Evidence map›Paper›PMID 28294170›Full record

ReviewEuropean journal of clinical nutrition2017

Exploring inter-organ crosstalk to uncover mechanisms that regulate β-cell function and mass.

J Shirakawa, D F De Jesus, R N Kulkarni

Abstract readReview
PubMed Publisher
In one paragraph

Review in European journal of clinical nutrition, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

22 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Beyond Deterministic Fetal Programming: Intrauterine Exposures and the Multifactorial Origins of Adiposity.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2026
    Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. Review
  11. A NovelFrontiers in endocrinology · 2020
    Article
  12. Article
  13. Strategy for achieving standardized bone models.Biotechnology and bioengineering · 2020
    Review
  14. Article
  15. Organ crosstalk: the potent roles of inflammation and fibrotic changes in the course of organ interactions.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2019
    Review
  16. Article
  17. Article
  18. Review
  19. Article
  20. Review
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

3 authors.

J ShirakawaIslet Cell and Regenerative Biology, Joslin Diabetes Center, Department of Medicine, Brigham and Women's Hospital, Harvard Stem Cell Institute, Harvard Medical School, Boston, MA, USA.
D F De JesusIslet Cell and Regenerative Biology, Joslin Diabetes Center, Department of Medicine, Brigham and Women's Hospital, Harvard Stem Cell Institute, Harvard Medical School, Boston, MA, USA.
R N KulkarniIslet Cell and Regenerative Biology, Joslin Diabetes Center, Department of Medicine, Brigham and Women's Hospital, Harvard Stem Cell Institute, Harvard Medical School, Boston, MA, USA.

Funding

Role of IGF-1 and Insulin Receptors Beta-Cell SurvivalR01DK067536 · NIDDK · JOSLIN DIABETES CENTER · PI ROHIT N. KULKARNI · 2004 to 2026
$8.0M
Role of SerpinB1 in beta cell growthR01DK103215 · NIDDK · JOSLIN DIABETES CENTER · PI KULKARNI, ROHIT N. · 2014 to 2018
$2.6M
NIDDK NIH HHS R01 DK067536NIDDK NIH HHS R01 DK103215
6 · The paper itself

Abstract

Impaired β-cell function and insufficient β-cell mass compensation are twin pathogenic features that underlie type 2 diabetes (T2D). Current therapeutic strategies continue to evolve to improve treatment outcomes in different ethnic populations and include approaches to counter insulin resistance and improve β-cell function. Although the effects of insulin secretion on metabolic organs such as liver, skeletal muscle and adipose is directly relevant for improving glucose uptake and reduce hyperglycemia, the ability of pancreatic β-cells to crosstalk with multiple non-metabolic tissues is providing novel insights into potential opportunities for improving β-cell function and/or mass that could have beneficial effects in patients with diabetes. For example, the role of the gastrointestinal system in the regulation of β-cell biology is well recognized and has been exploited clinically to develop incretin-related antidiabetic agents. The microbiome and the immune system are emerging as important players in regulating β-cell function and mass. The rich innervation of islet cells indicates it is a prime organ for regulation by the nervous system. In this review, we discuss the potential implications of signals from these organ systems as well as those from bone, placenta, kidney, thyroid, endothelial cells, reproductive organs and adrenal and pituitary glands that can directly impact β-cell biology. An added layer of complexity is the limited data regarding the relative relevance of one or more of these systems in different ethnic populations. It is evident that better understanding of this paradigm would provide clues to enhance β-cell function and/or mass in vivo in the long-term goal of treating or curing patients with diabetes.

Indexed as

AdiposityAnimalsBlood GlucoseDatabases, FactualDiabetes Mellitus, Type 2Disease Models, AnimalEndothelial CellsGastrointestinal MicrobiomeGastrointestinal TractHomeostasisHumansHyperglycemiaHypoglycemic AgentsInsulinInsulin-Secreting CellsInsulin SecretionBlood GlucoseHypoglycemic AgentsInsulin

Identifiers

PMID28294170

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.