MCP-1 contributes to macrophage infiltration into adipose tissue, insulin resistance, and hepatic steatosis in obesity
J. Clin. Invest. Hajime Kanda, et al. 116:1494 doi:10.1172/JCI26498 [Go to this article.]

Figure 2
Tissue distribution of MCP-1 mRNA and plasma concentration of MCP-1 in obese mice. (A) Total RNA was extracted from the indicated tissues of 8-week-old db/db or db/+m mice and subjected to Northern blot analysis with a probe specific for mouse MCP-1 mRNA. WAT, white adipose tissue; BAT, brown adipose tissue. (B) Plasma concentration of MCP-1 in 11-week-old db/+m and db/db mice. Data are mean ± SEM (db/+m, n = 8; db/db, n = 11). *P < 0.05 versus db/+m. (C) Total RNA, extracted from the indicated tissues of 18-week-old C57BL/6J mice fed either a high-fat diet (HFD) or normal chow for 12 weeks, was subjected to Northern blot analysis with a probe specific for MCP-1 mRNA. (D) Plasma concentration of MCP-1 in 18-week-old C57BL/6J mice fed normal chow or the high-fat diet for 12 weeks. Data are mean ± SEM (normal chow, n = 11; high-fat diet, n = 9). *P < 0.05 versus normal chow. (E) Total RNA (15 μg), extracted from the SVF and adipocyte fraction (Adipo) of epididymal fat tissue from 11-week-old db/db mice or 18-week-old C57BL/6J mice fed a high-fat diet for 12 weeks, was subjected to Northern blot analysis with a probe specific for MCP-1 mRNA. The intensity of the band corresponding to MCP-1 mRNA in each fraction was quantitated and expressed relative to the value for the SVF of mice fed a high-fat diet. Data are mean ± SEM of values from 3 independent experiments (n = 3).