I'm making myself a lab rat for n-acetylglucosamine

[Labrat2]

Three months, nothing. There are effects, good and bad, but nothing for MS. I'll keep messing with the glucosamine/sulfur at a much-reduced amount for other reasons, but wait for another inspiration for the MS (or of course for someone to come up with a miracle cure.)

[NHE]

The paper below discusses how glucosamine can help promote hepatitis B replication. I do not know if this would also hold true for n-acetylglucosamine.

Glucosamine promotes hepatitis B virus replication through its dual effects in suppressing autophagic degradation and inhibiting MTORC1 signaling
Autophagy. 2020 Mar;16(3):548-561.

Glucosamine (GlcN), a dietary supplement widely utilized to promote joint health and effective in the treatment of osteoarthritis, is an effective macroautophagy/autophagy activator in vitro and in vivo. Previous studies have shown that autophagy is required for hepatitis B virus (HBV) replication and envelopment. The objective of this study was to determine whether and how GlcN affects HBV replication, using in vitro and in vivo experiments. Our data demonstrated that HBsAg production and HBV replication were significantly increased by GlcN treatment. Confocal microscopy and western blot analysis showed that the amount of autophagosomes and the levels of autophagic markers MAP1LC3/LC3-II and SQSTM1 were clearly elevated by GlcN treatment. GlcN strongly blocked autophagic degradation of HBV virions and proteins by inhibiting lysosomal acidification through its amino group. Moreover, GlcN further promoted HBV replication by inducing autophagosome formation via feedback inhibition of mechanistic target of rapamycin kinase complex 1 (MTORC1) signaling in an RRAGA (Ras related GTP binding A) GTPase-dependent manner. In vivo, GlcN application promoted HBV replication and blocked autophagic degradation in an HBV hydrodynamic injection mouse model. In addition, GlcN promoted influenza A virus, enterovirus 71, and vesicular stomatitis virus replication in vitro. In conclusion, GlcN efficiently promotes virus replication by inducing autophagic stress through its dual effects in suppressing autophagic degradation and inhibiting MTORC1 signaling. Thus, there is a potential risk of enhanced viral replication by oral GlcN intake in chronically virally infected patients.

Free full text.

[NHE]

GlcN strongly blocked autophagic degradation of HBV virions and proteins by inhibiting lysosomal acidification through its amino group.

This effect of glucosamine described above would not be an issue with n-acetylglucosamine. Since the acetyl group is bonded directly to the nitrogen atom in n-acetylglucosamine, the primary amine is converted to an amide group. As such, the unshared pair of electrons on the nitrogen atom would have greatly reduced basicity since they would be involved in resonance with the neighboring carbonyl group. For reference, see the discussion of the basicity of amine groups on the following page.

Alkyl amine of glucosamine: pK_a ≈ 10.7
Amide of n-acetylglucosamine: pK_a ≈ -1.0

The larger pK_a yields a smaller pK_b and therefore a stronger base (pK_a + pK_b = pK_w = 14.0, acids have a pK_a less then 7.0, bases have a pK_a greater than 7.0).

With an alkyl amine the lone pair electrons are localized on the nitrogen. However, the lone pair electrons on an amide are delocalized between the nitrogen and the oxygen through resonance. This makes amides much less basic compared to alkylamines.

[NHE]

A dietary source of n-acetylglucosamine.

Chitin in mushrooms is listed as a dietary source of n-acetylglucosamine.
https://vitanetonline.com/forums/1/Thre ... essage1488

The chemical structure of chitin consists of a polymer of n-acetylglucosamine monomers linked in a beta 1-4 linkage.
https://en.wikipedia.org/wiki/Chitin

White button mushrooms contain 14.3% chitin by mass.
http://www.ijsrp.org/research-paper-081 ... -p8017.pdf

One white button mushroom weighs around 10 grams. This would provide 1.4 grams of n-acetylglucosamine.