Research

Hormonal

Loss of Bardet-Biedl syndrome (BBS) proteins causes leptin resistance and obesity by disrupting the physical interaction between BBS1 and the leptin receptor (LepRb), leading to defective intracellular trafficking and attenuated hypothalamic signaling.

This research identifies a specific biological mechanism where genetic defects prevent the brain from properly processing the 'fullness' signal (leptin) from fat cells. For individuals with Bardet-Biedl Syndrome or similar genetic variants affecting ciliary function, standard weight loss advice may fail because the body's internal signaling hardware is broken, not just the caloric balance. Future treatments may need to target the trafficking of the leptin receptor itself rather than just focusing on calorie intake.

GoodSupportsHIGH confidence
Our data indicate that BBS proteins mediate LepR trafficking and that impaired LepR signaling underlies energy imbalance in BBS. These findings represent a novel mechanism for leptin resistance and obesity.
Seongjin Seo et al. · Human Molecular Genetics · 2009

Why this rating

High-quality mechanistic evidence using multiple knockout mouse models (Bbs2, Bbs4, Bbs6) and in vitro assays, though findings are preclinical (mouse models).

Source

Requirement of Bardet-Biedl syndrome proteins for leptin receptor signaling

Seongjin Seo et al. · Human Molecular Genetics · 2009

DOI 10.1093/hmg/ddp031

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DOI resolved against Crossref · corpus check 2026-06-10

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