Pathophysiology Of Type 1 Diabetes

People with diabetes are able to eat exactly like the rest of their family does. Modern day nutrition guidelines for those with diabetes offer quite a few choices, they are flexible and allow diabetics to fit in special-occasion or favorite foods. A healthy diet consisting of whole grains, vegetable, fruits, heart healthy fats and lean proteins should be kept by everyone regardless of whether or not they are diabetic.

Fats that are found in oils, margarine and salad dressings do not immediately affect the blood glucose levels. That being said eating a fatty meal can slow down the process of digestion making it more difficult for your insulin to work, this could possibly cause elevated glucose levels hours after you have eaten.

Your blood cholesterol can be raised by some fats which increases the risk of a stroke or heart attack. These unhealthy fats are called trans fat and saturated fat and should be limited.
Shortening, butter, milk, cheese and red meat are all sources of saturated fat. Some snack foods, margarine and fast foods contain trans fats. Fat is also very high in calories so if your are trying to lose weight you should avoid it.


Insulin enables glucose uptake by adipose tissue and resting skeletal muscle. Insulin binds to receptor, initiates the synthesis of glucose transporters (GLUT 4) , the GLUT 4 transpor proteins are integrated into the cell membrane allowing glucose to be transported into the cell. In the absence or low of insulin, glucose cannot enter the cell. (Type 1 Diabetes) Normal liver cell. Insulin acts indirectly to alter glucose uptake in hepatocytes: in fed state liver cells take up glucose. Type 1 Dieabetes liver cell. A hepatocyte in the fasted state makes glucose and transports it out into the blood.

The major metabolic derangements, which result from insulin deficiency in IDDM are impaired glucose, lipid and protein metabolism which are explained in details as follows: -Effects on glucose metabolism Uncontrolled IDDM -Effect on lipid metabolis. -Effects on protein. Leads to Hyperglycemia -Life threatening medical emergency, high mortality rate. Characterized by Plasma osmolarity 340 mOsm/L or greater (normal: 280 -300) Blood glucose severely elevated, 600 – 1000 or 2000 (normal 70-110) Altered level of consciousness With progressive dehydration, acidosis, hyperosmolality, and diminished cerebral oxygen utilization, consciousness becomes impaired, and the patient ultimately becomes comatose.

Although other islet cell types [alpha cells (glucagon-producing), delta cells (somatostatin-producing), or PP cells (pancreatic polypeptide-producing)] are functionally and embryologically similar to beta cells and express most of the same proteins as beta cells, they are inexplicably spared from the autoimmune process.

Pathologically, the pancreatic islets are infiltrated with lymphocytes (in a process termed insulitis). After all beta cells are destroyed, the inflammatory process abates, the islets become atrophic, and most immunologic markers disappear. The precise mechanisms of beta cell death are not known but may involve the formation of nitric oxide metabolites, apoptosis, and direct CD8+ T cell cytotoxicity. The autoimmune destruction of pancreatic β-cells leads to a deficiency of insulin secretion. It is this loss of insulin secretion that leads to the metabolic derangements associated with IDDM.


In addition to the loss of insulin secretion, the function of pancreatic α-cells is also abnormal. There is excessive secretion of glucagon in IDDM patients. Normally, hyperglycemia leads to reduced glucagon secretion. However, in patients with IDDM, glucagon secretion is not suppressed by hyperglycemia. The resultant inappropriately elevated glucagon levels exacerbate the metabolic defects due to insulin deficiency .The most pronounced example of this metabolic disruption is that patients with IDDM rapidly develop diabetic ketoacidosis in the absence of insulin administration. Particularly problematic for long term IDDM patients is an impaired ability to secrete glucagon in response to hypoglycemia. This leads to potentially fatal hypoglycemia in response to insulin treatment in these patients.

Although insulin deficiency is the primary defect in IDDM, in patients with poorly controlled IDDM there is also a defect in the ability of target tissues to respond to the administration of insulin. There are multiple biochemical mechanisms that account for this impairment of tissues to respond to insulin. Deficiency in insulin leads to elevated levels of free fatty acids in the plasma as a result of uncontrolled lipolysis in adipose tissue. Free fatty acids suppress glucose metabolism in peripheral tissues such as skeletal muscle. This impairs the action of insulin in these tissues, i.e. the promotion of glucose utilization.

Additionally, insulin deficiency decreases the expression of a number of genes necessary for target tissues to respond normally to insulin such as Glucokinase in liver and the GLUT 4 class of glucose transporters in adipose tissue. The major metabolic derangements which result from insulin deficiency in IDDM are impaired glucose, lipid and protein metabolism.