By Afnan Ali Ibrahim, hamideh talei farkhondeh
Biotechnology Department, Faculty Of Applied Science
UCSI University, Malaysia

Diabetes mellitus is a serious, lifelong condition that represents a group of metabolic disorders in which there is impaired glucose utilization, inducing hyperglycemia. A defective or deficient insulin secretory response underlies the glucose underutilization. Fat and protein metabolism are also commonly affected. The cause of diabetes is a mystery, although both genetics and environment appear to play roles.
There are two major types of diabetes: Insulin-Dependent (type 1), Non-Insulin-Dependent (type2). Of all diabetic patients, 10% have type 1 and 90% have type 2. [4] Type 1 patients are unable to produce insulin and must receive exogenous insulin to survive. On the other hand, type 2 patients have at least partially preserved insulin secretion, but are often insulin resistant. [3,5] Generally these two major types of diabetes have different pathogenetic mechanisms and metabolic characteristics, the chronic, long-term complications in blood vessels (microangiopathy, atherosclerosis), kidneys (diabetic nephropathy), eyes (retinopathy) and nerves (neuropathy), occur in both types and are the major causes of morbidity and death in diabetes.[5,6] The pathogenesis of the two types will be discussed separately, but first we briefly discuss glucose homeostasis, since some aspects of insulin release and action are important in the discussion of pathogenesis. [5]

Maintenance of an adequate supply of glucose in the blood is essential for the proper functioning of neuronal cells. This task is accomplished by two hormones produced by the pancreas: insulin and glucagon. Glucose homeostasis is a physiologically well-balanced mechanism depending on three coordinated and simultaneously ongoing processes involving insulin secretion by the pancreas, glucose production in the liver and, uptake of glucose by peripheral tissues (mostly muscle tissue). Insulin secretion is modulated such that glucose production and utilization rise or fall to maintain normal blood glucose levels. [2] This diagram below shows how insulin and glucagon control blood glucose homeostasis

figure1 : Homeostasis of Insulin and Glucagon in Controlling Blood Glucose (Pearson education. Inc)

Insulin reduces blood glucose and fatty acids by facilitating entry of glucose into the cells of target tissues and helping to convert these substances for storage as glycogen, triglycerides, and protein. Glucagon works to preserve glucose and fatty acids from conversion and to increase glucose output by the liver. Insulin and glucagon (along with other hormones) balance the overall levels of glucose and fatty acids in the blood to maintain a steady state. Dysfunction in glucose metabolism is generally the result of either deficiencies or excess in these hormones, as well as resistance to hormone action by target tissues. [2]

The inability to secrete adequate amounts of insulin is known as type 1 diabetes mellitus caused by the reduction in the beta cell mass. This disorder usually develops in childhood, becoming manifest and severe at puberty. Generally patients require multiple daily injections of insulin to maintain blood glucose levels. Without insulin, they develop acute metabolic complications, such as ketoacidosis and coma. Its etiology appears to involve three interlocking mechanisms: genetic susceptibility, autoimmunity, and environmental insult, these factors are responsible for the islet cell destruction. [3,5] Much less is known, about the pathogenesis of non-Insulin-Dependent (type2) diabetes, which is by far the most common type that results from the body's inability to make enough or properly use insulin. The causes are largely unidentified genetic factors and the effects of unhealthy lifestyle, People suffering from this disorder are usually overweight and even obese.

Some of the warning signs and symptoms of type 1 and 2 diabetes are summarized below:-
Type 1 Diabetes:
Type 2 Diabetes:
§ Frequent urination(polyuria).
§ Unusual thirst (Polydipsia).
§ Extreme hunger.
§ Unusual weight loss.
§ Extreme fatigue
§ Irritability.
§ Any of the type 1 symptoms, plus
§ Frequent infections.
§ Blurred vision.
§ Cuts/bruises that is slow to heal.
§ Tingling/numbness in the hands or feet.
§ Recurring skin, gum, or bladder infections

figure 2 : Signs and symptoms illustration by Mikael Häggström

There is extreme variability among patients in the time of onset, the severity of these complications and the particular organ or organs involved. There are several Diabetes complications and it can be divided in two sections (Acute and chronic).

figure 2: complications of diabetes mellitus

An example of diabetes mellitus complication : The diabetic foot which is one of the common problems that diabetic people develop. It spreads so quickly at a little carelessness can make it severe.
figure 3 : gangrene

Diabetes mellitus is now a major global public health problem. The prevalence of diabetes is noted to vary with ethnicity. However, the developing and newly industrialized nations, and the disadvantaged community groups in the developed countries are said to be at highest risk of having diabetes. It has also been demonstrated that as age increases, the risk of having diabetes and hence the prevalence of diabetes increases. There are several approaches employed to reduce risk for diabetes. To reach the greatest success in reducing the incidence and prevalence of diabetes, both a high risk and a population-based approach should be employed. Pharmacologic therapy or lifestyle modification programs can be used to prevent the risk for development of type 2 diabetes. However, lifestyle modification should be considered first-line therapy. Life style modifications aimed at losing weight, getting more exercise and include establishing and maintaining healthy lifestyle behaviors (e.g. diet and physical activity) and achieving and maintaining a healthy body weight. Knowler. Et al.(2002).

Finally click here to watch this overview about Diabetes [1]

complications overview

1. Vincent J. M. Di Maio, Dominick J. Di Maio. 2001.Forensic pathology. 2nd edition. Page 79-81.
2. Phillip M. Kleespies . 2000. Emergencies in Mental Health Practice: Evaluation and Management. Guilford Press. Diabetes mellitus p-343.
3. Glucose Homeostasis and Diabetes.

4. Günter Klöppel and Andreas Clemens. (2007). Insulin-dependent diabetes mellitus: Islet changes in relation to etiology and pathogenesis. Endocrine Pathology, vol.8, No.4, 273-282.
5. Ramzi S.Cotran, Stanley L. Robbins , Vinay Kumar. (1994). Pathologic basis of disease. 5th edition. Saunders Company.
6. Long term complications of diabetes []
7. K. N. Mathur. 2001. Diabetes Mellitus. B. Jain Publishers.
8. Nicholas Vardaxis. 2010. A Textbook of Pathology. 2nd edition, p-448.

9. Knowler WC, Barrett-Connor E, Fowler SE, Hamman RF, Lachin JM. Reduction in the incidence of type 2 diabetes with lifestyle intervention or metformin. N Engl J Med 2002; 346: 393–403.
10. Dr. Tam Hoang Nguyen .diabetes mellitus . []
11. diabetic food care .[]