Evidence map›Paper›PMID 38241508›Full record

ReviewDiabetes2024

Adipose Signals Regulating Distal Organ Health and Disease.

Ankit Gilani, Lisa Stoll, Edwin A Homan, James C Lo

Open access · bronzeAbstract readReview
In one paragraph

Review in Diabetes, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed, 1 pooled it
19.3field-weighted citation impact, top 1% 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

51 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.

  1. New Mediators in the Crosstalk between Different Adipose Tissues.International journal of molecular sciences · 2024
    Pooled it
  2. Article
  3. Article
  4. Biochemistry and biophysics reports · 2026
    Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Adipogenesis Under Leptin Control: Mechanisms and Model-Specific Effects.International journal of molecular sciences · 2026
    Review
  13. Article
  14. Article
  15. Cold exposure-inducedActa pharmaceutica Sinica. B · 2026
    Article
  16. Article
  17. Review
  18. Article
  19. Review
  20. 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

4 authors at 1 institution in 1 country.

Ankit GilaniWeill Center for Metabolic Health, Cardiovascular Research Institute, Department of Medicine, Weill Cornell Medicine, New York, NY.
Lisa StollWeill Center for Metabolic Health, Cardiovascular Research Institute, Department of Medicine, Weill Cornell Medicine, New York, NY.
Edwin A HomanWeill Center for Metabolic Health, Cardiovascular Research Institute, Department of Medicine, Weill Cornell Medicine, New York, NY.
James C LoWeill Center for Metabolic Health, Cardiovascular Research Institute, Department of Medicine, Weill Cornell Medicine, New York, NY.ORCID 0000-0003-0244-1670
Cornell University · US

Funding

Dusp26 regulation of beta cell homeostasisR01DK121140 · NIDDK · WEILL MEDICAL COLL OF CORNELL UNIV · PI James C Lo · 2020 to 2026
$2.7M
An Obesity-Induced Kinase that Regulates Adipose Homeostasis and Metabolic DiseasesR01DK121844 · NIDDK · WEILL MEDICAL COLL OF CORNELL UNIV · PI LO, JAMES C · 2019 to 2023
$2.1M
Multidisciplinary Research Training in Cardiovascular DiseaseT32HL160520 · NHLBI · WEILL MEDICAL COLL OF CORNELL UNIV · PI Geoffrey S Pitt, Jonathan W. Weinsaft · 2022 to 2026
$2.0M
American Heart Association-American Stroke Association 908952NHLBI NIH HHS T32 HL160520NIDDK NIH HHS R01 DK121140NIDDK NIH HHS R01 DK121844NIH HHS 1 T32 HL160520
6 · The paper itself

Abstract

Excessive adiposity in obesity is a significant risk factor for development of type 2 diabetes (T2D), nonalcoholic fatty liver disease, and other cardiometabolic diseases. An unhealthy expansion of adipose tissue (AT) results in reduced adipogenesis, increased adipocyte hypertrophy, adipocyte hypoxia, chronic low-grade inflammation, increased macrophage infiltration, and insulin resistance. This ultimately culminates in AT dysfunction characterized by decreased secretion of antidiabetic adipokines such as adiponectin and adipsin and increased secretion of proinflammatory prodiabetic adipokines including RBP4 and resistin. This imbalance in adipokine secretion alters the physiological state of AT communication with target organs including pancreatic β-cells, heart, and liver. In the pancreatic β-cells, adipokines are known to have a direct effect on insulin secretion, gene expression, cell death, and/or dedifferentiation. For instance, impaired secretion of adipsin, which promotes insulin secretion and β-cell identity, results in β-cell failure and T2D, thus presenting a potential druggable target to improve and/or preserve β-cell function. The cardiac tissue is affected by both the classic white AT-secreted adipokines and the newly recognized brown AT (BAT)-secreted BATokines or lipokines that alter lipid deposition and ventricular function. In the liver, adipokines affect hepatic gluconeogenesis, lipid accumulation, and insulin sensitivity, underscoring the importance of adipose-liver communication in the pathogenesis of nonalcoholic fatty liver disease. In this perspective, we outline what is currently known about the effects of individual adipokines on pancreatic β-cells, liver, and the heart.

Indexed as

Diabetes Mellitus, Type 2Insulin ResistanceNon-alcoholic Fatty Liver DiseaseAdipokinesAdipose TissueAdipose Tissue, BrownAdiposityComplement Factor DHumansInflammationLipidsObesityRetinol-Binding Proteins, PlasmaAdipokinesComplement Factor DLipidsRBP4 protein, humanRetinol-Binding Proteins, Plasma

Identifiers

PMID38241508
PMCPMC10796297
OpenAlexW4391017353

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.