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Thus, we found that mesenteric arterioles of homozygous mice (GPx1 / ) and older heterozygous (GPx1 +/ ) knockout mice had a loss of NO-dependent vasodilatory responses to - methacholine and bradykinin, instead showing a vasoconstrictor response to these mediators that cause vasodilation in wildtype arterioles [39, 71]

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(2001, Int J Obes) showed that chronic treatment with AOD-9604 restored repressed beta-3 AR mRNA levels in obese mice toward lean-mouse values, characterizing a chronic-treatment mechanism that complements the fragment's acute lipolytic action