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.

Saturday, June 26, 2010

Increased weight and Insulin resistance lead to improved glycemic control

Somebody needs to explain this to me. This, once again, deals with Ketosis Prone Type 2 Diabetes but I don't care. This seems to go against everything that I know about being T2. This is from two of the seminal papers on Ketosis Prone Type 2 Diabetes so it isn't junk science. I went back and read these papers because I was researching what was meant by "near-normoglycemic remission".  This data caught my eye and when I looked at other papers, I found confirmation.

Ketosis Prone T2 Diabetics are known for the fact that they can suddenly go into acute insulin failure and essentially become T1's, some will even stay T1's, with no autoimmune factors. The others will recover their beta functioning incredibly fast, we are talking weeks, if given insulin therapy. Even though their IR hasn't receded on bit, they will still proceed to stabilize their blood sugars at or near normal levels. Many, can and do,  require only diet and exercise regimens. This is weird enough but this next part is inexplicable to me.

Weight does not really play a part in KPD. There are just as many thin KPD's as obese ones.They both are prone to DKA just as much. The recovery, however, is something different. The KPD's who recover fastest and have the lowest A1c's tend to be the ones who put on weight. Weight gain is the best predictor of  near-normoglycemic remission. If we follow the logic, these are people who gain glycemic control by increasing their insulin resistance. How? This makes no sense. The thin ones don't do as well as those who put on weight. It gets better. Those with metabolic syndrome actually do better than those without metabolic syndrome. I can not wrap my head around this. Here are some of the quotes from these papers

We also noted significant weight gain associated with improvement of glycemic control, regardless of what therapy was used. Insulin-treated patients gained more weight than individuals on other therapies.

Our study also indicates that weight-gain is a good clinical marker of improved glycemic control, regardless of what therapy is used.

There was a significant correlation between changes in HbA1c and weight changes (r 5 0.45, P , 0.001, n 5 54) in both treatment groups. Patients with greater improvement in HbA1c had greater weight gain. Weight gain after initiation of diabetes treatment was 6.6 6 12.5 kg, regardless of what therapy was used. However, 17 patients continued to lose weight during the years of follow-up. These patients had a follow-up HbA1c of 11.4 6 3.5%. Of the patients that lost weight during the study, 5 were on insulin and 12 were on diet and/or oral agent therapy (7 on diet therapy alone, 2 on glyburide/metformin, 2 on glyburide alone, and 1 on glyburide/troglitazone combination). In the 37 patients who gained weight, HbA1c was 8.0 6 2.5% at follow-up. Of the patients that gained weight, 28 were on insulin and 9 were on oral agents or diet. The patients in the insulin-therapy group that gained weight had a significantly lower HbA1c than the patients in the diet and/or oral agent group that gained weight (P 5 0.01; difference of 2.6%, 95% CI 0.83– 4.4%). There was also a significant difference of 3.4% in HbA1c in patients that gained weight (regardless of therapy) compared with those that lost weight during the observational period (P , 0.0001, 1.7–5.1%). The patients on insulin therapy had a mean weight gain of 11.0 6 11.2 kg (P , 0.0001, 6.6 –18.5kg) versus non–insulin-treated patients.
Other than weight gain, there was no difference in diabetes-related complications between treatment groups in this short study period.

  • Antonio Piñero-Piloña, MD

  • Patrick Litonjua, MD

  • Larissa Aviles-Santa, MD and  

  • Philip Raskin MD


    In conclusion, over 40% of patients in a multi-ethnic cohort of indigent patients with ketosis-prone diabetes have the MetS. These patients have better glycemic control, higher h-cell functional reserve, and a greater likelihood of following a noninsulin-dependent course, than do those who do not have the MetS.

    The glycemic control at baseline was very poor in both groups’ mean Hba1c of 13%; it significantly improved in both groups, but it was significantly better in the +MetS group. Improved glycemic control has been well described in ketosis-prone Type 2 diabetes mellitus 
    (Balasubramanyam et al., 1999; Banerji et al., 1994; Maldonado et al., 2003; Umpierrez et al., 1999).
    Preserved h-cell function is a feature of ketosis-prone Type 2 diabetes (Balasubramanyam et al., 1999; Banerji et al., 1994; Maldonado et al., 2003; Umpierrez et al., 1999). In both groups, the h-cell function was lower on presentation and improved significantly in both groups at 6 and 12 months of follow-up. Based on the C-peptide, C-peptide-to-glucose ratio, and C-peptide response to glucagon stimulation, the +MetS group had significantly higher h-cell functional reserve both at presentation and during follow-up. Autoantibodies against the h-cell were more frequently present in the MetS group.

    Presence of the metabolic syndrome distinguishes patients with ketosis-prone diabetes who have a Type 2 diabetic phenotype
    Max E. Otinianoa, Ashok Balasubramanyama,b, Mario Maldonadoa,b,
    Journal of Diabetes and Its Complications 19 (2005) 313– 318

    Don't think that this is some weird or isolated diabetes, a conservative estimate puts the number to be, at least, 1 million diabetics in this country alone, twice as high would be more realistic. Still this doesn't make much sense.


    It took me a couple of months but here is my answer to this post.


    1. yes. me too.. i need someone to explain it to me further for me to understand it. how is it related to gaining weight and weight loss. thank you

    2. Sorry, I'm at sea here. Increased IR means more insulin and obviously more weight gain. Rather than following the usual path of higher blood sugars as this occurs something intercedes in terms of beta cell functioning. The one thing that could be the case is a better 1st phase insulin response. What this points up is that the relationship between insulin, IR and weight are not as clear cut as once thought.

    3. Michael:

      I have been sitting on an article for months now, which is puzzling in the sense you describe here. Good research, pretty solid analysis, but puzzling results. So puzzling that the authors seem to sweep one of the key results under the rug.

      A theory is starting to form in my mind, and it has something to do with a particular kind of insulin sensitivity - body fat cell sensitivity. That's a kind of insulin sensitivity that many folks don't want to have, and it is related to GLUT-4 receptors in body fat cells. I talk a little bit about this in this post:

      I will write a post about the article soon, and certainly would like to know your opinion. The article is about growth hormone replacement therapy and resulting insulin resistance.

    4. Ed

      I look forward to reading your post even though I really don't need anymore confusion.

    5. On my blog I'm discussing physiologic v pathological insulin resistance right now -


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