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. Author manuscript; available in PMC: 2014 May 1.

Published in final edited form as: Atherosclerosis. 2013 Mar 4;228(1):124–135. doi: 10.1016/j.atherosclerosis.2013.02.026

Fig. 7 — Control wild-type (WT) and adiponectin receptor transgenic (AdR1-TG) mice were fed with the high fat diet for 20 weeks; and (A) macrophage, (B) adipose tissue, (C) skeletal muscle, and (D) liver were dissected. Total RNA was isolated from these cells/tissues, cDNAs were synthesized, and QPCR was performed with aP2, IL10, and MCP-1 gene primers for macrophages; LPL, MCP-1, and TNF-α for adipose tissue; PGC-1α, IL10, and IL6 for skeletal muscle; and SREBP1, HMGCR, and PCSK9 for liver. Mean ± SEM from three separate experiments with triplicate samples (n=9 for each group) were presented, *p < 0.05 and **p < 0.01.

Fig. 7 — Control wild-type (WT) and adiponectin receptor transgenic (AdR1-TG) mice were fed with the high fat diet for 20 weeks; and (A) macrophage, (B) adipose tissue, (C) skeletal muscle, and (D) liver were dissected. Total RNA was isolated from these cells/tissues, cDNAs were synthesized, and QPCR was performed with aP2, IL10, and MCP-1 gene primers for macrophages; LPL, MCP-1, and TNF-α for adipose tissue; PGC-1α, IL10, and IL6 for skeletal muscle; and SREBP1, HMGCR, and PCSK9 for liver. Mean ± SEM from three separate experiments with triplicate samples (n=9 for each group) were presented, *p < 0.05 and **p < 0.01.