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. 2021 Dec;32(12):958-959.
doi: 10.1016/j.tem.2021.08.001. Epub 2021 Aug 19.

Pericytic porters: helping leptin step in

Daniel J Torres  1 , Matthew W Pitts  2
Affiliations

Pericytic porters: helping leptin step in

Daniel J Torres et al. Trends Endocrinol Metab. 2021 Dec.

Abstract

A new mechanism of leptin extravasation from the bloodstream into the brain may have been discovered. According to recent findings by Butiaeva et al., pericytes within the blood-brain barrier (BBB) express the leptin receptor and, upon activation, facilitate the movement of the appetite-suppressing hormone into deeper regions of the hypothalamus.

Keywords: blood–brain barrier; hypothalamus; leptin; obesity; pericyte.

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Conflict of interest statement

Declaration of interests

The authors declare no conflicts of interest.

Figures

Figure 1.
Figure 1.. Pathways of leptin action in the hypothalamus.
(A) It is known that leptin (yellow) enters the median eminence (ME) of the hypothalamus by passing through the pores of the fenestrated capillaries. Leptin receptor-positive (LepR+) neurons within the arcuate nucleus (Arc) access leptin via projections into the ME, leading to changes in metabolism. Recent evidence suggests that leptin reaches LepR+ neurons in the deeper regions of the mediobasal hypothalamus (MBH) through a pathway regulated by LepR+ pericytes lining the blood–brain barrier (BBB). (B) Activation of LepR on pericytes by circulating leptin increases BBB permeability. This mechanism may involve the adjustment of VE- or N-cadherins at inter-endothelial junctions to allow paracellular flow of leptin into the brain, as suggested by Butiaeva et al. [2]. Abbreviation: 3V, third ventricle.
See this image and copyright information in PMC

Comment on

References

    1. Friedman JM (2019) Leptin and the endocrine control of energy balance. Nat. Metab 1, 754–764 - PubMed
    1. Butiaeva LI et al. (2021) Leptin receptor-expressing pericytes mediate access of hypothalamic feeding centers to circulating leptin. Cell Metab. 33, 1433–1448 - PubMed
    1. Burguera B et al. (2000) Obesity is associated with a decreased leptin transport across the blood–brain barrier in rats. Diabetes 49, 1219–1223 - PubMed
    1. Munzberg H and Myers MG Jr. (2005) Molecular and anatomical determinants of central leptin resistance. Nat. Neurosci 8, 566–570 - PubMed
    1. Balland E et al. (2014) Hypothalamic tanycytes are an ERK-gated conduit for leptin into the brain. Cell Metab. 19, 293–301 - PMC - PubMed