From: Steve Harris <sbharris@ix.netcom.com>
Newsgroups: sci.med.nutrition
Subject: Re: White Flour Contains Diabetes-Causing Contaminant Alloxan
Date: 22 Jun 2005 19:21:33 -0700
Message-ID: <1119493293.279544.88350@g47g2000cwa.googlegroups.com>

>>Scientists have known of the alloxan-diabetes connection for years; in
fact, researchers who are studying diabetes commonly use the chemical
to induce the disorder in lab animals. <<


COMMENT:

In LAB animals. This is one of those cases where humans differ quite a
lot from rodents and even dogs in toxicity of a given chemical. We're
not sure why. It may be that alloxan is toxic mainly in species that
make their own vitamin C.  In flour it probably only gives diabetes to
the Linus Pauling types who megadose. :)


Proc Natl Acad Sci U S A. 1994 Sep 27;91(20):9253-6.

Major species differences between humans and rodents in the
susceptibility to pancreatic beta-cell injury.

Eizirik DL, Pipeleers DG, Ling Z, Welsh N, Hellerstrom C, Andersson A.

Department of Medical Cell Biology, Uppsala University, Sweden.

The ability of beta cells to endure assaults may be relevant in the
development of insulin-dependent diabetes mellitus. This study examines
the susceptibility of human pancreatic islets to agents that are
cytotoxic for rodent beta cells--i.e., sodium nitroprusside (NP, a nitric
oxide donor), streptozotocin (SZ), or alloxan. After 5-8 days in tissue
culture, human or rodent islets were exposed for 14 h to NP (50-200
microM) or for 30 min to SZ or alloxan (1-3 mM).  Glucose oxidation by
human islets was not reduced by NP, but there was a dose-dependent
inhibition in rat (40-90% inhibition; P < 0.001) and mouse (10-60%
inhibition; P < 0.05) islet glucose oxidation. Glucose (16.7 mM)-induced
insulin release by human islets was not impaired after a 30-min exposure
to SZ or alloxan, at concentrations that inhibited insulin release from
rat (30-80% inhibition; P < 0.001) or mouse (10-70% inhibition; P < 0.05)
islets.  The viability of human beta cells purified by flow cytometry was
not affected by SZ or alloxan (5 mM), as judged 1 or 4 days after a
10-min exposure and subsequent culture; these conditions were cytotoxic
for rat beta cells, with 65-95% (P < 0.01) dead beta cells after 4 days.
Human islets transplanted under the kidney capsule of nude mice were not
affected by in vivo alloxan exposure, as suggested by preserved graft
morphology and insulin content, whereas the endogenous beta cells of the
transplanted mice were severely damage (80% decrease in pancreatic
insulin content and morphological signs of beta-cell destruction). Thus
human beta cells are resistant to NP, SZ, or alloxan at concentrations
that decrease survival and function of rat or mouse beta cells. These
marked interspecies differences emphasize the relevance of repair and/or
defense mechanisms in beta-cell destruction and raise the possibility
that such differences may also be present among individuals of the same
species.

PMID: 7937750 [PubMed - indexed for MEDLINE]