Type 1 diabetes

Type 1 diabetes is an autoimmune disease - the person's body has destroyed his/her own insulin-producing beta cells in the pancreas.

People with Diabetes Type 1 are unable to produce insulin. Most patients with Diabetes Type 1 developed the condition before the age of 40. Approximately 15% of all people with diabetes have Type 1.

Type 1 diabetes is fatal unless the patient regularly takes exogenous insulin. Some patients have had their beta cells replaced through a pancreas transplant and have managed to produce their own insulin again.

Type 1 diabetes is also known as juvenile diabetes or childhood diabetes. Although a large number of diabetes Type 1 patients become so during childhood, it can also develop after the age of 18. Developing Type 1 after the age of 40 is extremely rare.

Type 1, unlike Type 2, is not preventable. The majority of people who develop Type 1 are of normal weight and are otherwise healthy during onset. Exercise and diet cannot reverse Type 1. Quite simply, the person has lost his/her insulin-producing beta cells. Several clinical trials have attempted to find ways of preventing or slowing down the progress of Type 1, but so far with no proven success.

A C-peptide assay is a lab test that can tell whether somebody has Type 1 or Type 2. As external insulin has no C-peptide a lack of it would indicate Type 1. The test is only effective when ALL the endogenous insulin has left the body - this can take several months.



What is Type 1 Diabetes?
http://www.youtube.com/watch?v=_OOWhuC_9Lw




Type 2 diabetes

A person with diabetes type 2 either:

Does not produce enough insulin. Or
Suffers from 'insulin resistance'. This means that the insulin is not working properly.
The majority of people with Type 2 have developed the condition because they are overweight. Type 2 generally appears later on in life, compared to Type 1. Type 2 is the most common form of diabetes.

In the case of insulin resistance, the body is producing the insulin, but insulin sensitivity is reduced and it does not do the job as well as it should do. The glucose is not entering the body's cells properly, causing two problems:

A build-up of glucose in the blood.
The cells are not getting the glucose they need for energy and growth.
In the early stages of Type 2 insulin sensitivity is the main abnormality - also there are elevated levels of insulin in the blood. There are medications which can improve insulin sensitivity and reduce glucose production by the liver.

As the disease progresses the production of insulin is undermined, and the patient will often need to be given replacement insulin.

Many experts say that central obesity - fat concentrated around the waist in relation to abdominal organs - may make individuals more predisposed to develop Type 2 diabetes.

Central obesity does not include subcutaneous fat - fat under the skin. The fat around your waist - abdominal fat - secretes a group of hormones called adipokines. It is thought that adipokines may impair glucose tolerance.

The majority of people who develop diabetes Type 2 were overweight during the onset, while 55% of all Type 2 patients were obese during onset.


It is not uncommon for people to achieve long-term satisfactory glucose control by doing more exercise, bringing down their bodyweight and cutting down on their dietary intake of carbohydrates.

However, despite these measures, the tendency towards insulin resistance will continue, so the patient must persist with his/her increased physical activity, monitored diet and bodyweight.

If the diabetes mellitus continues the patient will usually be prescribed orally administered anti-diabetic drugs. As a person with Type 2 does produce his/her own insulin, a combination of oral medicines will usually improve insulin production, regulate the release of glucose by the liver, and treat insulin resistance to some extent.

If the beta cells become further impaired the patient will eventually need insulin therapy in order to regulate glucose levels.


What is Type 2 Diabetes?
http://www.youtube.com/watch?v=nBJN7DH83HA



This post has been edited by greenlife: Apr 30 2012, 04:15 PM

many unaware they have diabetes very late...




This post has been edited by greenlife: Apr 30 2012, 04:11 PM

Diabetes Types 1 and 2 are chronic medical conditions - this means that they are persistent and perpetual. Gestational Diabetes usually resolves itself after the birth of the child.

Symptoms of Diabetes

People can often have diabetes and be completely unaware. The main reason for this is that the symptoms, when seen on their own, seem harmless. However, the earlier diabetes is diagnosed the greater the chances are that serious complications, which can result from having diabetes, can be avoided.

