IR in LADA

[foxl]

Equivalent insulin resistance in latent autoimmune diabetes in adults (LADA) and type 2 diabetic patients
Harvey K. Chiu, a, , Elaine C. Tsaia, Rattan Junejaa, James Stoevera, Barbara Brooks-Worrella, Amit Goela and Jerry P. Palmera

aVeterans Affairs Puget Sound Health Care System, Department of Medicine, Division of Metabolism, Endocrinology and Nutrition, University of Washington Seattle, WA, United States


Received 15 August 2006; accepted 19 December 2006. Available online 17 January 2007.

Abstract
Insulin resistance is a primary component in the pathophysiology of type 2 diabetes. In latent autoimmune diabetes in adults (LADA), insulin resistance has been reported to be significantly lower than in autoantibody-negative type 2 diabetes (T2DM), but whether this might be related to differences in body mass index (BMI) has not been excluded. Furthermore, previous studies have used limiting inclusive criteria for LADA, requiring only the presence of GADA or IA-2A.

To apply more inclusive criteria for LADA, consistent with recent recommendations, we defined LADA by clinical manifestations characteristic of T2DM, but with the presence of any combination of GADA, IA-2A, ICA, or IAA. We recruited 43 LADA patients, 70 T2DM patients, and 150 non-diabetic controls. Insulin resistance was assessed by both the homeostasis model assessment and the quantitative insulin sensitivity check index, and BMI was calculated.

We found that insulin resistance in LADA is equivalent to that of T2DM. When insulin resistance is assessed as a function of BMI, both diabetic populations demonstrated an insulin resistance equally greater than normal controls. The interaction between insulin resistance and BMI in the two diabetic groups was significantly different from that demonstrated in non-diabetic controls. In summary, LADA demonstrates insulin resistance of similar magnitude to T2DM, but with the concurrent component of an immune attack against the pancreatic beta-cells. LADA patients may be at significant risk for metabolic consequences of insulin resistance other than glucose metabolism, such as those described in the metabolic syndrome. As complications and treatment regimens specific to LADA are realized, improved means of identification of LADA will become increasingly important.

Keywords: Latent autoimmune diabetes in adults (LADA); Body mass index (BMI); Homeostasis model assessment (HOMA); Insulin resistance; Pancreatic autoantibody

I feel that this article describes me ... perfectly. Taking to Endo!

[SB_Krista]

Interesting article, Linda....thanks for sharing! Any idea what they mean by "Insulin resistance was assessed by both the homeostasis model assessment and the quantitative insulin sensitivity check index"? For non-clinical trial patients, I thought the Endo's only tool for determining insulin resistance was assessing weight or BMI and measuring C-peptide levels (a normal or elevated level indicating insulin resistance). Am I missing something?

[foxl]

Interesting article, Linda....thanks for sharing! Any idea what they mean by "Insulin resistance was assessed by both the homeostasis model assessment and the quantitative insulin sensitivity check index"? For non-clinical trial patients, I thought the Endo's only tool for determining insulin resistance was assessing weight or BMI and measuring C-peptide levels (a normal or elevated level indicating insulin resistance). Am I missing something?

They refer to the test in the full article as Quicki-IR and compare it to the HOMA-IR ... not sure how broadly available it might be. Does NOT turn up in a google, other than this article. May be experimental only at this time.

[foxl]

Bumping for ACSTOKES and general interest, as well!

[zoelula]

Bumping for ACSTOKES and general interest, as well!

Uhhh....run that by me again, Linda??

[foxl]

Bumping the thread since ACSTOKES (boardname) was talking about insulin resistance in LADA in his thread, and I wanted to make sure he saw this abstract.

