ArticleEBioMedicine2016
Catecholamines Facilitate Fuel Expenditure and Protect Against Obesity via a Novel Network of the Gut-Brain Axis in Transcription Factor Skn-1-deficient Mice.
Article in EBioMedicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 28 citations in OpenAlex.
- Adaptive remodeling of rat adrenomedullary stimulus-secretion coupling in a chronic hypertensive environment.Cellular and molecular life sciences : CMLS · 2024Article
- Differentiated Epithelial Cells of the Gut.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Stimulation of Alpha-1-Adrenergic Receptor Ameliorates Obesity-Induced Cataracts by Activating Glycolysis and Inhibiting Cataract-Inducing Factors.Endocrinology and metabolism (Seoul, Korea) · 2022Article
- Tuft cell integration of luminal states and interaction modules in tissues.Pflugers Archiv : European journal of physiology · 2021Review
- Unexpected obesity, rather than tumorigenesis, in a conditional mouse model of mitochondrial complex II deficiency.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- Thallium Toxicity in Caenorhabditis elegans: Involvement of the SKN-1 Pathway and Protection by S-Allylcysteine.Neurotoxicity research · 2020Article
- Skn-1a/Pou2f3 functions as a master regulator to generate Trpm5-expressing chemosensory cells in mice.PloS one · 2017Article
- Expanding frontiers in weight-control research explored by young investigators.The journal of physiological sciences : JPS · 2017Review
- Tuft Cells: New Players in Colitis.Trends in molecular medicine · 2016Article
- Article
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Taste signals and nutrient stimuli sensed by the gastrointestinal tract are transmitted to the brain to regulate feeding behavior and energy homeostasis. This system is referred to as the gut-brain axis. Here we show that both brush cells and type II taste cells are eliminated in the gastrointestinal tract of transcription factor Skn-1 knockout (KO) mice. Despite unaltered food intake, Skn-1 KO mice have reduced body weight with lower body fat due to increased energy expenditure. In this model, 24-h urinary excretion of catecholamines was significantly elevated, accompanied by increased fatty acid β-oxidation and fuel dissipation in skeletal muscle and impaired insulin secretion driven by glucose. These results suggest the existence of brain-mediated energy homeostatic pathways originating from brush cells and type II taste cells in the gastrointestinal tract and ending in peripheral tissues, including the adrenal glands. The discovery of food-derived factors that regulate these cells may open new avenues the treatment of obesity and diabetes. RESEARCH CONTEXT: Taste signals and nutrient stimuli sensed by the gastrointestinal tract are transmitted to the brain to regulate feeding behavior and energy homeostasis along the gut-brain axis. We propose the concept that taste-receiving cells in the oral cavity and/or food-borne chemicals-receiving brush cells in the gut are involved in regulation of the body weight and adiposity via the brain. The discovery of food-derived factors that regulate these cells may open new avenues for the treatment of obesity and diabetes.
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Registered trials
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