Pathology of type 2 diabetes

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skyemt

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Hi...

recently heard a professor lecture about type 2 diabetes...

the pathology, according to her, lies with a problem with the insulin receptors... they do not all function properly, and at many sites, the insulin is not binding to the receptors, causing an inability of the body to use blood glucose, even though it is present, as is the insulin itself...

however, since then, i've had two instructors tell me that information is not accurate, and in fact the pathology is unknown, other than to say the body does not use the insulin "efficiently", known as insulin resistance.

does anyone have a take on this? bit confusing...

thanks
 
Ha. We just covered insulin in physio yesterday.

The problem with type 2 is twofold.

1. Defects in the second messanger cascade.
2. Down regulation of receptors from being constantly activated.
 
JPINFV said:
Ha. We just covered insulin in physio yesterday.

The problem with type 2 is twofold.

1. Defects in the second messanger cascade.
2. Down regulation of receptors from being constantly activated.
Click to expand...

okay... i appreciate your answers, but without explanations, i'm not really going to follow you...

my goal is not just to see how much everyone else knows, but to actually learn something here...

awaiting more details...

thanks!
 
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Both of the answers are correct. Those are theories that is how pathology of Diabetes, there is so much literature and research out there this forum could not hold it. I recommend looking at ADA web site, and some others for more detail explanation.

R/r 911
 
The very basic and simple explanation is as follows (since the full pathological/physiological theories are quite intricate, however if you want more info, I would be happy to dig into my old physio notes and look it up)

Obesity is often correlated with type 2 diabetes because the repetitive increase in glucose consumption cause the insulin receptors to become desensitized. The desensitization of these insulin receptors decrease the levels of insulin release thus causing the spike in blood sugar. Experts often say that to treat type 2, you must control your diet and exercise. This is because if you decrease the amount of glucose intake, there is a possibility of regaining insulin sensitivity.

Kind of the same physiological effects like sleep apnea. Snoring is the number contributing factor to sleep apnea. Since snoring is disrupting the normal flow of air and normal gas exchange, and because humans breath based on carbon dioxide levels, the CO2 receptors become desensitized due to the high concentration of CO2 present when snoring. These receptors become desensitized and may cause the individual to stop breathing, literally.

So moral of the story? Too much of a bad thing is....well bad.
 
Obesity:

1. Intracellular free fatty acids and fatty acid metabolism products decrease insulin sensitivity.

2. Obesity causes the level of hormones produced by fat cells to change (both up and down). These changes are associated with insulin resistance.

Beta cell dysfunction:

Physio primer: Insulin secretion following a meal has two peaks. The first peak is a sharp increase and represents the release of insulin that was produced and packaged between meals. The second peak is smother and smaller and represents fresh production and release of insulin.

Path:
As resistance increases, B-cells attempt to compensate by producing more insulin than unaffected individuals would. Overtime this leads to b-cell failure. This is initial seen by a decrease in insulin cycling. Overtime, this results in the destruction of the islets of Langerhans.

-Kumar, V., Abbas, A., Fausto, N., Mitchell, R. Robins Basic Pathology. 8 ed. Philadelphia: Saunders Elsevier. 2007. pg. 778-780

One of the reasons for insulin resistance is a down regulation and destruction of insulin receptors in peripheral cells due to elevated levels of resting insulin. This results in a lower density of insulin receptors on a cell. The internalization and destruction of receptor-ligand complexes is normal, the problem is the high rate of activation seen with elevated blood glucose levels. This is what leads to the lower density compared to unaffected individuals.

-Dice, J. MBS 206: Physiology. Syllabus. Tufts University School of Medicine. Unpublished. 2007. pg. E85-E87.
 
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so in addition to they type 2 pathologies, over time, if not corrected, these patients will also suffer the same maladies affecting type 1 patients, with regard to the destruction of the B cells (islet cells)?

am i understanding that correctly?
 
Under the current body of knowledge (the current model is a combination of animal testing and looking at humans after they've developed it), yes to an extent. The key difference between type 1 and type 2 is that type 1 is caused by antibodies targeted at the beta cells themselves. You won't see that in type 2.
 
JPINFV said:
Ha. We just covered insulin in physio yesterday.

The problem with type 2 is twofold.

1. Defects in the second messanger cascade.
Click to expand...
JP, which cascade is this in reference to?
 
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