BMJ Sub-Journal: Loss of GPR21 improves glucose homeostasis and inhibits the CCL2-CCR2 axis through different mechanisms

Chronic low-grade inflammation is part of the pathogenesis of obesity-induced insulin resistance, manifested by immune cells infiltrating adipose tissue
.

The number of metabolic and immune cells (including fat cells and macrophages) parallels the activation of various pro-inflammatory receptors and signaling pathways, establishing a mechanical link between insulin resistance and inflammation

Chronic low-grade inflammation is part of the pathogenesis of obesity-induced insulin resistance, manifested by immune cells infiltrating adipose tissue

The potential role of the

The results of the study showed that the high-fat feeding study of Gpr21 mice had improved glucose tolerance and slight changes in the expression of inflammatory genes
.

Gpr21−/− monocytes and peritoneal macrophages have impaired chemotaxis selectivity to monocyte chemoattractant protein (MCP)-1, although the expression of Ccr2 has not changed

Into the genotype analysis further showed that chemotaxis damage due to monocyte polarization caused by imbalance

After the 16-week feeding period, the wild-type control group fed a high-fat diet (HFD) showed an expected increase in body weight compared to animals fed a normal diet (NC) (Figure 2A, B, n=6-12)
.

Gpr21−/− Compared with the control mice, the animals taking HFD gained less weight, and during the whole experiment, whether they took HFD or NC, the weight gain was the same (Figure 2B, n=6-12)

After the 16-week feeding period, the wild-type control group fed a high-fat diet (HFD) showed an expected increase in body weight compared to animals fed a normal diet (NC) (Figure 2A, B, n=6-12)

Overall, human and mouse data indicate that GPR21 affects glucose homeostasis and MCP-1/CCL2-CCR2-driven monocyte migration

References: RiddyDM ,KammounHL ,MurphyAJ RiddyDM Riddy KammounHL Kammoun MurphyAJ Murphy , et al.
BMJ Open Diabetes Research and Care 2021; 9: e002285.
doi:10.
1136/bmjdrc-2021-002285 doi:  10.
1136/bmjdrc -2021-002285 doi: leave a message here