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In agreement with these findings, old Dkk1 mutant mice show improved memory consolidation and affective behaviour (Seib et al. 2013).
Nox2 knockout mice show improved endothelial dysfunction in a model of renovascular hypertension [ 17] but no change in basal blood pressure [ 5] or the hypertensive response to chronic angiotensin II infusion [ 16], nor to chronic activation of the renin-angiotensin system [ 28].
However, these mice show improved insulin sensitivity and lowered HGP when excess pyruvate and lactate are used for synthesis of TG (Sun et al., 2012).
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Although this is severe model, PTP1B−/− mice showed improved GTT and ITT.
Although this severe model, PTP1B−/− mice showed improved GTT and ITT.
Confirming the proposed insulinotropic effect of betacellulin, transgenic mice showed improved glucose tolerance.
Both the diabetic and non-diabetic RAGE-/ mice showed improved angiogenesis compared to the RAGE+/+ mice (WT diabetic and non-diabetic) based on greater uptake of radiolabeled RGD targeting αvβ3 expression, a biomarker of tissue changes accompanying early angiogenesis.
On day 14 (Fig. 2D), both wild type and Atxn2 ko mice showed improved performance (2-way ANOVA, P<0.0001, Bonferroni posttests, p<0.001 for Atxn2 ko and p<0.05 for wt).
Ad5ASM-infected mice showed improved glucose tolerance.
Ucn3+ mice showed improved glucose tolerance across a GTT (Fig. 2f).
ARC transgenic mice showed improved cardiac remodeling, as assessed by myocardial cross-sectional area and collagen content.
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