Thursday, October 15, 2009

Help From Biotechnology for Diabetes Mellitus

Biotechnology Help for Diabetes Mellitus

Current research has indicated that up to four injections per day of insulin is protocol. Even better, an insulin pump to reduce vascular and renal complications of Type I diabetics.

Now, if you add a glucose sensor and a miniature computer to an insulin pump you have just manufactured an artificial pancreas that would dispense insulin as needed.

Mist inhalers and insulin patches are other methods of administering insulin.

Pancreatic Islet Cell Transplants are increasing in their ability to help Type I diabetics. The limiting factor in islet transplantations is the need for long-term immunosuppression.

The side effects from immunosupressant drugs may cause complications. Thus, pancreatic islet transplantations are only used for patients that cannot control their diabetes any other way.

For those of you that have Type II diabetes the worry about ketoacidosis is far less but the other complications that afflict Type I diabetics still exist for you. Heredity or a familial predisposition is very strong for Type II diabetics. An estimated 25 to 30 percent of Americans carry a gene that predisposes them to Type II diabetes, with non-white populations at a far greater risk.

Most Type II diabetics produce insulin but the insulin receptors on body cells are unable to respond to it, a phenomenon called insulin resistance. Mutations in any one of several genes could lead to insulin resistance. One example is a gene called PC-1. That gene, a membrane protein gene, causes that membrane protein to react strongly to insulin receptor that prevents the receptor from being activated.

Lifestyle can play a role. Diabetics are almost all overweight and sedentary. Adipose cells of obese folks overproduce a number of hormone-like chemicals including tumor necrosis factor alpha and adiponectin which may alter the cascade sequence triggered by insulin binding that makes it possible for your body cells to absorb glucose for metabolism.

The good news is that many Type II diabetics can control their diabetes by exercise, weight loss and a healthy diet. Some diabetics benefit from oral medications like Orinase. There is a number of drugs that are referred to as insulin resistance reducers such as Avandia.

Wednesday, October 14, 2009

Polyuria, Polydipsia and Polyphagia - Three Signs of Diabetes

Polyuria, Polydipsia and Polyphagia

We know that excess glucose in the blood that doesn't go away without some help is diabetes. This is how the three signs above are created in diabetes.

The excess glucose in the urine filtrate acts as an osmotic diuretic. Wow! big words again for us to master. 

First, a simple definition of osmosis that will never get you into trouble, well seldom, never is an impossible situation.

Osmosis is the movement of water through a selective permeable membrane (think cell membrane if you have a tiny mind like me!)from an area of low solute concentration (anything dissolved in water (the solvent) into a area of high solute concentration.

In this illustration, due to the large amount of excess glucose in the filtrate, (what the kidney filters from the blood under pressure) the glucose is the "solute molecule" and causes the concentration of solutes in the kidney filtrate to be higher than the solute concentration in the blood. Net result, instead of water being returned to the blood it is flushed out of the body in the urine! Thats called diuresis.

A diuretic, in this case, is something that inhibits water reabsorption by the blood from the kidney tubules that results in a hugh urine output that is called Polyuria.

The polyuria results in decreased blood volume and dehydration. Thats why a diabetic person experiences excessive thirst. Lets look at how that "thirst" occurs technically.

Along with water loss, which is a solvent, serious electrolytelosses also occur as the body rids itself of excess ketones.

The ketone bodies are negatively charged particles called ions. Keep in mind a balance is maintained between positive and negative ions in the body. But, in mass movements involving negative charged ketone bodies, they attract and carry positve charged ions like sodium (Na+) and potassium (K+)out of the body fluids as well. 

This creates an electrolyte imbalance in you, if you are a diabetic out of control. Because of this imbalance you get abdominal pains and may vomit, and the stress reaction  ("flight, fright and frolic") about diabetes mellitus just accelerates even more.

Vomiting expels even more water from the body and carries with it more important electrolytes. This rapid water loss, or dehydration, stimulates the hypothalmic thirst centers causing polydipsia or excerssive thirst.

