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1000
Control
δ
β
Captopril
800
Tamoxifen
#
600
#
ψ
β
β
400
β
#
ψ
β
δ
200
#
0
CW
CG
TDW
TDG
TSW
TSG
Fig. 8.5 Comparison of pancreatic insulin secretion among groups ( CW control with water intake
alone, CW + Cap CW plus captopril treatment, CW + Tam CW plus tamoxifen treatment, CG con-
trol with high sugar intake, CG + Cap CG plus captopril treatment, CG + Tam CG plus tamoxifen
treatment, TDW perinatal taurine depletion with water intake alone, TDW + Cap TDW plus capto-
pril treatment, TDW + Tam TDW plus tamoxifen treatment, TDG perinatal taurine depletion with
high sugar intake, TDG + Cap TDG plus captopril treatment, TDG + Tam TDG plus tamoxifen
treatment, TSW perinatal taurine supplementation with water intake alone, TSW + Cap TSW plus
captopril treatment, TSW + Tam TSW plus tamoxifen treatment, TSG perinatal taurine supplemen-
tation with high sugar intake, TSG + Cap TSG plus captopril treatment, TSG + Tam TSG plus
tamoxifen treatment; * p < 0.05 compared to untreated control of same taurine status; # p < 0.05 com-
pared to CW of same treatment; b p < 0.05 compared to CG of same treatment; d p < 0.05 compared
to TDW of same treatment; y p < 0.05 compared to TSW of same treatment)
RAS contributes importantly to the pathogenesis of many disorders including
diabetes mellitus and hypertension. Long-term inhibition of the RAS by angio-
tensin-converting enzyme inhibitors or angiotensin receptor antagonists improves
insulin sensitivity and insulin secretion in type 2 diabetes mellitus (Henriksen 2007 ) .
Its initial effect is to increase insulin secretion rather than increase tissue insulin
sensitivity (Rodriguez et al. 2012 ; Suzuki et al. 2008 ), but the long-term effect of the
RAS treatment is to improve glucose-insulin regulation. Similarly, in humans and
animal models, acute angiotensin II infusion increases insulin sensitivity in basal
state or during euglycemic insulin clamp (Buchanan et al. 1993 ; Fliser et al. 2000 ;
Jonk et al. 2010 ; Patiag et al. 2000 ; Townsend and DiPette 1993 ). This may be the
result of redistribution of blood flow to muscles since angiotensin II has a potent and
immediate vasoconstrictor action but little immediate metabolic effect. This mecha-
nism may explain why short-term captopril treatment increases insulin secretion
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