(August 21, 2019)
Very interesting research. Thank you for posting. It will be interesting to see what the future holds. But I still have good numbers and no complications. Sometime things do just happen with this disease. .Nancy 50
“…new research at the University of Kentucky shows that changes to mitochondria—the powerhouse of cells—drive chronic inflammationfrom cells exposed to certain types of fats, shattering the prevailing assumption that glucose was the culprit.”
I wonder what types of fats. Interesting article!
The unhealthy fats that drive inflammation are the industrial (not natural) fats such as vegetable oils and trans fats.
Thanks Jim. I’m aware that unsaturated fats are better for heart health. It seems like this would be an issue for anyone, not just people with Type 2. I’m wondering if there may be particular fats that are more harmful to people with Type 2 and why those fats would affect them more than the general population.
I’ll try to look up the study to see if they give more detail on the fats that were identified in the experiment.
If you find anything more definitive please let us know @katers87
Here’s a link to the study: https://www.cell.com/cell-metabolism/fulltext/S1550-4131(19)30377-8
Looks like you have to pay to get the full version. There’s a lot of scientific jargon in the abstract, so it’ll take me some time to try to get the gist of what their conclusion is. Maybe a scientist with a background in this will come along and explain it to us…
“Mechanisms that regulate metabolites and downstream energy generation are key determinants of T cell cytokine production, but the processes underlying the Th17 profile that predicts the metabolic status of people with obesity are untested. Th17 function requires fatty acid uptake, and our new data show that blockade of CPT1A inhibits Th17-associated cytokine production by cells from people with type 2 diabetes (T2D). A low CACT:CPT1A ratio in immune cells from T2D subjects indicates altered mitochondrial function and coincides with the preference of these cells to generate ATP through glycolysis rather than fatty acid oxidation. However, glycolysis was not critical for Th17 cytokines. Instead, β oxidation blockade or CACT knockdown in T cells from lean subjects to mimic characteristics of T2D causes cells to utilize 16C-fatty acylcarnitine to support Th17 cytokines. These data show long-chain acylcarnitine combines with compromised β oxidation to promote disease-predictive inflammation in human T2D.”
Good find. I think what they’re trying to say is some individuals have genetic disorders that may result in underproduction of acetyl-CoA and dysfunction of the Krebs cycle.
This paper sums it up nicely (see 4. Carnitine, β-Oxidation and Health)