Hi Jean-Claude,
Cholecystokinin is usually referred to as CCK. It is a hormone that is
mostly produced in the small intestine. Production of CCK is stimulated by
the arrival of fats in the part of the small intestine that is closest to
the stomach. Once produced, CCK is absorbed into the bloodstream, where it
travels to the gall bladder. Upon arrival, it signals the gall bladder to
contract. These contractions push bile into the common bile duct, which
leads back to the small intestine.  The muscular action of the digestive
system mixes the bile from the gall bladder with the fats in the small
intestine. The resulting fat particles, called micelles, are very small, and
may thus be more easily absorbed into the lymph system. Without CCK, we do
not absorb fat very well, which is why patients who have undergone gall
bladder removal are encouraged to avoid fats.

CCK production is almost always compromised in untreated celiac disease. The
researchers in question must have ruled out celiac disease, since they
conducted microscopic examinations of the intestinal biopsies taken, but
without the original report in the NEJM, we can't tell what criteria they
used to rule it out..... sometimes methods can lag well behind current
knowledge and pathologists examining biopsy tissues need to be well versed
in the histology (microscopic study of tissues) of celiac disease before
they can accurately read these biopsies. It is common, especially among
those who are not well versed in this area, to erroneously rule out celiac
disease simply due to the absence of villous atrophy. However, current
research reveals that is an inappropriate approach. Gluten can produce a
wide range of  injuries to a wide range of human tissues, both directly, and
through activation of an autoimmune dynamic. There is also some evidence to
suggest that other food proteins, especially milk may also induce damage at
the cellular level.

Perhaps this patient, and many more of the 20% mentioned, would benefit from
dietary exclusion of gluten. Certainly antibody testing for immune reactions
to a variety of dietary proteins would be an excellent starting place.

I hope my comments are helpful.
best wishes,
Ron



>
> MALABSORPTION IN AUTOIMMUNE POLYGLANDULAR SYNDROME TYPE I LINKED TO
> CHOLECYSTOKININ DEFICIENCY
> Many cases of malabsorption in patients with autoimmune polyglandular
> syndrome type I may result from cholecystokinin deficiency, according to a
> report in the January 25th issue of the New England Journal of Medicine.
> http://diabetes.medscape.com/33132.rhtml?srcmp=endo-020201
>
>
> <...Though about 20% of many patients with autoimmune polyglandular
syndrome
> type I develop fat malabsorption, its cause is unknown, the authors
> explain.... >
>
> does someone knows what is cholecystokinin , where is it produced and how
> can we become deficient.?
> jean-claude