What Is The Difference Between Diabetes 1 And Diabetes 2?

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Main Category: Diabetes
Also Included In: Endocrinology
Article Date: 15 May 2009 - 0:00 PDT

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Before we look at the difference between diabetes 1 and diabetes 2, let's firstly look at diabetes in general: Diabetes, termed diabetes mellitus, is a metabolism disorder. Metabolism refers to how the body uses and digests food for growth and energy. Most of the food we consume is broken down into glucose. Glucose is a type of sugar in the blood - it is the main source of food for our bodies (our cells). When food is digested it eventually enters our bloodstream in the form of glucose. Cells utilize the glucose for growth and energy. However, without the help of insulin, the glucose cannot enter our cells. Insulin, a hormone, is produced in the pancreas. After consuming food the pancreas automatically releases an appropriate quantity of insulin to transport the blood glucose into the cells, thus lowering blood sugar levels.

If you have diabetes, the amount of blood glucose is too high - a condition called hyperglycemia. This happens for one of two main reasons:

• The body is producing no insulin - this is Diabetes Type 1
• The cells do not respond correctly to the insulin - this is Diabetes Type 2

Consequently, excessive amounts of glucose accumulate in the blood. This blood glucose overload is eventually passed out of the body in urine. Even though the blood has plenty of insulin, the cells of a person with diabetes are not getting their crucial energy and growth requirements.

What is type 1 diabetes?

In Type 1 Diabetes, the person's own body has destroyed the insulin-producing beta cells in the pancreas. When your own body destroys good stuff in your body it has what is called an autoimmune disease. Diabetes Type 1 is known as an autoimmune disease.

Quite simply - a person with Diabetes Type 1 does not produce insulin. In the majority of cases this type of diabetes appears before the patient is 40 years old. That is why this type of diabetes is also known as Juvenile Diabetes or Childhood Diabetes. Diabetes Type 1 onset can appear after the age of 40, but it is extremely rare. About 15 per cent of all diabetes patients have Type 1.

People with Type 1 have to take insulin regularly in order to stay alive.

Diabetes Type 1 is not preventable, it is in no way the result of a person's lifestyle. Whether a person is fat, thin, fit or unfit, makes no difference to his or her risk of developing Type 1. In the case of Diabetes Type 2, much of its onset is the result of bodyweight, fitness and lifestyle. The vast majority of people who develop Type 1 are not overweight, and are otherwise healthy during onset. You cannot reverse or prevent Type 1 by doing lots of exercise or eating carefully. Quite simply, the Diabetes Type 1 patient has lost his/her beta cells. The beta cells are in the pancreas; they produce insulin.

What is type 2 diabetes?

Person with Diabetes Type 2 has one of two problems, and sometimes both:

1. Not enough insulin is being produced.
2. The insulin is not working properly - this is known as insulin resistance.

The vast majority of patients who develop Type 2 did so because they were overweight and unfit, and had been overweight and unfit for some time. This type of diabetes tends to appear later on in life. However, there have been more and more cases of people in their 20s developing Type 2, but it is still relatively uncommon.

Approximately 85% of all diabetes patients have Type 2.

Insulin resistance

The body produces insulin, but its insulin sensitivity is undermined and does not work as it should do - glucose in not entering the body's cells properly. Consequently, blood sugar levels rise, and the cells are not getting their required nutrients for energy and growth.

The problem is with the cells - they are not responding to insulin like they used to. Experts are not sure what exactly is happening when cells stop responding well to insulin. Below is a simple explanation of why insulin resistance happens:

• Cells build up insulin resistance anyway
  Each time your cells are exposed to insulin they build up a bit of resistance.


• Lots of food triggers more insulin production
  If a person is eating a lot he will be producing more insulin than somebody who doesn't.


• Too much insulin is toxic for the cells
  If the exposure to insulin is high the cell will try to protect itself from intoxication - it will down-regulate its receptor activity and the number of receptors so that it does not have to be subjected to all that stimuli all the time.


• Frequent high insulin speeds up the process
  If the cell's exposure to high insulin is frequent the insulin resistance will grow faster.


• The pancreas puts out more insulin
  If the insulin is not doing its job properly the pancreas will put out more of it - a vicious circle.

The insulin resistance will reach a point in which the amount of insulin produced by the pancreas is not enough to make up for the cells lower response. At this point the person will have to take additional insulin.

Lack of physical activity, being overweight, and some genetic factors make it much more likely that the cells build up insulin resistance more quickly. It is important to remember that insulin resitance is not the insulin not responding properly, it is the cells not responding properly to insulin.

Unfortunately, insulin resistance can lock a patient into a another vicious circle, because insulin resistance itself promotes weight gain. So, if people are insulin resistant because they are overweight, the excess pounds are harder to get rid of because of it.

According to Medilexicon's medical dictionary, insulin resistance is a "diminished effectiveness of insulin in lowering plasma glucose levels, arbitrarily defined as a daily requirement of at least 200 units of insulin to prevent hyperglycemia or ketosis; usually due to binding of insulin or insulin receptor sites by antibodies; associated with obesity, ketoacidosis, and infection."

Written by Christian Nordqvist

Original article date: 21 Apr 2004
Article updated: 15 May 2009

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