ArticlePLoS genetics2016
The BBSome Controls Energy Homeostasis by Mediating the Transport of the Leptin Receptor to the Plasma Membrane.
Article in PLoS genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers.
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Who cites it
83 citing papers in PubMed, 129 citations in OpenAlex.
- Quality of life improvements following one year of setmelanotide in children and adult patients with Bardet-Biedl syndrome: phase 3 trial results.Orphanet journal of rare diseases · 2023Trial
- Primary cilia: master conductors of cellular communication in development and disease.Nature reviews. Nephrology · 2026Review
- Setmelanotide Response Variability in Two Genetically Confirmed Pediatric Kidney Transplant Recipients with Bardet-Biedl Syndrome.International journal of molecular sciences · 2026Article
- Recent Dominant Transposition Events Affect Gene Regulatory Regions, but Not Coding Sequences, in Polar and Brown Bear Genomes.Current issues in molecular biology · 2026Article
- Hypothalamic wars: the last nanodelivery.Reviews in endocrine & metabolic disorders · 2026Review
- BBSome: An essential component of hypothalamic regulation of energy homeostasis.Reviews in endocrine & metabolic disorders · 2026Review
- Primary cilia in the hypothalamic AgRP neurons mediate metabolic effects of butyrate.Nature communications · 2026Article
- The genetics of obesity: aetiology, prevention and therapy.Nature metabolism · 2026Review
- SerpinA3N in leptin-sensitive neurons is required for energy and glucose homeostasis and autonomic regulation.Metabolism: clinical and experimental · 2025Article
- Research Progress on Leptin in Metabolic Dysfunction-associated Fatty Liver Disease.Journal of clinical and translational hepatology · 2025Review
- Central leptin pathways in metabolic homeostasis.Clinical science (London, England : 1979) · 2025Review
- Hyperphagia in Bardet-Biedl syndrome: Pathophysiology, burden, and management.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2025Review
- Metabolic reprogramming in polycystic kidney disease and other renal ciliopathies.EMBO molecular medicine · 2025Review
- The Primary Cilia are Associated with the Axon Initial Segment in Neurons.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The intraflagellar transport cycle.Nature reviews. Molecular cell biology · 2025Review
- BBSome deficiency in Lotmaria passim reveals divergent functions in trypanosomatid parasites.Parasites & vectors · 2025Article
- Control of tuberal hypothalamic development and its implications in metabolic disorders.Nature reviews. Endocrinology · 2025Review
- A methylome-wide association study of major depression with out-of-sample case-control classification and trans-ancestry comparison.Nature. Mental health · 2025Article
- Follistatin like-1 (Adipocyte · 2024Article
- Treatment of Hypothalamic Obesity With GLP-1 Analogs.Journal of the Endocrine Society · 2024Review
23 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Bardet-Biedl syndrome (BBS) is a highly pleiotropic autosomal recessive disorder associated with a wide range of phenotypes including obesity. However, the underlying mechanism remains unclear. Here, we show that neuronal BBSome is a critical determinant of energy balance through its role in the regulation of the trafficking of the long signaling form of the leptin receptor (LRb). Targeted disruption of the BBSome by deleting the Bbs1 gene from the nervous system causes obesity in mice, and this phenotype is reproduced by ablation of the Bbs1 gene selectively in the LRb-expressing cells, but not from adipocytes. Obesity developed as a consequence of both increased food intake and decreased energy expenditure in mice lacking the Bbs1 gene in LRb-expressing cells. Strikingly, the well-known role of BBS proteins in the regulation of ciliary formation and function is unlikely to account for the obesogenic effect of BBS1 loss as disruption of the intraflagellar transport (IFT) machinery required for ciliogenesis by deleting the Ift88 gene in LRb-expressing cells caused a marginal increase in body weight and adiposity. Instead, we demonstrate that silencing BBS proteins, but not IFT88, impair the trafficking of the LRb to the plasma membrane leading to central leptin resistance in a manner independent of obesity. Our data also demonstrate that postnatal deletion of the Bbs1 gene in the mediobasal hypothalamus can cause obesity in mice, arguing against an early neurodevelopmental origin of obesity in BBS. Our results depict a novel mechanism underlying energy imbalance and obesity in BBS with potential implications in common forms of human obesity.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.