FUDiabetes

Changes to mitochondria drive inflammation in type 2 diabetes, not glucose

Dr Ponder shared this on Facebook the other day. This is potentially a big deal and course change in the understanding of diabetes complications

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@Jim_YYC posted a similar article on TUD. It looks pretty groundbreaking.

It sounds like she hasn’t identified which fats are responsible or why yet. It’d be interesting to know if people with type 1 experience similar mitochondrial defects.

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Hard to know, but my gut instinct would be to think that since the complications are so similar that it’d be most likely that their mechanism and etiology would be too

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Hmm. I have a mitochondrial myopathy, though that was diagnosed nearly 4 years before I was diagnosed w/type 1 (and the myopathy diagnosis was after an 8 year search for answers). I’d considered the fact that mito put me more at risk for diabetes (and there’s some debate on an association with autoimmune diseases in general), but never thought about diabetes possibly causing more issues in my mitochondria. :thinking:

This is not super surprising. When you look at genes that are tied to increased risk of type 2 diabetes, a number are in regions associated with mitochondrial respiration.

Also, they’re not saying that high sugar levels don’t cause complications in type 2, but that the driver of inflammation in cells (in a petri dish) is not glucose levels. Obviously, we have robust data showing that highly elevated A1Cs are tied to complications in T1Ds and also in T2Ds. There are probably other cells that cause damage besides Th17 cells.

I think the question is more in the sub 8 A1C region – are you going to improve the situation a lot if you push the A1C down but at the expense of exposing cells to high levels of fatty acids from your diet? Or would it be better to have a slightly higher A1C but eat a diet that reduces your cellular exposure to those fatty acids.

I’ve anecdotally seen this with my dad. He has heart failure and T2. He’s never had A1Cs over a 7, despite pretty lax treatment and no insulin. But his health continued to deteriorate until he (well, my mom) became stricter about his following a heart failure diet. Very low in fat, low in salt and with moderate carb in take (45 to 50 g per serving). Almost zero meat. He’s stopped having edema and his heart failure stabilized, and coincidentally his A1C has improved.

As for T1s, that’s an interesting question. I did remember seeing a few studies suggesting initial inflammation in pancreatic cells is what triggered the autoimmune attack in the first place. And some of that may have been mitochondrial dysfunction? But the long-term complications, I’m not sure if they have data on.

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