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. 2018 Mar 21;11:33–46. doi: 10.1016/j.molmet.2018.03.008

Figure 4.

Figure 4

DMH Glp1r KD rats develop hepatic steatosis and insulin resistance. (A) Plasma TG levels (n = 6/8; Student t-test; *p < 0.001). (B) Representative pictures of oil red O staining (Scale bar: 100 μm) and ORO area quantification in liver of AAV-control and AAV-GLP-1R rats (n = 5/5; Student t-test; p < 0.0005). (C) Relative mRNA expression in liver: n = 6/8; Student t-test; *p < 0.05 for FAS * p < 0.01 for PEPCK1; *p < 0.005 for G6Pase. p = 0.06 for ACC, ns: FGF21 and PGC1α. (D) Western blot for enzymes involved in do-novo lipogenesis: n = 7/8; Student t-test; *p < 0.05 for FAS and ACC. ns: pACC and pACC/ACC. (E) Relative mRNA expression in inguinal fat pad: n = 6/8; Student t-test; *p < 0.05 for FAS. ns: ATGL, HSL, and ACC. (F) Blood glucose profile during an IPGTT (2 g/kg glucose) in AAV-control and AAV-GLP-1R rats. The bar graph shows the area under curve. (G) Blood insulin profile during an IPGTT in AAV-control and AAV-GLP-1R rats. The bar graph shows the area under curve (n = 4/6; Student t-test; *p < 0.05). (H) Fasting plasma insulin levels in AAV-control and AAV-GLP-1R rats (n = 4/6; Student t-test; *p < 0.05). Data are mean ± SEM.