GPR182 and the reframing of lacteal chylomicron uptake
Liqing Yu
Liqing Yu
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Commentary

GPR182 and the reframing of lacteal chylomicron uptake

Abstract

Historically, research on chylomicron entry into intestinal lymphatic vessels (lacteals) has been polarized between paracellular and transcellular transport models. In this issue of the JCI, Sun et al. identified GPR182 as a lipoprotein receptor in lymphatic endothelial cells (LECs), profoundly advancing our understanding of intestinal lipid absorption. They observed poor fat absorption in GPR182-deficient mice and demonstrated the role of GPR182 in transporting chylomicrons across the LECs into the lacteal lumen. This discovery establishes a molecular basis for transcellular transport of chylomicrons, challenging the traditional view that lacteal lipid entry is predominantly paracellular. By linking receptor-mediated uptake to impaired fat absorption and protection against fat-induced obesity and steatosis, this study expands the biological and translational implications of lacteal transport. Consequently, rather than favoring a single model, future research should investigate the integration of both paracellular and transcellular transport models in vivo.

Authors

Liqing Yu

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Figure 1

Paracellular and transcellular transport of chylomicrons into the lacteal.

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Paracellular and transcellular transport of chylomicrons into the lactea...
Chylomicrons in the lamina propria enter the lacteal lumen via two distinct routes. In the paracellular pathway, chylomicrons pass through the junctions between adjacent LECs. The findings of Sun et al. highlight the transcellular pathway’s contributions to chylomicron uptake, showing that chylomicrons bind to the GPR182 receptor, undergo endocytosis and vesicular transport through the LEC body, and are ultimately exocytosed into the lumen (17).