Trial reportObesity (Silver Spring, Md.)2010
A preliminary candidate genotype-intermediate phenotype study of satiation and gastric motor function in obesity.
Trial report in Obesity (Silver Spring, Md.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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
13 citing papers in PubMed, 17 citations in OpenAlex.
- Obesity candidate genes, gestational weight gain, and body weight changes in pregnant women.Nutrition (Burbank, Los Angeles County, Calif.) · 2018Trial
- Influence of Receptor Polymorphisms on the Response to α-Adrenergic Receptor Blockers in Pheochromocytoma Patients.Biomedicines · 2022Article
- The Association between Obesity-Risk Genes and Gestational Weight Gain Is Modified by Dietary Intake in African American Women.Journal of nutrition and metabolism · 2018Article
- Variation in the αPharmacogenomics · 2017Article
- Association of UCP-3 rs1626521 with obesity and stomach functions in humans.Obesity (Silver Spring, Md.) · 2015Article
- The 'Fat Mass and Obesity Related' (FTO) gene: Mechanisms of Impact on Obesity and Energy Balance.Current obesity reports · 2015Review
- Gastrointestinal morbidity in obesity.Annals of the New York Academy of Sciences · 2014Review
- Association of melanocortin 4 receptor gene variation with satiation and gastric emptying in overweight and obese adults.Genes & nutrition · 2014Article
- Genome-wide association and systems genetic analyses of residual feed intake, daily feed consumption, backfat and weight gain in pigs.BMC genetics · 2014Article
- Effect of high fat-diet and obesity on gastrointestinal motility.Annals of translational medicine · 2013Article
- Association of genetic variation in cannabinoid mechanisms and gastric motor functions and satiation in overweight and obesity.Neurogastroenterology and motility · 2011Article
- Association of TCF7L2 allelic variations with gastric function, satiation, and GLP-1 levels.Clinical and translational science · 2011Article
- Genetic approaches to functional gastrointestinal disorders.Gastroenterology · 2010Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Stomach motility contributes significantly to fullness sensation while eating and cessation of food intake in humans. Genes controlling adrenergic and serotonergic mechanisms (ADRA2A, GNB3, and SLC6A4) affect gastric emptying (GE), volume (GV), and satiation. Fat mass and obesity-associated gene (FTO) is linked with satiety. Our aim was to examine the association of these candidate genes with stomach functions that signal postprandial fullness: GE, GV, and maximum tolerated volume (MTV). These biomarkers constitute a component of the intermediate phenotype of satiation. A total of 62 overweight or obese participants underwent genotyping of the candidate genes, and validated measurements of GE of solids and liquids by scintigraphy, fasting and postprandial change in GV by SPECT (single photon emission computed tomography), and MTV by nutrient drink test. These markers of satiation were compared for 38 genetic variants in ADRA2A, ADR2C, ADRB3, uncoupling protein (UCP)-2 and -3, GNB3, FTO, and SLC6A4 using a recessive model of inheritance. ADRA2A, ADR2C, UCP-3, GNB3, and FTO loci were significantly associated with the intermediate phenotype markers of satiation: ADR2C (Ins-Del322_325) with accelerated GE; GNB3 (rs1047776) with delayed GE; ADRA2A (rs491589 and rs553668) and GNB3 (rs2269355, rs10849527, and rs3759348) with decreased postprandial GV; ADRA2A (rs3750625) and GNB3 (rs4963517 and rs1129649) with increased postprandial GV; UCP-3 (rs1685356) with increased MTV, and FTO (rs9939609) decreased MTV. Genetic susceptibility to postprandial satiation can be identified through intermediate phenotype markers. With independent validation, these markers may guide patient selection of weight-loss therapies directed at gastric motor functions.
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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.