Modulation of Gr1 low monocyte subset impacts insulin sensitivity and weight gain upon high-fat diet in female mice

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Background/objectives Blood monocytes are expanded during obesity. However, the differential contribution of monocyte subsets in obesity-related metabolic disorders remains unknown. The aim of the study was to define the role of the Gr1 low monocyte subset upon high-fat diet (HFD). Methods We used transgenic female mouse models allowing the modulation of circulating Gr1 low monocyte number (decreased number in CX3CR1 -/- mice and increased number in CD11c-hBcl2 mice) and studied obesity upon HFD. Results We reported here that HFD induced monocytosis in mice, preferentially due to Gr1 low monocyte expansion, and was associated with a specific upregulation of CD11c on that subset. Using mice models with altered Gr1 low monocyte number, we found a striking correlation between Gr1 low monocytes, bodyweight (BW) and insulin resistance (RT) status. Indeed, CX3CR1 -/- female mice, with reduced Gr1 low monocytes upon HFD, showed increased RT and a pro-inflammatory profile of the adipose tissue (AT) despite a lower BW. Conversely, mice expressing the anti-apoptotic gene hBcl2 in CD11c-expressing cells have increased Gr1 low monocytes, higher insulin sensitivity upon HFD and an anti-inflammatory profile of the AT. Finally, increasing Gr1 low monocytes in Gr1 low -defective CX3CR1 -/- mice rescued BW loss in these mice. Conclusions By using transgenic female mice and adoptive transfer exp

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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