If the general body cells cannot take up glucose for metabolism to take place you develop excessive hunger pangs and increase your food consumption accordingly. This is called polyphagia. You sense, correctly, that you are starving to death. Although you have plenty of glucose available, it cannot be used, and the body begins to use the fat and protein stores for metabolism.

If you are a Type I Diabetic you can develop long term vascular and neural problems. The lipidemia and high blood cholesterol levels, characteristic of the disease, can lead to severe vascular complications like atherosclerosis, strokes, heart attacks, renal shutdown, gangrene and blindness.

Hope this helps with your understanding of the course that diabetes follows in a Type I diabetic.

Homeostatic Imbalance - Diabetes mellitus - A Trip of Complications

Homeostatic Imbalance - Diabetes Mellitus

Diabetes mellitus results from either hyposecretion or hypoactivity of insulin. After a meal, when insulin is either absent or deficient, blood glucose levels remain high because glucose is unable to enter most tissue cells.

Ordinarily, when blood glucose levels rise, hyperglycemic hormones are not released, but when hyperglycemia becomes excessive, you start to feel nauseated. 

The nausea causes your body to enter the "flight-fright-frolic" response. This is a series of changes brought about by the Autonomic Nervous System and prolonged by certain members of your Endocrine System

The results are inappropriate because they normally occur in the hypoglycemic (fasting state) to make glucose available. The nausea triggers glycogenolysis (breakdown of glycogen), lipolysis (breakdown of fat) and gluconeogenesis.

These cause the already high glucose levels to soar even higher and excess glucose begins to leave the body in the urine (glycosuria).

When simple sugars, such as glucose, cannot be used as cellular fuel, more fats are mobilized and broken down for fuel. The fats produce a high fatty acid level in the blood, a condition called lipidemia or lipemia. The presence of acids in the blood increases a persons free H+ ion count which results in a lower than normal pHThis is referred to as acidosis

When a H+ ion is free, by itself, it contributes to acidity. The purpose of buffering is to combine the free H+ and take it out of body fluids. When that happens the pH of the blood increases (Becomes Basic).

In severe cases of diabetes mellitus, blood levels of fatty acids and their metabolites (acetoacetic acid, acetone and others) rise dramatically. The metabolites, collectively called ketones or ketone bodies are organic acids. They work to push down your pH even more. Your acidosis becomes more severe. Since this is due to ketones the acidosis is renamed ketoacidosis. Excess ketones spill over into the urine from the kidneys. This is called ketonuria.

Severe ketoacidosis is life threatening. One of the very good reasons to see your friendly Diabetologist if you suspect you are starting to lose control of your condition.

The severe ketoacidosis causes the nervous system to initiate rapid deep breathing (hyperpnea) to blow off carbon dioxide from the blood with the net result of temporarily increasing your pH (buffers the blood).

If ketoacidosis continues unchecked it will disrupt heart activity and oxygen transport, severely depress the nervous system which leads to coma and death.

Detection, education and control are the keys to managing diabetes.

Monday, October 12, 2009

Signaling Mechanisms for Insulin

Signaling Mechanisms for Insulin

Insulin appears to work without second messengers generated when a hormone binds to a receptor on the plasma membrane of its tissue cells, referred to as target cells.

A hormone stimulus typically produces one or more of the following changes:

1. Alters plasma membrane permeability or membrane potential , or both, by opening or closing ion channels.

2. Stimulates synthesis of proteins or regulatory molecules such as enzymes within the cell.

3. Activates or deactivates enzymes.

4. Induces secretory activity.

5. Stimulates mitosis.

The insulin receptor is a tyrosine kinase enzyme that is activated by autophosphorylation (addition of the phosphate complex ion to several of its own tyrosines ) when insulin binds. This activated insulin receptor provides docking sites for intracellular relay proteins that, in turn, initiate a series of protein phosphorylations that trigger specific cell responses.

The phosphorylated proteins begin the cascade that leads to increased glucose uptake by the cells in the body.

After glucose enters a target cell, insulin binding triggers enzymatic activities that:

2. Join glucose molecules together to form glycogen.

3. Convert glucose to fat (particularly in adipose tissue.)

Signals, whether neural, hormonal or both are important to homeostasis and your health.