nr. 477 - 2011 - Institut for Natur, Systemer og Modeller (NSM)

3.3 Gastrin 15
eration in situ Urusova et al. (2004). The findings reported Urusova et al. (2004) are
corroborated in Brubaker and Drucker (2004).
Though we have several other articles on GLP-1 we stop here, and present a summary
of GLP-1-related positive effects that could be included in a mathematical model:
• Regulates differentiation of pancreatic progenitor cells (Urusova et al., 2004, p.27)
• It causes β-cell proliferation in the islets (Urusova et al., 2004, p.28)
• Protects β-cells from apoptosis (Urusova et al., 2004, p.30-31)
• Increases replication of duct cells (Suarez-Pinzon et al. (2008))
• Has an intermittent effect on the autoimmune response (Suarez-Pinzon et al.
(2008))
We would like to reiterate that the results of Suarez-Pinzon et al. (2008) are for GLP-1
and gastrin, while those of Urusova et al. (2004) and Brubaker and Drucker (2004) are
for GLP-1 alone. In the following section we will turn our attention to gastrin.
3.3 Gastrin
Rooman and Bouwens (2004) tested the effects of gastrin and epidermal growth factor
(EGF), as well as gastrin only and EGF only on (C57Bl6/J 1 ) alloxan 2 treated mice.
They also treated healthy specimens, that were not to be given alloxan, with the combination
to see if it had any effect on these.
On the first day the mice that were not chosen as control specimens were given intravenous
injections of alloxan. The mice that were treated with gastrin and EGF all
became normoglycemic after eight days of treatment, and normoglycemia persisted until
6 weeks after administration of alloxan, at which point the mice were terminated.
The mice that were treated with gastrin only or EGF only were unsuccessful in reaching
normoglycemia (Rooman and Bouwens, 2004, p.261). Rooman and Bouwens (2004)
speculates that duct cells are responsible for regeneration in the pancreas (Rooman and
Bouwens, 2004, p.264). In the mice that were given gastrin only neogenesis of β-cells
was observed.
Again we see that the desired effects depend on a combination of gastrin and another
drug – in this case epidermal growth factor.
3.4 Dendritic Cells
Dendritic cells (DC) may play a crucial part in the initiation T1D, but they also have a
part to play in regards of possible therapeutic advances. Immature DCs are responsible
for keeping the immune system from initiating autoimmune attacks, by making T cells
tolerant to autoantigens. 3 However under certain (pathological) circumstances the DC’s
travel to the lymph nodes where they activate the immune system, thus initiating an
1 The C57Bl6 mouse is the most commonly used laboratory mouse. The “J” in C57BL6/J indicates
that it is an C57Bl6 mouse that has been (genetically) altered (Pociot (2009)).
2 Alloxan is a medicament used to induce experimental diabetes (Szkudelskii (2001)).
3 Autoantigens are recognized by the adaptive immune system – if the immune system recognizes the
autoantigens as foreign antigens, then an autoimmune response may occur leading to cell destruction
(Seeley et al., 2008, p.798-801).