Human Anatomy, Physiology, and Medicine. Anything human!

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Post by mrsmile » Sun Jan 03, 2010 9:43 am

Ok...guys...here's a passage from an article i read a few days ago...
it says:
"Before diabetes sets in, a person develops insulin resistance and suffers from it in silence for amny , many years. This condition affects your muscle, fat, and liver cells. The receptors in these cells become less sensitive to insulin and are not able to utilise the hormone properly. glucose, therefore, is unable to gain access into these cells.
The resulting high blood glucose level continues to signal the pancreas to release more insulin into the bloodstream, while the liver produces excessive glucose in response to the energy-starved cells.
Eventually, this compensation mechanism fails to work. The poor pancreas- under great pressure- is unable to meet insulin demand after meals, resulting in excess glucose in the bloodstream.
Many people with insulin resistance have high levels of blood glucose and insulin simultaneously circulating in the bloodstream." (taken from HealthToday Magazine)

(Apologies if there's any typing error....and sorry i could only provide so much information...)

So, here are some questions:
1) How does insulin resistance(of the cell) happen?
2) How does insulin help cells in making entry for glucose into cells?
3) What does "the pancreas is unbale to meet the insulin demands" in paragraph 4 means? Does this mean that the pancreas fail? If so, how?

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Post by Hodag » Sun Jan 03, 2010 2:01 pm

When food is digested, the sugars wind up in the blood stream. Insulin is a protein that can bind to the glucose molecules and to surface receptors on cells. When blood sugar spikes due to eating a meal or drinking something sweet, the pancreas produces insulin which then binds all the glucose and serves as a transporter mechanism to get the sugar to the cells.

When insulin spikes too often (i.e. too much sugar in the diet) the cells react by producing fewer surface receptors. Over time, there are fewer and few receptors available for the insulin and the patient becomes "insulin resistent". Certain "fast sugars" do not need insulin for transport, but they still upregulate insulin production which leaves the body craving sugar because the insulin has nothing to transport. Some junk foods contain a high ratio fo these fast sugars that bump your insulin levels but leave you craving for more food.

However, this is not a lost cause as insulin resistence is not necessarily permanent! Increasing the amount of exercise you get will increase the number of mitochondria in the body, and all those hungry little mitochondria need to be fed! The only energy mitochondria use is ATP and the source of ATP is conversion of glucose, so increasing the number of mitochondria will force your body to produce more insulin receptors. Getting certain other foods in the diet, such as "good fats" will stimulate a different class of receptor, PPAR-gamma, which regulates metabolism and when properly stimulated will make the body more insulin sensitive (a good thing).

If you a really interested in this topic, I can suggest the bood "Ultrametabolism" by Mark Hyman as a starting point. The science is well researched and is presented in layman's terms, although the writing style is a tad repetitive. It was a NY Times best seller a few years ago and your local library probably has several copies.

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Post by Darby » Mon Jan 04, 2010 11:35 pm

There are a few things wrong with the initial description -

Insulin increases uptake in cells (but insulin does not bind directly to glucose, or any sugar for that matter) that are going to store it - this does not interfere with their being able to take glucose in for their own uses. They don't get energy-starved, and the release of the liver's stored glucose wouldn't be affected.

And I'm afraid that the stuff about mitochondria and insulin receptors makes no metabolic sense at all.

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