy store of the body (Advanced Medical Assistant Custom Web Design, LLC 2007). There is a physiological regulation of blood glucose in the body; at an approximate range of about 125 mg/dL of blood and above this triggers the release of this hormone and thus conversion of the excess sugar in blood circulation into glycogen. Two types of diabetes are can be either Type 1 (primary) diabetes found in early childhood, in which the body fails to produce adequate insulin; and its etiology is associated with autoimmune or viral or Type 2 (secondary) diabetes which is the most common in our community and is mostly a consequence of changes in lifestyle choices for instance obesity, lack of or inadequate levels of exercise and the consumption of detrimental foods (poor diets). Rarely, there is a third type of diabetes which is known as Type 3/gestational diabetes, which affects women at times during pregnancy but it regresses away after pregnancy; however, half of these cases will progress into Type 2 diabetes within a duration of about five years on parturition (Sateesh & Behera, 2007).

Biological molecules involved

Blood sugar level regulation (glucose homeostasis) is a physiologically well-balanced system that depends on three synchronized and simultaneously continuing processes linking insulin secretion by the pancreas’ beta cells, hepatic glucose yield and glucose uptake by splanchnic and peripheral tissues stores. Glucose is the only source of energy for the brain and it is also preferentially utilized during initial stages of muscle exercise. Due to a minute amount of glucose in the extracellular fluid (only 20 g.), continuous provision of glucose to the brain and other tissues is therefore vital, hence there is a need for metabolic fuels storage in form of glycogen. Despite this, the amount of available glycogen storage capacity is approximately 75 g in the liver and 400 g in the muscles, and these stores are limited since the Liver (which is a major glycogen store) can supply glucose for no longer than 16 h (Sateesh & Behera, 2007). This occurs temporarily before the body attains a safeguarded continuous supply of glucose for prolonged periods through the transformation of noncarbohydrate compounds into glucose during gluconeogenesis.

What physiological systems are affected and affected by this imbalance

Digestion of the ingested food materials converts sugars (from foods) into glucose (a simple sugar), and this sugar forms the body’s primary fuel when this blood glucose is broken down to release energy in form of ATP and water in the process of glycolysis. The beta cells of the pancreas as stimulated by the increased blood sugar levels beyond 125 mg/dL, release the hormone insulin which enables glucose to pass from the bloodstream into the body’s cells as glycogen (stored energy) for a later use as the body’s energy requirements. Usually this stored body energy, on top of the energy body requirement is deposited in liver and muscle cells as glycogen, and this can be converted back into glucose by another hormone (glucagon) especially when the blood glucose levels in the body diminish. However, if the receptors for insulin stimulus are lost (insulin resistance development), then normal levels of insulin fail to produce a normal insulin response, even if there is elevated production of the hormone by the Beta cells. This then limits the glucose absorption into the cells with its deficiency, and there will be a lack or improper storage of glycogen in the liver and muscles. Glucose blood remains high and the pancreas responds by attempting to produce more insulin, but this can ultimately exhaust the beta cells, which will no longer continue to produce more insulin for elevated blood glucose (Sateesh & Behera, 2007). Later on the beta cells, themselves become dysfunctional, with less insulin production (insulin deficiency) at the same time as blood glucose levels continue to increase. This can finally cause beta-cell apoptosis, or programmed cell death and further worsen the situation of diabetes.

Diabetic patients lack or have only trace amounts of insulin hormone in plasma but the plasma levels of glucagon hormone are highly elevated. This leads to an inability of their bodies to convert blood glucose into glycogen for storage, and this leads to hyperglycemia (elevated blood sugar levels). This consequently inhibits the process of glycolysis and lipogenesis and on the other hand stimulates physiological processes such as glycogenolysis, lipolysis, ketogenesis, and gluconeogenesis. The liver becomes a principal producer of glucose and this increased endogenous glucose secretion plus impaired glucose transfer leads to fasting hyperglycemia. Excess production of acetyl CoA also stimulates Ketogenesis and if there are no compensatory mechanisms the patient develops ketonemia and consequently ketonuria (Guyton & Hall, 2005). Excess production of acetoacetic and beta-hydroxybutyric acids lowers blood pH, below the normal range of 7.37-7.44 hence metabolic acidosis results. Eventually, renal excretion of a large quantity of glucose leads to osmotic diuresis and the patient develops polydipsia of polyuria and dehydration via fluid loss and this diabetic ketoacidosis is a life-threatening disease.

Prevention of diabetes

Diabetes can be prevented through proper diet and subjection to exercises, to make use of the glucose which is found in the blood.

References

  1. Advanced Medical Assistant Custom Web Design, LLC (2007), Blood Sugar Regulation (Homeostasis), the important roles of insulin and glucagon: an article on Diabetes and Hypoglycemia
  2. Guyton A.C. & Hall J.E., (2005), Insulin, Glucagon and diabetes mellitus: Textbook of Medical Physiology; 11 ed. 961-978
  3. Sateesh B., & Dayanidhi Behera (2007), Glucose Homeostasis and Diabetes: Our e-journal “Pharmaceutical Reviews “(ISSN 1918-5561), Pharmainfo.net journal.
  4. Rang H.P, Dale M.M, Ritter J.M and Moore P.K. (2003), Endocrine disorders: Pharmacology; 5 ed. 384-385