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. 2010 Jan 26;59(4):916–925. doi: 10.2337/db09-1403

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© 2010 by the American Diabetes Association.

Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. See http://creativecommons.org/licenses/by-nc-nd/3.0/ for details.

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FIG. 3. — Hepatic RMCs are morphologically, functionally, and transcriptionally distinct from KCs. A: Representative histogram plot depicting the distribution of side (indicating relative granularity, left panel) and forward (indicating relative size, right panel) light scatter values obtained from FACS analysis of RMCs and KCs from lean (Lep^+/+) and leptin-deficient obese (Lep^ob/ob) mice. B: KCs are larger than RMCs as seen in hematoxylin and eosin (H&E)-stained isolated cells (bar equals 10 microns). C: Relative expression of Ccr2 was more than 100× higher in RMCs than in KCs (KC expression is set at 100 arbitrary units [AU]) (n = 5–6). D: The relative expression of genes associated with classically (M1) or alternatively (M2) activated cells is not consistently associated with either RMCs or KCs isolated from livers of obese mice (Lep^ob/ob) mice (□, KC Lep^ob/ob; ■, RMC Lep^ob/ob) (n = 5–6). For C and D, data represent mean ± SD. *P < 0.05; ***P < 0.005. (A high-quality digital representation of this figure is available in the online issue.)