# Changes to mitochondria drive inflammation in type 2 diabetes, not glucose **URL:** \ **Category:** D-News\ **Created:** [August 28, 2019, 2:11am UTC](https://forum.fudiabetes.org/t/changes-to-mitochondria-drive-inflammation-in-type-2-diabetes-not-glucose/8205 "2019-08-28T02:11:20Z")\ **Posts on this page:** 5\ **Page:** 1
**Author:** ![Sam](https://yyz2.discourse-cdn.com/flex030/user_avatar/forum.fudiabetes.org/sam/32/10595_2.png) [@Sam](https://forum.fudiabetes.org/u/Sam)\ **Post date:** [August 28, 2019, 2:11am UTC](https://forum.fudiabetes.org/t/changes-to-mitochondria-drive-inflammation-in-type-2-diabetes-not-glucose/8205/1 "2019-08-28T02:11:20Z")
Dr Ponder shared this on Facebook the other day. This is potentially a big deal and course change in the understanding of diabetes complications > **[Changes to mitochondria drive inflammation in type 2 diabetes, not glucose](https://www.news-medical.net/news/20190821/Changes-to-mitochondria-drive-inflammation-in-type-2-diabetes-not-glucose.aspx?sfns=mo)** > > To date, the underlying causes of inflammation in obesity and type 2 diabetes mellitus have been poorly understood, which has hampered efforts to develop treatments to prevent complications from a disease that is the third leading cause of death in... ---
**Author:** ![Katers87](https://avatars.discourse-cdn.com/v4/letter/k/a9adbd/32.png) [@Katers87](https://forum.fudiabetes.org/u/Katers87)\ **Post date:** [August 28, 2019, 2:17am UTC](https://forum.fudiabetes.org/t/changes-to-mitochondria-drive-inflammation-in-type-2-diabetes-not-glucose/8205/2 "2019-08-28T02:17:55Z")
@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. ---
**Author:** ![Sam](https://yyz2.discourse-cdn.com/flex030/user_avatar/forum.fudiabetes.org/sam/32/10595_2.png) [@Sam](https://forum.fudiabetes.org/u/Sam)\ **Post date:** [August 28, 2019, 3:39am UTC](https://forum.fudiabetes.org/t/changes-to-mitochondria-drive-inflammation-in-type-2-diabetes-not-glucose/8205/3 "2019-08-28T03:39:41Z")
> [@Katers87](#): > > It’d be interesting to know if people with type 1 experience similar mitochondrial defects. 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 ---
**Author:** ![Pianoplayer7008](https://yyz2.discourse-cdn.com/flex030/user_avatar/forum.fudiabetes.org/pianoplayer7008/32/1507_2.png) [@Pianoplayer7008](https://forum.fudiabetes.org/u/Pianoplayer7008)\ **Post date:** [August 28, 2019, 4:47am UTC](https://forum.fudiabetes.org/t/changes-to-mitochondria-drive-inflammation-in-type-2-diabetes-not-glucose/8205/4 "2019-08-28T04:47:08Z")
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. 🤔 ---
**Author:** ![TiaG](https://yyz2.discourse-cdn.com/flex030/user_avatar/forum.fudiabetes.org/tiag/32/594_2.png) [@TiaG](https://forum.fudiabetes.org/u/TiaG)\ **Post date:** [August 28, 2019, 9:28am UTC](https://forum.fudiabetes.org/t/changes-to-mitochondria-drive-inflammation-in-type-2-diabetes-not-glucose/8205/5 "2019-08-28T09:28:01Z")
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. > > > The complex etiology of type 1 diabetes (T1D) is the outcome of failures in regulating immunity in combination with beta cell perturbations. Mitochondrial dysfunction in beta cells and immune cells may be involved in T1D pathogenesis. Mitochondrial energy production is essential for the major task of beta cells (the secretion of insulin in response to glucose). Mitochondria are a major site of reactive oxygen species (ROS) production. Under immune attack, mitochondrial ROS (mtROS) participate in beta cell damage. Similarly, T cell fate during immune responses is tightly regulated by mitochondrial physiology, morphology, and metabolism. Production of mtROS is essential for signaling in antigen-specific T cell activation. Mitochondrial dysfunction in T cells has been noted as a feature of some human autoimmune diseases. Recent Advances: Preclinical and clinical studies indicate that mitochondrial dysfunction in beta cells sensitizes these cells to immune-mediated destruction via direct or indirect mechanisms. Sensitivity of beta cells to mtROS is associated with genetic T1D risk loci in human and the T1D-prone nonobese diabetic (NOD) mouse. Mitochondrial dysfunction and altered metabolism have also been observed in immune cells of NOD mice and patients with T1D. This immune cell mitochondrial dysfunction has been linked to deleterious functional changes.It remains unclear how mitochondria control T cell receptor signaling and downstream events, including calcium flux and activation of transcription factors during autoimmunity.Mechanistic studies are needed to investigate the mitochondrial pathways involved in autoimmunity, including T1D. These studies should seek to identify the role of mitochondria in regulating innate and adaptive immune cell activity and beta cell failure.