ArticlePloS one2015
Reduced Gut Acidity Induces an Obese-Like Phenotype in Drosophila melanogaster and in Mice.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- Extracts ofHylotelephiumerythrostictum (miq.) H. Ohba ameliorate intestinal injury by scavenging ROS and inhibiting multiple signaling pathways in Drosophila.BMC complementary medicine and therapies · 2024Article
- Nutrient Sensing via Gut inInternational journal of molecular sciences · 2022Review
- Anatomy and Physiology of the Digestive Tract ofGenetics · 2018Review
- The Drosophila model for microbiome research.Lab animal · 2018Review
- Proton pump inhibitors as risk factor for metabolic syndrome and hepatic steatosis in coeliac disease patients on gluten-free diet.Journal of gastroenterology · 2018Observational
- Organ-to-Organ Communication: AFrontiers in cell and developmental biology · 2017Review
- Molecular mechanism and functional significance of acid generation in the Drosophila midgut.Scientific reports · 2016Article
- Preventing Age-Related Decline of Gut Compartmentalization Limits Microbiota Dysbiosis and Extends Lifespan.Cell host & microbe · 2016Article
Corrections and comments
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Authors and funding
11 authors at 7 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In order to identify genes involved in stress and metabolic regulation, we carried out a Drosophila P-element-mediated mutagenesis screen for starvation resistance. We isolated a mutant, m2, that showed a 23% increase in survival time under starvation conditions. The P-element insertion was mapped to the region upstream of the vha16-1 gene, which encodes the c subunit of the vacuolar-type H+-ATPase. We found that vha16-1 is highly expressed in the fly midgut, and that m2 mutant flies are hypomorphic for vha16-1 and also exhibit reduced midgut acidity. This deficit is likely to induce altered metabolism and contribute to accelerated aging, since vha16-1 mutant flies are short-lived and display increases in body weight and lipid accumulation. Similar phenotypes were also induced by pharmacological treatment, through feeding normal flies and mice with a carbonic anhydrase inhibitor (acetazolamide) or proton pump inhibitor (PPI, lansoprazole) to suppress gut acid production. Our study may thus provide a useful model for investigating chronic acid suppression in patients.
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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.