Evidence map›Paper›PMID 27489309›Full record

ArticleDiabetes2016

SERCA2 Deficiency Impairs Pancreatic β-Cell Function in Response to Diet-Induced Obesity.

Xin Tong, Tatsuyoshi Kono, Emily K Anderson-Baucum, Wataru Yamamoto, Patrick Gilon, Djamel Lebeche, Richard N Day, Gary E Shull, Carmella Evans-Molina

Open access · greenAbstract read
In one paragraph

Article in Diabetes, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed, 1 pooled it
7.8field-weighted citation impact, top 2% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

61 citing papers in PubMed, 1 synthesis or guideline pooled it, 88 citations in OpenAlex.

  1. Pooled it
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  3. Review
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  7. Review
  8. Article
  9. Review
  10. SERCA blockade as a treatment strategy for obesity.European journal of applied physiology · 2025
    Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Review
  17. Article
  18. Review
  19. Article
  20. Role of cytosolic and endoplasmic reticulum CaPflugers Archiv : European journal of physiology · 2024
    Review

1 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 5 institutions in 2 countries.

Xin TongDepartment of Cellular and Integrative Physiology, Indiana University School of Medicine, Indianapolis, IN.
Tatsuyoshi KonoDepartment of Medicine, Indiana University School of Medicine, Indianapolis, IN.
Emily K Anderson-BaucumDepartment of Medicine, Indiana University School of Medicine, Indianapolis, IN.
Wataru YamamotoDepartment of Cellular and Integrative Physiology, Indiana University School of Medicine, Indianapolis, IN.
Patrick GilonPôle d'endocrinologie, diabète et nutrition, Institut de recherche expérimentale et clinique, Université catholique de Louvain, Brussels, Belgium.
Djamel LebecheCardiovascular Research Institute and Diabetes Obesity and Metabolism Institute, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, NY.
Richard N DayDepartment of Cellular and Integrative Physiology, Indiana University School of Medicine, Indianapolis, IN.
Gary E ShullDepartment of Molecular Genetics, Biochemistry, and Microbiology, University of Cincinnati College of Medicine, Cincinnati, OH.
Carmella Evans-MolinaDepartment of Cellular and Integrative Physiology, Indiana University School of Medicine, Indianapolis, IN Department of Medicine, Indiana University School of Medicine, Indianapolis, IN Department of Biochemistry and Molecular Biology, Indiana University School of Medicine, Indianapolis, IN Herman B Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN Roudebush VA Medical Center, Indianapolis, IN cevansmo@iu.edu.
Indiana University – Purdue University Indianapolis · USIndiana University School of MedicineIcahn School of Medicine at Mount Sinai · USUCLouvain · BEUniversity of Cincinnati Medical Center · US

Funding

Translation CoreP30DK097512 · NIDDK · INDIANA UNIVERSITY INDIANAPOLIS · PI JEFFREY S ELMENDORF · 2015 to 2026
$17.4M
Mechanisms of Beta Cell Function in Health and DiseaseR01DK093954 · NIDDK · INDIANA UNIVERSITY INDIANAPOLIS · PI EVANS-MOLINA, CARMELLA · 2011 to 2019
$3.5M
Biomarkers Of Beta Cell Stress In Type 1 Diabetes (BetaMarker)UC4DK104166 · NIDDK · INDIANA UNIVERSITY INDIANAPOLIS · PI EIZIRIK, DECIO LAKS, EVANS-MOLINA, CARMELLA · 2014 to 2014
$2.4M
Targeting Diabetes With Novel SERCA Allosteric ActivatorsR01DK111417 · NIDDK · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI LEBECHE, DJAMEL · 2018 to 2022
$2.3M
Targeting Diabetes With Novel Small Molecule TherapeuticsR56DK100624 · NIDDK · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI LEBECHE, DJAMEL · 2015 to 2015
$170k
Regulation of Calcium Homeostasis in the Pancreatic Beta CellI01BX001733 · VA · RLR VA MEDICAL CENTER · PI Carmella Evans-Molina · 2013 to 2026
–
BLRD VA I01 BX001733NIDDK NIH HHS P30 DK097512NIDDK NIH HHS R01 DK093954NIDDK NIH HHS R01 DK111417NIDDK NIH HHS R56 DK100624NIDDK NIH HHS UC4 DK104166
6 · The paper itself

Abstract

The sarcoendoplasmic reticulum (ER) Ca(2+) ATPase 2 (SERCA2) pump is a P-type ATPase tasked with the maintenance of ER Ca(2+) stores. Whereas β-cell SERCA2 expression is reduced in diabetes, the role of SERCA2 in the regulation of whole-body glucose homeostasis has remained uncharacterized. To this end, SERCA2 heterozygous mice (S2HET) were challenged with a high-fat diet (HFD) containing 45% of kilocalories from fat. After 16 weeks of the HFD, S2HET mice were hyperglycemic and glucose intolerant, but adiposity and insulin sensitivity were not different between HFD-fed S2HET mice and HFD-fed wild-type controls. Consistent with a defect in β-cell function, insulin secretion, glucose-induced cytosolic Ca(2+) mobilization, and the onset of steady-state glucose-induced Ca(2+) oscillations were impaired in HFD-fed S2HET islets. Moreover, HFD-fed S2HET mice exhibited reduced β-cell mass and proliferation, altered insulin production and proinsulin processing, and increased islet ER stress and death. In contrast, SERCA2 activation with a small molecule allosteric activator increased ER Ca(2+) storage and rescued tunicamycin-induced β-cell death. In aggregate, these data suggest a critical role for SERCA2 and the regulation of ER Ca(2+) homeostasis in the β-cell compensatory response to diet-induced obesity.

Indexed as

AnimalsBlood GlucoseCalciumCell ProliferationCytosolDiet, High-FatEndoplasmic ReticulumHomeostasisInsulinInsulin ResistanceInsulin-Secreting CellsIslets of LangerhansMaleMiceObesitySarcoplasmic Reticulum Calcium-Transporting ATPasesAtp2a2 protein, mouseBlood GlucoseCalciumInsulinSarcoplasmic Reticulum Calcium-Transporting ATPases

Identifiers

PMID27489309
PMCPMC5033263
OpenAlexW2490120783

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.