Understanding the pathogenesis of lean non-autoimmune diabetes ...

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Eddy Edson

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Relationship to Diabetes
Type 2
... in a Ugandan population.


Conclusions/interpretation

Approximately one-third of participants with incident adult-onset non-autoimmune diabetes had BMI <25 kg/m2. Diabetes in these lean individuals was more common in men, and predominantly associated with reduced pancreatic secretory function rather than insulin resistance. The underlying pathological mechanisms are unclear, but this is likely to have important management implications.

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Thanks for posting this. interesting read, especially for my particular case. Would make a lot of sense for me, I spent most of my teenage years undernourished (my own fault, not bad parents ) I’ve kind of always thought I may of done this to myself.
 
Interesting stuff 🙂 It's a shame they didn't do any of these tests on me at diagnosis to see if it was autoimmune. I wasn't just lean though, I was decidedly skinny with a BMI of around 17 at diagnosis due to very rapid weight loss in the final week prior to diagnosis, but I was around 19 before that anyway, and always had been. Also, I had DKA and of course I needed basal (20 lantus) and bolus (45 units novorapid) for several years afterwards, so it's unlikely I would have ever been bracketed as Type 2. I think I'm just an outlier, really.
 
Maybe a bit interesting: even the non-lean subjects in this study didn't seem to have very elevated BP or cholesterol levels, despite having high body fat, big waists, high BG.


Median HbA1c 86 mmol/mol, non-HDL cholesterol 3.1, trigs 1.4, LDL 2.6, HDL 0.9. SBP 127. Apart from the HbA1c, a lot of people would say those numbers are *not bad*.

I was much leaner than this group at DX, at BMI of 25 point something, with a similar HbA1c of 89, but my non-HDL was 4.7, trigs 3.2, LDL 3.6, HDL 0.8, SBP 180 ... I don't think my numbers were very bad, relative to a European late middle age poorly controlled T2D population, but they were way worse than the Ugandan overweight/obese T2D group in this study.

How much due to different nutrition, activity levels etc, how much to genetics? How if at all does it relate to the apparent higher prevalence of the beta cell issues identified here?

I don't know enough about the biology to have an opinion on whether the biochem metabolic syndrome markers the paper discusses look betetr or worse than in other populations, but it would be interesting to see a comparison.
 
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