ArticleAmerican journal of physiology. Endocrinology and metabolism2012
Transformation of postingestive glucose responses after deletion of sweet taste receptor subunits or gastric bypass surgery.
Article in American journal of physiology. Endocrinology and metabolism, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 38 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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
38 citing papers in PubMed, 66 citations in OpenAlex.
- Ileal brake activation: macronutrient-specific effects on eating behavior?International journal of obesity (2005) · 2015Trial
- Artificial sweeteners stimulate adipogenesis and suppress lipolysis independently of sweet taste receptors.The Journal of biological chemistry · 2013Trial
- Taste receptor downregulation in diet-induced obesity reveals circumvallate papillae-specific taste-inflammatory networks.Frontiers in nutrition · 2026Article
- Genetic controls of Tas1r3-independent sucrose consumption in mice.Mammalian genome : official journal of the International Mammalian Genome Society · 2021Article
- Sweet Taste Is Complex: Signaling Cascades and Circuits Involved in Sweet Sensation.Frontiers in human neuroscience · 2021Review
- An alternative pathway for sweet sensation: possible mechanisms and physiological relevance.Pflugers Archiv : European journal of physiology · 2020Review
- Loss of the nutrient receptor Tas1R3 reduces atherosclerotic plaque accumulation and hepatic steatosis in ApoEJournal of physiology and biochemistry · 2020Article
- Factors Influencing Mitochondrial Function as a Key Mediator of Glucose-Induced Insulin Release: Highlighting Nicotinamide Nucleotide Transhydrogenase.International journal of molecular and cellular medicine · 2020Review
- Taste and the Gastrointestinal tract: from physiology to potential therapeutic target for obesity.International journal of obesity supplements · 2019Review
- 3-Deoxyglucosone Induces Glucagon-Like Peptide-1 Secretion from STC-1 Cells via Upregulating Sweet Taste Receptor Expression under Basal Conditions.International journal of endocrinology · 2019Article
- Sugars, Sweet Taste Receptors, and Brain Responses.Nutrients · 2017Review
- Gastrointestinal hormones and the gut connectome.Current opinion in endocrinology, diabetes, and obesity · 2017Review
- Impact of obesity on taste receptor expression in extra-oral tissues: emphasis on hypothalamus and brainstem.Scientific reports · 2016Article
- Carbohydrate-induced secretion of glucose-dependent insulinotropic polypeptide and glucagon-like peptide-1.Journal of diabetes investigation · 2016Review
- Accumulation of intestinal tissue 3-deoxyglucosone attenuated GLP-1 secretion and its insulinotropic effect in rats.Diabetology & metabolic syndrome · 2016Article
- Bile Acids Trigger GLP-1 Release Predominantly by Accessing Basolaterally Located G Protein-Coupled Bile Acid Receptors.Endocrinology · 2015Article
- Sugar-induced cephalic-phase insulin release is mediated by a T1r2+T1r3-independent taste transduction pathway in mice.American journal of physiology. Regulatory, integrative and comparative physiology · 2015Article
- Farnesoid X receptor inhibits glucagon-like peptide-1 production by enteroendocrine L cells.Nature communications · 2015Article
- Return of the glucoreceptor: Glucose activates the glucose-sensing receptor T1R3 and facilitates metabolism in pancreatic β-cells.Journal of diabetes investigation · 2015Review
- Gut chemosensing mechanisms.The Journal of clinical investigation · 2015Review
Corrections and comments
- Retraction · 2015-09-01Falsification/Fabrication of Data · Investigation by Company/Institution · Manipulation of Images · Results Not Reproducible ·
- Commented on by
- Commented on by
- RetractedRetraction.2015
Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
The glucose-dependent secretion of the insulinotropic hormone glucagon-like peptide-1 (GLP-1) is a critical step in the regulation of glucose homeostasis. Two molecular mechanisms have separately been suggested as the primary mediator of intestinal glucose-stimulated GLP-1 secretion (GSGS): one is a metabotropic mechanism requiring the sweet taste receptor type 2 (T1R2) + type 3 (T1R3) while the second is a metabolic mechanism requiring ATP-sensitive K(+) (K(ATP)) channels. By quantifying sugar-stimulated hormone secretion in receptor knockout mice and in rats receiving Roux-en-Y gastric bypass (RYGB), we found that both of these mechanisms contribute to GSGS; however, the mechanisms exhibit different selectivity, regulation, and localization. T1R3(-/-) mice showed impaired glucose and insulin homeostasis during an oral glucose challenge as well as slowed insulin granule exocytosis from isolated pancreatic islets. Glucose, fructose, and sucralose evoked GLP-1 secretion from T1R3(+/+), but not T1R3(-/-), ileum explants; this secretion was not mimicked by the K(ATP) channel blocker glibenclamide. T1R2(-/-) mice showed normal glycemic control and partial small intestine GSGS, suggesting that T1R3 can mediate GSGS without T1R2. Robust GSGS that was K(ATP) channel-dependent and glucose-specific emerged in the large intestine of T1R3(-/-) mice and RYGB rats in association with elevated fecal carbohydrate throughout the distal gut. Our results demonstrate that the small and large intestines utilize distinct mechanisms for GSGS and suggest novel large intestine targets that could mimic the improved glycemic control seen after RYGB.
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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.