Insulin/Proinsulin/etc. in Normal, IGT and T2 Diabetics

One more on the measurement side of things since these type posts are easier to put the finishing touches on to get out the door.  This is another older paper, and I'm trying to track down more info on newer/current analyses and their specificity.  Unlike the last discussion here, I want to focus on the secretory capacity of the  β-cell through the progression of diabetes.  

Serum proinsulin levels at fasting and after oral glucose load in patients with Type 2 (non-insulin-dependent) diabetes mellitus (1988).  

• 40 newly diagnosed with T2 diabetes + 21 IGT -- No medications or special diet
• BMI < 27 in men, < 25 in women
• Controls were weight matched to study group participants.

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Blood Sugar 140: Context is Everything II: The OGTT

In the last installment, I discussed the context of blood glucose readings over 140 mg/dL in diabetics vs. non-diabetics.  In this installment I'm going to discuss it in the context of an Oral Glucose Tolerance Test, OGTT.   The crux of this post is that the results of this study do not justify the Ruhl/Jaminet/(and I'll add Kresser) takeaway message vis a vis diabetes complications and "spikes" in blood glucose.   The fact that 50% of the neuropathy subjects to whom OGTT's were administered had 2 hr. glucose levels over 140 (e.g. diagnosed as Impaired Glucose Tolerance, IGT) simply does not support:  Nerve Damage Occurs when Blood Sugars Rise Over 140 mg/dl (7.8 mmol/L) After Meals as stated on Ruhl's site and in Perfect Health Diet (Kindle Locations 712-716).  (This seems to have been repeated by Chris Kresser as well).

What is an OGTT?  The most common form is conducted in the fasted state, at least 8 hrs, studies seem to favor 10 or 12 hrs.  It involves ingesting 75g of liquid glucose solution in a short period of time.  Glucose (and often insulin) levels are sampled at 30 min (sometimes shorter at early time periods)  intervals for 2 to 3 hours.  There are two values that are assessed:

• 1 hour and/or peak BG:  under 200 mg/dL = normal , 200 mg/dL or over = IGT or diabetic
• 2 hour BG:  under 140 mg/dL = normal, 140-199 mg/dL = IGT, 200 mg/dL or over = diabetic

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Abnormal OGTT Results - The many causes

direct image link

As often happens, when looking for something a bit more specific, I came across this image at right, which led me to this webpage:  Laboratory Testing for Diabetes Mellitus.

Curve 1 is a normal OGTT, Curve 6 is a diabetic.  The other causes are listed:

Pathologic conditions causing impaired, or diabetic, glucose tolerance results:

• Hypercorticism - curve 5.
• Acromegaly - between curves 4 and 5
• Hyperthyroidism - curve 4.
• Pheochromacytoma (or "emotional hyperglycemia") - between curves 4 and 5

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Blood Sugar 140: Where did the 140 mg/dL threshold come from?

This post (that is going to be a series to keep post lengths manageable) has been brewing for quite a while, but I was reminded of it because Jenny Ruhl came out with a diet book recently, and appeared recently as an "expert" on Jimmy Moore's Ask the Low Carb Experts podcast.  After listening to her previous podcast with Jimmy, I had some mixed reviews.  Jenny is certainly articulate, well-read (though I disagree with many of her interpretations) on the topic, and quite a bit more moderate/measured about controlling diabetes and the efficacy of low carb.   But she also seems to view all diabetes through her own MODY eyes.  MODY (Mature Onset Diabetes of the Young) is a rare genetic form (there are actually several rare genetic forms classified as MODY) that is lumped quite often under the category of Type 1.5.  One of these days I need to address some other things on Jenny's website, as it (and her book) is one of the more definitive internet sources for diabetes info in LC circles.    Her book, Blood Sugar 101, more specifically this Amazon review , as well as this page on her website, is where I took the title of this post from.  On the website she writes:

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Insulin Resistance II ~ The Complexity of "Hormone Resistance" Phenomena

It's been a while since Part I of this series ... too many irons in too many fires and all that jazz.  But one research track I went down recently reminded me of this lingering series and I thought I'd finish up this second installment. We hear all the time truisms such as that the acute effects of a hormone differ from the chronic effects, and whenever a hormone is present in excess of normal levels, the term "fill in hormone here resistance" is sure to be close behind.  Now there is no doubt that hormone resistance is a very real phenomenon, but what does it mean, specifically?

The concept of insulin resistance, IR, is highly complicated by the fact that insulin has varying actions in various tissues and organs.  I do intend to discuss tissue-specific IR in more depth as this series unfolds.  But for today, I am going to limit the discussion to insulin and the muscle cell.  After all, when general IR is discussed, it is usually systemic or skeletal muscle insulin resistance.   

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