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Fig. 14.2 ( a ) Fed plasma insulin ( n = 5-16) and ( b ) glucose-induced insulin secretion in isolated
pancreatic islets ( n = 8) from NP, NPT, LP, and LPT mice. Values are mean ± SEM; different letters
over bars indicate statistical difference; P < 0.05 (two-way ANOVA, Newman-Keuls post hoc
test)
15 min ( P < 0.05) and returned to normal levels after 1 h (Fig. 14.3f ). Akt
phosphorylation was not altered by acute incubation with TAU (Fig. 14.3g ).
Despite no modification in islet protein ER stress maker profile in LP islets,
p-PERK and BIP protein expression in the liver of LP mice was higher than in NP
mice ( P < 0.05; Fig. 14.4a, b ). Increased liver ER stress marker expression in LPT
mice was prevented by TAU supplementation.
14.4
Discussion
Here, we describe that mice fed on a low-protein diet have lower BW and plasma
insulin and isolated islets from these mice secrete less insulin in response to glucose
(Figs. 14.1 and 14.2 ). These findings are in accordance with previous studies from
our group (Amaral et al. 2010 ; Filiputti et al. 2010 ; da Silva et al. 2012 ) and others
(Chen et al. 2009 ; Theys et al. 2009 ) .
In this study, TAU supplementation enhanced glucose-stimulated insulin
secretion (GSIS) in isolated islets from control and malnourished mice
(Fig. 14.2b ). TAU supplementation was already reported to enhance beta cell
responsiveness to nutrients and other stimuli (Carneiro et al. 2009 ; Ribeiro et al.
2009 ). These effects of TAU were mainly due to the improvement upon beta cell
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