Publication: A surgical model of short bowel syndrome induces
a long-lasting increase in pancreatic beta-cell mass
Authors
Pérez-Arana, G. ; Camacho-Ramírez, A. ; Segundo-Iglesias, M.C. ; Lechuga-Sancho, A.M. ; Sancho-Maraver, E. ; Aguilar-Diosdado, M.
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Publisher
F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología
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DOI
https://doi.org/10.14670/HH-30.479
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info:eu-repo/semantics/article
Description
Abstract
Several surgical techniques are used
nowadays as a severe treatment for obesity and diabetes
mellitus type 2. These techniques are aggressive due to
drastic changes in the nutrient flow and non-reversible
modifications on the digestive tube. In this paper we
present the effects of a massive intestinal resection on
the pancreas. Results have shown that short bowel
technique is less aggressive to normal anatomy and
physiology of the intestinal tract than Gastric bypass or
biliopancreatic diversion (e.g.). In this paper we
reproduce a model of short bowel syndrome (SIC), with
similar surgical conditions and clinical complications as
seen in human cases. This work was conducted on
normal Wistar rats, with no other concurrent factors, in
order to determine the effects on normal pancreas islets.
We measured pancreatic implications by histomorphometric studies, which included beta-cell mass by
immunocytochemistry, and apoptosis/proliferation test
with TUNEL technique and Ki-67. Briefly, we reported
on an increased relative area of the islets of the pancreas,
as well as an increase in the average size of islets in the
SIC versus the control group. Furthermore we stated that
this increase in size of the pancreatic islets is due to the
mechanisms of proliferation of beta cells in animals
undergoing SIC. These goals could reveal a direct
influence of surgical modification of the digestive tract
over the pancreatic beta cell homeostasis. In this sense,
there are many potential stimulators of intestinal
adaptation, including peptide hormones and growth
components which are associated or involved as
effectors of the endocrine pancreas.
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