WHY WE CANNOT USE GLUTAMINE AND ANTISTRESS THERAPY IN C HEPATITIS?
By Renato Cocchi, MD
Yaqoob, 1999, asserted GLN as a well-known preferred fuel of
cells of the immune system and able to promote in vitro lymphocyte proliferation.
By summarizing some recent research, Yaqoob suggested
that the increasing of oral availability of GLN could promote immune responses
involving macrophage- or T cell-derived cytokines.
There is
in increased consumption of GLN during inflammatory processes such as
infections, because GLN is the main substrate of stimulated monocytes
and macrophages, or hepatocytes in the liver.
These
cells release inflammatory mediators such as interleukin-1, interleukin-6 and
tumour necrosis factor alpha, or, as for the liver, "acute phase
proteins".
Why then
we cannot use glutamine as a promoter of hepatocytes
proliferation and in this way as a helper of liver resistance to c hapatitis? The individual resistance to this viral
infection, that exists as we habitually are seeing in our clinical work, can be
modulated in this way?
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