Still looking at this strain,
Bifidobacterium longum ssp. longum 35624, previously classified as Bifidobacterium longum ssp. infantis 35624, classified as Bifidobacterium infantis 35624 before that and still marketed as such. It is sold under the brand name Align in the US and Canada and Alflorex in Ireland, the UK and other European countries. It is patented. This strain was isolated directly from the epithelium of the terminal ileum of a healthy human subject
Seeing where retinol may accumulate.
This is something I have mentioned, the vitamin a might already be there.
Im looking at possible lack of synthesis from absent bacteria or dysbiosis.
Retinyl esters (RE), all-trans retinol (ROL), and all-trans RA
were extracted from the duodenum, jejunum, and ileum
mice had comparable amounts of REs, indicating that the RA
deficit is not due to a lack of vitamin A absorption or storage
Restoring Retinoic Acid Attenuates Intestinal Inflammation
You could maybe take out “intestinal” and this could still be a true statement.
RA plays a major role in skin “dysbiosis” or homeostasis as well.
Hydration, color, thickness, fine lines and wrinkles, wound repair.
I am just going to say right now, I think this could go in the other direction as well. Commensal bacteria or lack of could cause RA deficiency as well as dysbiosis.
Commensal Bacteria Regulate Vitamin A Metabolism
and Storage
Animals cannot synthesize vitamin A de novo but obtain the
molecules as micronutrients from the diet. IECs are the main
cell type responsible for the uptake of dietary vitamin A (Chelstowska et al., 2016). After uptake by IECs, diet-derived vitamin
A or retinol can either be processed into retinyl esters or further
metabolized to RA by two sequential oxidation steps (Figure 1A). To assess whether gut bacteria play a role in modulating vitamin A metabolism, we quantified the amount of
various vitamin A metabolites (collectively called retinoids) in intestinal and extra-intestinal tissue of germ-free (GF) and conventional (CV) mice by liquid chromatography coupled to
mass spectrometry (LC-MS). We found that GF mouse small intestine had significantly higher concentration of active metabolite (RA) compared to small intestine of conventionally raised
mouse (Figure 1B). Concurrently, we observed lower concentration of precursor form (retinol) (Figure 1C) and storage form
(retinyl esters) (Figure 1D) in the intestinal tissue of GF mouse
compared to CV mouse. This indicates that gut bacteria suppressed the conversion of vitamin A into RA and promoted conversion into retinyl esters in the intestine. To assess whether
this accumulation of retinyl esters in the intestinal tissue of
CV mice corresponded with higher retinoids in liver where
80% of vitamin A of the whole body is stored, we also quantified retinoids in the liver. We detected significantly higher quantities of retinol and retinyl esters (Figures 1F and 1G) but not RA
in the liver of CV mice (Figure 1E), suggesting that the presence
of bacteria directed vitamin A metabolism away from RA synthesis in the intestinal tissue and toward vitamin A storage in
liver. These results imply that bacteria regulate the amount of
active metabolite of vitamin A locally