[zoelula]

Thanks for the translation..lol

[rak1978]

Thanks for sharing this! All of the things that I have read say that insulin resistance is NOT a characteristic of LADA. Yet, I am insulin resistant and I have LADA. I have had great ongoing confusion over characterization of the types. I seem to have some qualities of all types. I have insulin resistance, positive gad65 antibodies, am insulin dependent, and was 26 yrs old and not overweight at time of dx.
Thanks for bringing me SOME clarity.
You are a well of information! :)

[foxl]

Thanks for sharing this! All of the things that I have read say that insulin resistance is NOT a characteristic of LADA. Yet, I am insulin resistant and I have LADA. I have had great ongoing confusion over characterization of the types. I seem to have some qualities of all types. I have insulin resistance, positive gad65 antibodies, am insulin dependent, and was 26 yrs old and not overweight at time of dx.
Thanks for bringing me SOME clarity.
You are a well of information! :)

Well, I think insulin resistance is a characteristic of humanity, and of aging. But it does not define LADA, as it does type 2, but seems rather to coexist with it. Hoepfully this does not mean the usefulness of oral meds is not overlooked ... !

Glad I can help ... I figure I might as well share my groping in the dark! :D

[rak1978]

Well, I think insulin resistance is a characteristic of humanity, and of aging. But it does not define LADA, as it does type 2, but seems rather to coexist with it. Hoepfully this does not mean the usefulness of oral meds is not overlooked ... !

Glad I can help ... I figure I might as well share my groping in the dark! :D

That makes sense. It's nice to read something that acknowledges that.
By the way, I recently started taking Glucophage again and have seen some improvements (especially in my fasting #).
It seems odd to me when people immediately discontinue oral meds upon a type 1 or 1.5 dx.
As long as you have insulin resistance, they should be at least somewhat effective, right?

And PLEASE keep sharing your "groping in the dark"!
This thread especially has really been helpful for me! Thanks!

[foxl]

That makes sense. It's nice to read something that acknowledges that.
By the way, I recently started taking Glucophage again and have seen some improvements (especially in my fasting #).
It seems odd to me when people immediately discontinue oral meds upon a type 1 or 1.5 dx.
As long as you have insulin resistance, they should be at least somewhat effective, right?

And PLEASE keep sharing your "groping in the dark"!
This thread especially has really been helpful for me! Thanks!

Let us know how the met goes ... I promise to do the same!

[Subby]

I spent years asking my endos why my insulin dose was high. They shrugged. I asked them if I was somehow resisting insulin. They shrugged. And blamed diet/mistakes/whatever they could for as long as they could, a suggestion that there's nothing to be done about needing a lot of insulin, or finding food and basal reqs hard and highly unpredictable, because - let's face it, you're always going to be stuffing up, aren't you? And how can any self respecting endo be expected to do any work of give further aide, until the patient illustrates complete stability first with vanilla approaches?

Then, when over a year ago I went on the pump and the dosing paradigm became I:C ratios, ie, something that definitively illustrated that some people need more insulin than others, and the context was closer control through pump settings - suddenly, insulin resistance *existed!* (it's hard to talk about some of the extreme differences between I:C ratios and pump settings, without acknowledging the idea of IR). Hallelujuh!

But were they prepared to do anything about it? No, that's just asking far too much... you're complicated enough as a type 1, they don't want to be dealing with the whole type 2/ IR side AS WELL if they can just keep upping doses (or not - I had to break with warnings to find an adequate basal dose) and shrugging shoulders.

I have a mission to find an endo who won't take this attitude that a type 1 uses insulin and nothing else. So far I'm about 8 down, over the years. The slow move to drugs like met have to give me hope too. I've got some calling around to do and appointments to line up.

[foxl]

Subby I DO hope you find a decent Endo! I feel bad for you, going through this BS.

I am about to go see if I can find a current Joslin's in the stacks, to check out ... MD's can be intimidating, especially with terminology, and I want to acquire enough background to get past that.

Of course we are still dependent on their clinical experience ... but it sounds to me like you got the song and dance I got. Why should they ask the why questions, as long as the prescription pad and pen are handy?