BleuCheese
Member
- Joined
- Jun 15, 2020
- Messages
- 15
Abstract (click here for study)
Background and aims: The aim of the present study was to examine the protective effect of a dietary high-amylose cornstarch (HAS) against D-galactosamine (D-GalN)-induced liver injury, focusing specifically on intestinal endotoxin translocation.Methods: Male Wistar rats fed a HAS-free basal diet or a 30% HAS-supplemented diet were injected intraperitoneally with D-GalN. Serum transaminase activities, serum concentrations of tumor necrosis factor (TNF)-alpha, and portal venous endotoxin concentrations were determined at various time points. Ileal mucosal proliferation, small intestinal immunoglobulin (Ig)A and mucin, and the size of the cecal short-chain fatty acids (SCFA) pool were also determined.
Results: High-amylose cornstarch ingestion significantly reduced the increase in serum transaminase activities at 22 h after the injection of D-GalN. Rats fed the HAS diet showed a greater cecal SCFA production as measured by pool size than those fed the basal diet. Luminal IgA and mucin content were significantly greater in rats fed the HAS diet. Protein, DNA and RNA contents in the ileal mucosa were also higher in rats fed the 30% HAS diet. In a further experiment, portal venous endotoxin concentrations in rats fed the basal diet reached 72 ng/L at 4 h after D-GalN administration, but endotoxin was not detected in rats fed the HAS diet. At this time, portal endotoxin concentrations were significantly and positively correlated with the serum concentrations of TNF-alpha and serum alanine aminotransferase activities.
Conclusion: These data support the view that HAS ingestion may reduce D-GalN-induced liver injury as a result of an inhibitory effect on endotoxin influx from the intestinal tract, at least in part as a result of alterations in the mucosal barrier functions.
This study was posted but wasn't discussed in any meaningful way. I see it this way, if resistant starch is capable of providing energy substrate for bacteria that produce butyrate for the colonocytes, and energy is, as Ray Peat describes, the primary way in which an organism maintains its structure, then RS might have a reinforcing effect on the digestive tract by providing immediately useable energy substrate, aka butyrate.
Except I suppose in situations of dysbiosis when RS could be used by bad bacteria/ infections.
This review article says "Butyrate is a primary energy source for colonocytes and also maintains intestinal homeostasis through anti-inflammatory actions (17, 18). At the cellular level, SCFAs can have direct or indirect effects on processes such as cell proliferation, differentiation, and gene expression. They may be absorbed by passive diffusion, but uptake by intestinal epithelial cells is greatly enhanced by dedicated transporters, e.g., the monocarboxylate transporter 1 (MCT1; encoded by SLC16A1) and the sodium-coupled monocarboxylate transporter 1 (SMCT1; encoded by SLC5A8). Moreover, SCFAs act as ligands for G-protein coupled receptors (GPCRs), including GPR109A, GPR43, and GPR41, thereby activating anti-inflammatory signaling cascades (5, 19–24). Importantly, IBD patients not only show reduced levels of dominant SCFAs-producing bacteria (like Faecalibacterium prausnitzii and Roseburia intestinalis) in intestinal mucosa and feces, but the actual steady state levels of SCFAs herein also appear to be lower compared to healthy controls (25–29)."
So essentially, IBD patients are lacking bacteria capable of producing readily available local energy for the digestive tract, which gives the intestines the energy needed to reinforce their structure, and maintain proper functioning. It makes sense really.
Just a shitty hypothesis I whipped up in 30 seconds, because RS is doing something amazing for me right now. Lmk what you guys think.
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