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M1-M2 balancing act in white adipose tissue browning – a new role for RIP140

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Pages 146-148 | Received 09 Sep 2014, Accepted 23 Oct 2014, Published online: 07 Jan 2015

Figures & data

Figure 1. The function of ATM recruitment and contribution to adipose tissue. Left panel: In lean mice fed a normal diet (or ND), the function of ATMs as M2 type maintains adipose tissue homeostasis and normal insulin sensitivity. Middle panel: In HFD-induced obese mice, RIP140 is overexpressed in monocytes/macrophages compared with ND-fed WT mice, resulting in M1 over M2 ATM infiltration and in situ polarization, triggering WAT adiposity and insulin resistance. Right panel: Attenuation of RIP140 in the monocytes/macrophages could result in M2 over M1 ATM polarization, triggering WAT browning and alleviating HFD–induced insulin resistance.

Figure 1. The function of ATM recruitment and contribution to adipose tissue. Left panel: In lean mice fed a normal diet (or ND), the function of ATMs as M2 type maintains adipose tissue homeostasis and normal insulin sensitivity. Middle panel: In HFD-induced obese mice, RIP140 is overexpressed in monocytes/macrophages compared with ND-fed WT mice, resulting in M1 over M2 ATM infiltration and in situ polarization, triggering WAT adiposity and insulin resistance. Right panel: Attenuation of RIP140 in the monocytes/macrophages could result in M2 over M1 ATM polarization, triggering WAT browning and alleviating HFD–induced insulin resistance.

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