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1 Introduction In the past decade, obesity and related co-morbidities have become critical public health problems and serious medical conditions worldwide ( 2 )

However, since the GLP-2 treatment ex vivo was for 45 min ( eNOS / mice) display normal radiolabel appearance into plasma as wild-type controls, however, GLP-2 treatment in these mice did not increase plasma 3 H compared to treatment in wild-type mice ( eNOS / mice compared to wild-type mice, independent of GLP-2 treatment ( eNOS / mice compared to wild-type mice, again independent of GLP-2, suggesting that eNOS is involved in the release of stored TG as large chylomicrons rather than absorbed dietary TG and this is upregulated by exogenous GLP-2 ( Regulation of Intestinal Growth and Response Injury GLP-1R Interestingly, Gcgr / mice have increased circulating GLP-1 and GLP-2 ( Gcgr / mice have significantly increased small and large intestinal length and weight due to the elevated levels of gut-derived hormones ( 2 )GLP-2 and exendin-4 increases small intestinal weight and length to a greater extent compared to the agonists administered alone ( Gcgr / :Glp2r / mice, the authors demonstrate that GLP-1R signaling can still increase small intestinal length and weight compared to wild type, although not to the same extent as in Gcgr / mice ( Gcgr / mice appears to be driven by GLP-1R signaling as these parameters are unchanged in Gcgr / :Glp2r / mice ( Glp1r / mice ( Glp1r / mice lose significantly more weight, exhibit significantly increased disease activity scores and greater colon damage than wild-type controls in response to DSS-induced colitis (Yusta et al., 2015)