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Old 02-21-2006, 01:57 AM   #1 (permalink)
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Question Hyperinsulinism

I'm kinda confused on this...I found out last week (after waiting for a month for my test results) that I have PCOS and Hyperinsulinism.
My dr said my body is producing 6x the normal amount of insulin its supposed to, and my body is still rejecting it...so he put me on 1500mg of Metformin.
I've looked and looked everywhere online and can't find much info on it. Is it type 2 diabetes? Or something totally different?
I didnt ask my dr because I was too upset over the diagnosis to even think of questions to ask.

TIA!
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Old 02-21-2006, 06:03 AM   #2 (permalink)
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Alexis,

Before you panic, its just basically telling you the cause of your PCOS... you are insulin resistant, meaning your cells don't take in the insulin like they are supposed to and medications such as metformin re-sensitize the cells so they take and use the insulin like they are supposed to. Here is a site that explains it well. http://en.wikipedia.org/wiki/Hyperinsulinism
The part you have to take seriously is that anyone w/ insulin resistance has high risk of developing diabetes if they do not follow a healthy diet and exercise. I hope that helps some!

(((HUGS)))

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Old 02-21-2006, 04:00 PM   #3 (permalink)
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Thank you so much, I couldnt find any info on it except the deffinition of it online..LOL
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Old 02-22-2006, 01:48 AM   #4 (permalink)
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I just want to point out that there is newer research which seems to show that in many women with PCOS there is a beta cell dysfunction which causes increased insulin production, aside from insulin resistance. So our bodies make more insulin than we need, and our cells don't use the insulin efficiently. It's a double whammy. Here's a link to a study about this:

http://jcem.endojournals.org/cgi/content/full/90/1/310

Here are this study's "implications":

Insulin resistance is clearly found in many subjects with PCOS and may contribute to increased risk of the metabolic syndrome, development of type 2 diabetes, and cardiovascular disease (6). However, this study demonstrates the under-recognized importance of ß-cell function in PCOS. ß-Cell function, not insulin resistance, was an important correlate of bioavailable testosterone levels. Women with PCOS demonstrated an altered relationship between insulin resistance and insulin secretion, consistent with an intrinsic ß-cell defect wherein insulin resistance leads to an excessive amount of compensatory insulin secretion, with attendant consequences on androgen production and SHBG levels. Insulin hypersecretion may also help to explain the intense hunger experienced by PCOS patients and their ability to gain large amounts of weight in a short period of time. Possibly this insulin hypersecretion was evolutionarily advantageous in times of nutritional deprivation. More research, both at the clinical and cellular levels, is needed to better understand the importance of insulin secretion in PCOS. If ß-cell function is indeed a central pathogenic defect in PCOS, therapies that directly modulate insulin secretion may achieve greater success than insulin-sensitizing therapies commonly used today.

Linda
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