Evidence map›Paper›PMID 35147704›Full record

ArticleDiabetes2022

The Essential Role of Pancreatic α-Cells in Maternal Metabolic Adaptation to Pregnancy.

Liping Qiao, Sarah Saget, Cindy Lu, Tianyi Zang, Brianna Dzyuba, William W Hay, Jianhua Shao

Open access · bronzeAbstract read
In one paragraph

Article in Diabetes, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
3.1field-weighted citation impact, top 9% 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

13 citing papers in PubMed, 14 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Pregnancy-acquired memory CD4Nature communications · 2025
    Article
  6. Article
  7. Review
  8. Maternal GLP-1 receptor activation inhibits fetal growth.American journal of physiology. Endocrinology and metabolism · 2024
    Article
  9. Beta-cell compensation and gestational diabetes.The Journal of biological chemistry · 2023
    Review
  10. Article
  11. The human α cell in health and disease.The Journal of endocrinology · 2023
    Review
  12. Review
  13. Impact of Placental SLC2A3 Deficiency during the First-Half of Gestation.International journal of molecular sciences · 2022
    Article
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

7 authors at 2 institutions in 1 country.

Liping QiaoDepartment of Pediatrics, University of California, San Diego, La Jolla, CA.
Sarah SagetDepartment of Pediatrics, University of California, San Diego, La Jolla, CA.
Cindy LuDepartment of Pediatrics, University of California, San Diego, La Jolla, CA.
Tianyi ZangDepartment of Pediatrics, University of California, San Diego, La Jolla, CA.
Brianna DzyubaDepartment of Pediatrics, University of California, San Diego, La Jolla, CA.
William W HayUniversity of Colorado, Denver, CO.
Jianhua ShaoDepartment of Pediatrics, University of California, San Diego, La Jolla, CA.ORCID 0000-0002-3586-3602
University of California San Diego · USUniversity of Colorado Denver · US

Funding

Hypoadiponectinemia and Gestational DiabetesR01DK113007 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI Jianhua Shao · 2018 to 2026
$3.5M
The maternal-fetal adiponectin differential and fetal fat depositionR01DK095132 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI SHAO, JIANHUA · 2012 to 2021
$2.9M
Alpha cell-derived Extracellular Vesicles and Maternal Insulin ProductionR21HD112143 · NICHD · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI SHAO, JIANHUA · 2023 to 2024
$435k
NICHD NIH HHS R21 HD112143NIDDK NIH HHS R01 DK095132NIDDK NIH HHS R01 DK113007
6 · The paper itself

Abstract

Pancreatic α-cells are important in maintaining metabolic homeostasis, but their role in regulating maternal metabolic adaptations to pregnancy has not been studied. The objective of this study was to determine whether pancreatic α-cells respond to pregnancy and their contribution to maternal metabolic adaptation. With use of C57BL/6 mice, the findings of our study showed that pregnancy induced a significant increase of α-cell mass by promoting α-cell proliferation that was associated with a transitory increase of maternal serum glucagon concentration in early pregnancy. Maternal pancreatic GLP-1 content also was significantly increased during pregnancy. Using the inducible Cre/loxp technique, we ablated the α-cells (α-null) before and during pregnancy while maintaining enteroendocrine L-cells and serum GLP-1 in the normal range. In contrast to an improved glucose tolerance test (GTT) before pregnancy, significantly impaired GTT and remarkably higher serum glucose concentrations in the fed state were observed in α-null dams. Glucagon receptor antagonism treatment, however, did not affect measures of maternal glucose metabolism, indicating a dispensable role of glucagon receptor signaling in maternal glucose homeostasis. However, the GLP-1 receptor agonist improved insulin production and glucose metabolism of α-null dams. Furthermore, GLP-1 receptor antagonist Exendin (9-39) attenuated pregnancy-enhanced insulin secretion and GLP-1 restored glucose-induced insulin secretion of cultured islets from α-null dams. Together, these results demonstrate that α-cells play an essential role in controlling maternal metabolic adaptation to pregnancy by enhancing insulin secretion.

Indexed as

Glucagon-Secreting CellsIslets of LangerhansAnimalsFemaleGlucagonGlucagon-Like Peptide 1Glucagon-Like Peptide-1 ReceptorGlucoseInsulinMiceMice, Inbred C57BLMice, KnockoutPregnancyReceptors, GlucagonGlucagonGlucagon-Like Peptide 1Glucagon-Like Peptide-1 ReceptorGlucoseInsulinReceptors, Glucagon

Identifiers

PMID35147704
PMCPMC9044124
OpenAlexW4211070912

What Socratic 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 Socratic graph.