Here is a list of the most common diabetes symptoms:

Frequent urination
Have you been going to the bathroom to urinate more often recently? Do you notice that you spend most of the day going to the toilet? When there is too much glucose (sugar) in your blood you will urinate more often. If your insulin is ineffective, or not there at all, your kidneys cannot filter the glucose back into the blood. The kidneys will take water from your blood in order to dilute the glucose - which in turn fills up your bladder.

Disproportionate thirst
If you are urinating more than usual, you will need to replace that lost liquid. You will be drinking more than usual. Have you been drinking more than usual lately?

Intense hunger
As the insulin in your blood is not working properly, or is not there at all, and your cells are not getting their energy, your body may react by trying to find more energy - food. You will become hungry.

Weight gain
This might be the result of the above symptom (intense hunger).

Unusual weight loss
This is more common among people with Diabetes Type 1. As your body is not making insulin it will seek out another energy source (the cells aren't getting glucose). Muscle tissue and fat will be broken down for energy. As Type 1 is of a more sudden onset and Type 2 is much more gradual, weight loss is more noticeable with Type 1.

Increased fatigue
If your insulin is not working properly, or is not there at all, glucose will not be entering your cells and providing them with energy. This will make you feel tired and listless.

Irritability
Irritability can be due to your lack of energy.

Blurred vision
This can be caused by tissue being pulled from your eye lenses. This affects your eyes' ability to focus. With proper treatment this can be treated. There are severe cases where blindness or prolonged vision problems can occur.

Cuts and bruises don't heal properly or quickly
Do you find cuts and bruises take a much longer time than usual to heal? When there is more sugar (glucose) in your body, its ability to heal can be undermined.

More skin and/or yeast infections
When there is more sugar in your body, its ability to recover from infections is affected. Women with diabetes find it especially difficult to recover from bladder and vaginal infections.

Itchy skin
A feeling of itchiness on your skin is sometimes a symptom of diabetes.

Gums are red and/or swollen - Gums pull away from teeth
If your gums are tender, red and/or swollen this could be a sign of diabetes. Your teeth could become loose as the gums pull away from them.

Frequent gum disease/infection
As well as the previous gum symptoms, you may experience more frequent gum disease and/or gum infections.

Sexual dysfunction among men
If you are over 50 and experience frequent or constant sexual dysfunction (erectile dysfunction), it could be a symptom of diabetes.

Numbness or tingling, especially in your feet and hands
If there is too much sugar in your body your nerves could become damaged, as could the tiny blood vessels that feed those nerves. You may experience tingling and/or numbness in your hands and feet.




This post has been edited by greenlife: May 1 2012, 10:53 AM

What is insulin?
Insulin is a hormone. It makes our body's cells absorb glucose from the blood. The glucose is stored in the liver and muscle as glycogen and stops the body from using fat as a source of energy.

When there is very little insulin in the blood, or none at all, glucose is not taken up by most body cells. When this happens our body uses fat as a source of energy. Insulin is also a control signal to other body systems, such as amino acid uptake by body cells. Insulin is not identical in all animals - their levels of strength vary.

Porcine insulin, insulin from a pig, is the most similar to human insulin. Humans can receive animal insulin. However, genetic engineering has allowed us to synthetically produce 'human' insulin.

This post has been edited by greenlife: May 2 2012, 09:10 AM

The EVGN/EMVBM Meeting report also provides a putative molecular explanation that may contribute to the outcome of "PROactive", a broad clinical study that very recently demonstrated that pioglitazone significantly reduced the combined risk of heart attacks, strokes and death by 16% in high-risk patients with type 2 diabetes.

All In One: A Diabetes Drug, An Anticancer Drug And An Antiocclusive Drug

Thiazolidinediones (also called glitazones), drugs used to treat insulin-resistance in patients with type 2 diabetes, inhibit vascular cell proliferation by activating a known cancer suppressor gene: p16. This result, which could lead to the development of selective and non-invasive therapies for post-bypass surgery, was shown today during the Second Annual European Vascular Genomics (EVGN – evgn) Conference.

medical journal reports on PPARs

http://ajpendo.physiology.org/content/288/2/E287.full

Like the role of vitamins in 20th century, PPARs (Peroxisome Proliferators Activated Receptors) will represent the most important biomedical molecules in the 21st century.

