Studies on the benefits of odd chain fats and stearic acid
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Regulation of pyruvate dehydrogenase during infusion of fatty acids of varying chain lengths in the perfused rat heart (Latipää PM, et al., J Mol Cell Cardiol. 1985).
https://pubmed.ncbi.nlm.nih.gov/4087305/"The PDHa content of the tissue was higher during infusion of odd carbon number fatty acids than during infusion of even carbon number fatty acids.""Propionate caused an almost maximal (93%) activation of PDH."
Odd-chain fatty acids like propionate lower the NADH/NAD+ ratio compared to even-chain fats, keeping PDH more active; the study showed this ratio dropped during odd-chain infusions, sparing PDH from inhibitionDietary stearic acid regulates mitochondria in vivo in humans (Senyilmaz-Tiebe et al., Nat Commun. 2018).
https://pubmed.ncbi.nlm.nih.gov/30087348/"We show here that C18:0 ingestion rapidly and robustly causes mitochondrial fusion in people within 3 h after ingestion.""This occurred in both healthy and diabetic subjects... with 19 of the 21 subjects (90% of subjects) having more fused mitochondria after ingestion of C18:0.""Analysis of this factor confirmed that mitochondria became more fused upon ingestion of the C18:0 drink... Together, these data indicate that dietary C18:0 rapidly induces mitochondrial fusion in human neutrophils."
Computational Identification of Stearic Acid as a Potential Inhibitor of PDK for the Treatment of Early Stages of Multiple Sclerosis (Mitchel J, et al., Front Neurol. 2021)
"Using computational modeling and docking studies, we identified stearic acid as a potential inhibitor of PDK.""Stearic acid bound to PDK with high affinity, potentially preventing phosphorylation and inactivation of PDH, thereby supporting pyruvate entry into the TCA cycle.""This inhibition could enhance mitochondrial energy production and reduce lactate accumulation, beneficial for early MS pathologyA high-stearic acid diet does not impair glucose tolerance and insulin sensitivity in healthy women
A high-stearic acid diet does not impair glucose tolerance and insulin sensitivity in healthy women (Louheranta AM et al., Metabolism. 1998).Key lines on stearic acid effects:"No differences were found in the insulin sensitivity index (mean+/-SEM, 5.4+/-1.9 v 5.2+/-1.6 x 10(-4) min(-1) x microU(-1) x mL(-1), nonsignificant [NS]), glucose effectiveness (0.026+/-0.006 v 0.026+/-0.003 min(-1), NS), or first-phase insulin reaction ([FPIR] 368+/-57 v 374+/-66 mU/L x min, NS).""The concentration of serum lipids and lipoproteins and blood coagulation factors did not differ after the diet periods.""In conclusion, a diet rich in stearic acid did not deteriorate glucose tolerance or insulin action in young healthy female subjects as compared with a diet rich in oleic acid."
A Diet Enriched in Stearic Acid Protects Against the Progression of Type 2 Diabetes in Leptin Receptor Deficient Mice (db/db) (Valerie L. Reeves, University of Kentucky Dissertation, 2012).
"The stearic acid enriched diet prevented increases in blood glucose levels independently of weight loss in db/db mice compared to an oleic acid or chow diet.""Diabetic mice fed stearic acid maintained insulin responsiveness and pancreatic islet organization compared to the db/db mice fed chow and oleic diets.""Switching to stearic acid after prolonged hyperglycemia had a rescue effect on blood glucose levels... mice switched to a high fat diet enriched in stearic acid, but not one enriched in oleic acid diet, had significant reductions in blood glucose levels."The Cellular Stability Hypothesis: Evidence of Ferroptosis and Accelerated Aging-Associated Diseases as Newly Identified Nutritional Pentadecanoic Acid (C15:0) Deficiency Syndrome (Venn-Watson S et al., Metabolites. 2024).
"Pentadecanoic acid (C15:0), an odd-chain saturated fat, is an essential fatty acid with the primary roles of stabilizing cell membranes and repairing mitochondrial function. By doing so, C15:0 reverses the underpinnings of ferroptosis."
A pathophysiology of a newly identified nutritional C15:0 deficiency syndrome (“Cellular Fragility Syndrome”) is provided that demonstrates how C15:0 deficiencies (≤0.2% total circulating fatty acids) can increase susceptibilities to ferroptosis, dysmetabolic iron overload syndrome, type 2 diabetes, cardiovascular disease, and NAFLD.""Under the proposed “Cellular Stability Hypothesis”, evidence is provided to show that cell membranes optimally need >0.4% to 0.64% C15:0 to support long-term health and longevity... Further, evidence is provided that C15:0 supplementation can reverse the described C15:0 deficiency syndrome, including the key components of ferroptosis."