Publication: Effect of diabetic state on co-localization of substance P and serotonin in the gut in animal models
Authors
Spangeus, A. ; Forsgren, Sture ; El-Salhy, M.
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Publisher
Murcia : F. Hernández
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DOI
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info:eu-repo/semantics/article
Description
Abstract
Changes in the numbers of serotonin- and
substance P-immunoreactive (IR) cells occur in severa1
animal models of diabetes. It is not known, however,
whether these changes are a result of actual ceii loss or
are caused by modified gene expression in ceíls showing
co-localization of serotonin and substance P. The pattern
of mono- and co-expression of serotonin, as well as of
substance P, was therefore investigated in
gastrointestinal endocrine cells from animal models of
human type 1 and type 2 diabetes, namely non-obese
diabetic (NOD) and obese diabetic (oblob) mice.
Immunocytochemical staining by the avidin-biotin
complex method was performed for computerized image
analysis of each cell type, and by immunofluorescence
double staining to study co-localization. Tissues from
antrum, proximal duodenum and dista1 colon were
investigated. Co-localization of serotonin- and substance
P-IR was found in al1 investigated parts of the gut. In
antrum, substance P immunoreactivity was found
exclusively in serotonin-IR cells. In both NOD and
oblob mice there was a reduced number of substance PIR
cells, but an unchanged serotonin-IR cell count,
which thus tallies with a shut-off of substance P
expression in antral enterochromaffin cells. In
duodenum, both diabetes models showed a decreased
number of serotonin-IR cells. Furthermore there was a
decreased number of substance P-IR cells in the type 2 model. The proportion of serotonin-IR cells showing
substance P-immuno-reactivity was decreased in both
diabetic models, thus indicating a shut-off of substance
P-gene expression. However, this does not fully explain
the changes in duodenum, but the diabetic state probably
affects the number of mono-expressed cells as well. In
colon, no change was found in diabetic mice regarding
co-localization of substance P and serotonin. However,
pre-diabetic NOD mice showed a decreased proportion
of substance P in serotonin-IR cells, which might be
explained by the increased number of serotonin-IR cells, combined with an unchanged number of substance P-IR
cells. In conclusion, diabetic animal models of both type
1 and type 2 appear to have a combination of decreased
expression of substance P in serotonin-IR cells of both
antrum and duodenum, as well as a change in the
number of mono-expressed cells. The pattern in colon,
on the other hand, seems to be unaffected.
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