PPARγ-mediated insulin sensitization: the importance of fat versus muscle

Peroxisome proliferator-activated receptor-γ (PPARγ) is a nuclear hormone receptor that functions as a transcriptional regulator in a variety of tissues. PPARγ activation, e.g., through binding of the synthetic glitazones or thiazolidinediones (TZD), results in a marked improvement in type 2 diabetic patients of insulin and glucose parameters resulting from an improvement of whole body insulin sensitivity. The role of different metabolic tissues (fat, skeletal muscle, liver) in mediating PPARγ function in glucose and insulin homeostasis is still unclear. Recently, the function of PPARγ in adipose tissue and skeletal muscle has been intensively characterized by using targeted deletion of PPARγ in those tissues. In those studies, adipose PPARγ has been identified as an essential mediator for the maintainance of whole body insulin sensitivity. Two major mechanisms have been described. 1) Adipose PPARγ protects nonadipose tissue against excessive lipid overload and maintains normal organ function (liver, skeletal muscle); and 2) adipose PPARγ guarantees a balanced and adequate production of secretion from adipose tissue of adipocytokines such as adiponectin and leptin, which are important mediators of insulin action in peripheral tissues. In contrast to studies in adipose-specific PPARγ-deficient mice, the data in muscle-specific PPARγ−/− mice demonstrate that whole body insulin sensitivity is, at least in part, relying on an intact PPARγ system in skeletal muscle. Finally, these early and elegant studies using tissue-specific PPARγ knockout mouse models pinpoint adipose tissue as the major target of TZD-mediated improvement of hyperlipidemia and insulin sensitization.

peroxisome proliferator-activated receptor-γ (PPARγ) belongs to the family of PPARs, which also includes the isoforms PPARα and PPARδ. The PPARγ gene gives rise to at least three mRNAs, PPARγ1, PPARγ2, and PPARγ3, that differ at their 5′ end as a consequence of alternate promoter usage and splicing.

http://www.medscape.org/viewarticle/514729
Targeting Insulin Resistance: PPARs, Type 2 Diabetes, and Cardiovascular Risk

Introduction
Insulin resistance (IR) is widely recognized as a core physiologic defect contributing to the development of both type 2 diabetes and cardiovascular disease (CVD).The majority of individuals with type 2 diabetes are known to be insulin-resistant, and this IR, when coupled with an inadequate pancreatic beta-cell response, results in hyperglycemia.[1] Both clinical and epidemiologic data support the association between IR and an increase in CVD risk. IR is associated with the development of a cluster of characteristic CVD risk factors, including hypertension; an atherogenic dyslipidemia (characterized by low high-density lipoprotein cholesterol [HDL-C], increased triglycerides, and an increase in the prevalence of small, dense low-density lipoprotein [LDL] particles); and a proinflammatory, prothrombotic vascular environment, all of which likely contribute to the increase in CVD risk observed.

Given the accepted role of IR in the pathogenesis of diabetes and CVD, therapies that improve insulin action are used commonly for the management of hyperglycemia in diabetes. Moreover, there is significant interest in diabetes therapies that may limit CVD risk. Specifically, the impact of peroxisome proliferator activating receptor (PPAR)-gamma agonists, such as the thiazolidinediones (TZDs) on both diabetes control and CVD risk, has been widely discussed. These PPAR activators are well known to improve glucose control -- in great part by improving insulin action in the periphery -- and may improve a number of CVD risk factors, including hypertension, dyslipidemia, and the vascular, hemodynamic, and hemostatic abnormalities that are common in those with diabetes.

This post has been edited by greenlife: May 4 2012, 09:20 PM

Diabetes is NO MORE Silent Killer, Crypto PPARS
http://forum.lowyat.net/topic/2261881

this is the impact of peroxisome proliferator activating receptor (PPAR)-gamma agonists, such as the thiazolidinediones (TZDs) on both diabetes control and CVD risk, has been widely discussed...
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