ArticleJCI insight2019
TMEM16B determines cholecystokinin sensitivity of intestinal vagal afferents of nodose neurons.
Article in JCI insight, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
9 citing papers in PubMed, 11 citations in OpenAlex.
- Lipid flip-flop in biological membranes: through the lens of TMEM16F.Physiological reviews · 2026Review
- Vagal neuropathies: An underrecognized potential driver of physical, mental, and immune symptoms.Brain, behavior, & immunity - health · 2026Review
- RISING STARS: Endocrine regulation of metabolic homeostasis via the intestine and gut microbiome.The Journal of endocrinology · 2023Review
- A tree-based gene-environment interaction analysis with rare features.Statistical analysis and data mining · 2022Article
- Four evolving concepts in molecular and clinical autonomic research.Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2021Article
- Nutritional Regulation of Human Brown Adipose Tissue.Nutrients · 2021Review
- Roles, molecular mechanisms, and signaling pathways of TMEMs in neurological diseases.American journal of translational research · 2021Review
- Estrogen and gut satiety hormones in vagus-hindbrain axis.Peptides · 2020Review
- Molecular/Ionic Basis of Vagal Bronchopulmonary C-Fiber Activation by Inflammatory Mediators.Physiology (Bethesda, Md.) · 2020Review
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
The satiety effects and metabolic actions of cholecystokinin (CCK) have been recognized as potential therapeutic targets in obesity for decades. We identified a potentially novel Ca2+-activated chloride (Cl-) current (CaCC) that is induced by CCK in intestinal vagal afferents of nodose neurons. The CaCC subunit Anoctamin 2 (Ano2/TMEM16B) is the dominant contributor to this current. Its expression is reduced, as is CCK current activity in obese mice on a high-fat diet (HFD). Reduced expression of TMEM16B in the heterozygote KO of the channel in sensory neurons results in an obese phenotype with a loss of CCK sensitivity in intestinal nodose neurons, a loss of CCK-induced satiety, and metabolic changes, including decreased energy expenditure. The effect on energy expenditure is further supported by evidence in rats showing that CCK enhances sympathetic nerve activity and thermogenesis in brown adipose tissue, and these effects are abrogated by a HFD and vagotomy. Our findings reveal that Ano2/TMEM16B is a Ca2+-activated chloride channel in vagal afferents of nodose neurons and a major determinant of CCK-induced satiety, body weight control, and energy expenditure, making it a potential therapeutic target in 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.