The accepted knowledge is that Diabetes destroys gradually over years. Ketosis Prone Type 2 diabetes is an acute form of type 2. This type 2 can reach fasting blood sugars of 300 or higher in months. This blog brings together all the documentation that I could find in the world and my speculation of what it means for KPD’s in specific and diabetics in general. I ask you to leave your stories about what happened to you so that we can all gain a better understanding of what we are dealing with.

Monday, August 23, 2010

Multi-Tissue resistance in KPD's

I've been away doing research and other things but now I'm back.

KPD's don't have enough insulin therefore the body hovers at a high bg level. I originally was going to write another piece about the oddness of KPD and weight gain and then obtaining acceptable levels of blood sugar but I thought I had published this piece.  Sorry, I'm doing it now.

It has been noted that insulin resistance is a big part of being Type 2. This is why many Type 2's have high insulin numbers because the pancreas has to put out more insulin to overcome this resistance. KPD is Type 2, at least most of the time. What they have found to be different about KPD's is that all systems in the body seem to have relatively high insulin resistance.

This is the first investigation of diabetic patients in a metabolic state close to normoglycemia without insulin treatment. The multiorgan insulin resistance observed in near-normoglycemia suggests that these defects are primary rather than secondary to the diabetic state.
Multitissue Insulin Resistance Despite Near-Normoglycemic Remission in Africans With Ketosis-Prone Diabetes
Table 2—
Metabolic parameters and indexes of insulin action
KPDControl subjectsP
Fasting plasma glucose (mmol/l)6.3 ± 0.24.9 ± 0.1<0.001
Fasting plasma insulin (μU/ml)9.4 ± 1.96.7 ± 1.00.33
Insulinogenic index (mU/mmol)4.6 ± 0.921.3 ± 5.40.001
HOMA-IR3.1 ± 0.61.1 ± 0.20.005
SSPI1 (μU/ml)20.9 ± 3.317.4 ± 1.20.82
SSPI2 (μU/ml)189.6 ± 20.5181.5 ± 14.80.89
TGD (mg · kg−1 · min−1)7.5 ± 0.810.5 ± 0.90.018
TGD × insulinogenic index28.1 ± 4.0193.3 ± 46.1<0.001
bEGP (mg · kg−1 · min−1)4.0 ± 0.33.0 ± 0.10.001
rEGP1 (mg · kg−1 · min−1)1.6 ± 0.20.6 ± 0.10.004
bEGP × FPI (mg · kg−1 · min−1 · mU · l−1)35.9 ± 7.220.7 ± 3.60.04
rEGP1 × SSPI1 (mg · kg−1 · min−1 · mU · l−1)33.2 ± 7.210.9 ± 2.80.006
rEGP2 × SSPI2 (mg · kg−1 · min−1 · mU · l−1)50.3 ± 22.100.007
Fasting NEFA (μmol/l)1,936.7 ± 161.41,230.0 ± 174.10.002
SSNEFA1 (μmol/l)706.6 ± 96.5381.6 ± 55.90.015
SSNEFA2 (μmol/l)187.8 ± 27.7116.1 ± 11.20.05
Fasting IRNEFA (103 · μmol · mU · l−2)17.7 ± 3.28.0 ± 1.70.009
IRNEFA1 (103 · μmol · mU · l−2)17.4 ± 4.66.9 ± 1.40.05
IRNEFA2 (103 · μmol · mU · l−2)40.2 ± 9.221.2 ± 2.60.06

  • Data are means ± SE. SSNEFA, steady-state nonesterified fatty acid; IRNEFA, insulin resistance index to NEFA disappearance (1 and 2denote the last 20 min of the first and second steps of the glucose clamp, respectively).
I'm not going to go through all these numbers but they are meant to represent calculated indexes of insulin resistance. It would have been nice, if the comparison had been made to regular Type 2's. It would have been great, if they could have tested this before people went DKA but, as you know, there is no way to distinguish KPD before it occurs. It suffices to say that, metabolically, we aren't the most normal group on the planet.
If you look at these numbers and toss in glucose toxicity, you can get an idea of why we go DKA quickly. 

Despite an increasing number of reports of ketoacidosis in populations with Type 2 diabetes mellitus, the pathophysiology of the ketoacidosis in these patients is unclear. We therefore tested the roles of three possible mechanisms: elevated stress hormones, increased free fatty acids (FFA), and suppressed insulin secretion.
Conclusions  At the time of hospital presentation, the predominant mechanism for ketosis in KPDM2 is likely to be greater insulinopenia.

Pathophysiology of ketoacidosis in Type 2 diabetes mellitus
P. Linfoot C. Bergstrom and E. Ipp    Diabetic Medicine   Volume 22 Issue 10, Pages 1414 - 1419

The question I have is: when did this start? Is this part and parcel of our lives as youths? Have we always been KPD and it took bad diet to get us here. There is plenty of documentation that this is present in the young. 
again more research needs to be done.

Purely from an anecdotal perspective, looking back at my childhood and viewing my present day symptoms, I would say they were present then. The problem is we really don't know what KPD is. It is described by its most dramatic symptom, which is its acute presentation. What is going on before that? Is it the same syndrome in children? How insidious is it? What is the continuum of its behavior?

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