Cited by 178Regulation of Appetite and ObesityAdipokines, Inflammation, and Metabolic DiseasesHypothalamic control of reproductive hormones

The DOI matches its Crossref record; 175 of the 177 references it cites were found in a registry or an index; none of the 212 sources its claims cite is checked for support yet.

Inter‐organ communication: a gatekeeper for metabolic health

Open access
Castillo‐Armengol, Judit, Fajas, Lluis, Lopez‐Mejia, Isabel C·2019·The EMBO Reports

Abstract

Multidirectional interactions between metabolic organs in the periphery and the central nervous system have evolved concomitantly with multicellular organisms to maintain whole‐body energy homeostasis and ensure the organism's adaptation to external cues. These interactions are altered in pathological conditions such as obesity and type 2 diabetes. Bioactive peptides and proteins, such as hormones and cytokines, produced by both peripheral organs and the central nervous system, are key messengers in this inter‐organ communication. Despite the early discovery of the first hormones more than 100 years ago, recent studies taking advantage of novel technologies have shed light on the multiple ways used by cells in the body to communicate and maintain energy balance. This review briefly summarizes well‐established concepts and focuses on recent advances describing how specific proteins and peptides mediate the crosstalk between gut, brain, and other peripheral metabolic organs in order to maintain energy homeostasis. Additionally, this review outlines how the improved knowledge about these inter‐organ networks is helping us to redefine therapeutic strategies in an effort to promote healthy living and fight metabolic disorders and other diseases.

Overview

AI snapshot

Written from the paper’s full text.

TL;DR

This review describes how hormones, cytokines, myokines, adipokines, and neural signals coordinate gut, brain, liver, muscle, adipose, and pancreas to maintain energy homeostasis in feeding, fasting, cold exposure, and exercise. It also summarizes how these inter-organ networks are altered in obesity and type 2 diabetes and discusses therapeutic strategies, especially GLP-1 receptor agonists.

Key findings

  • In feeding, gut hormones such as GLP-1, secretin, and LEAP2 signal to the brain to reduce food intake; GLP-1 and GIP potentiate glucose-stimulated insulin secretion; FGF19 represses hepatic bile acid synthesis; and leptin suppresses food intake. In fasting, ghrelin increases appetite and adiposity, asprosin promotes hepatic glucose production and food intake, FGF21 increases adipose lipolysis and hepatic fatty acid oxidation/ketogenesis, and glucagon drives glycogenolysis and gluconeogenesis.
  • Cold-induced thermogenesis involves hypothalamic orexin/BMP8b, sympathetic norepinephrine, thyroid hormones, FGF21, and bile acids acting on brown adipose tissue; a UCP1-independent pathway mediated by PM20D1 is also described. Exercise-induced IL-6, irisin, and cathepsin B mediate muscle crosstalk with pancreas, liver, adipose tissue, and brain.
  • In obesity and related disorders, inter-organ communication is altered: leptin resistance, increased NPY, decreased adiponectin, increased FGF21 and asprosin, ghrelin resistance, altered GLP-1 after bariatric surgery, and proinflammatory adipokines are reported. The review notes that in pathological situations WAT can account for more than 50% of human body weight.
  • Therapeutic efforts include GLP-1 receptor agonists, which promote satiety and reduce food intake; leptin therapy alone failed to induce significant weight loss or insulin sensitization; FGF21 variants showed only a small trend toward glucose lowering in humans; and an asprosin-neutralizing antibody reduced appetite, body weight, and blood glucose in obese mice. The review also states that more than 15% of the protein-coding genome encodes roughly 3,000 secreted proteins, but only a handful have been properly annotated.

Methods

  • Design: narrative review summarizing well-established concepts and recent advances in inter-organ communication.
  • Data or sample: Not stated in the paper; no primary dataset or systematic sample is reported. The review synthesizes cited literature and includes figures and a table.
  • Main analysis: qualitative synthesis organized by physiological states—feeding/fasting cycles, non-shivering thermogenesis, exercise, and obesity—and by therapeutic implications.

Limitations

  • Stated: the review explicitly excludes the role of the immune system in energy homeostasis, noting it has been discussed elsewhere. It also identifies unresolved or controversial areas, including the role of FGF21, the normal physiology of Lcn5 and Metrnl, and the central mechanism of ghrelin action.
  • Evident: as a narrative review, it does not report a systematic search strategy, inclusion criteria, quality assessment, or meta-analysis.
  • Evident: therapeutic conclusions rely on cited preclinical and early clinical studies and are not systematically appraised.

Model-written summary. Check it against the paper before relying on it.

Integrity signals

Registry

Crossref · 10.15252/embr.201947903

Cites

175 of 175 references verified0 citation errors · 0 not checkable

Statistics

Nothing to recompute.

Verification

Claims the paper makes

0 of 212 cited sources checked · 0 supported · 0 flagged

Show all 90 claims

  • It may state two separate claims as one. 65
  • Probably not a substantial claim. 5
  • The quote only partly states this claim. 1
69 of 69
  • The paper relies on this without support.

    Multidirectional interactions between peripheral metabolic organs and the central nervous system maintain whole-body energy homeostasis and ensure adaptation to external cues.

    “Multidirectional interactions between metabolic organs in the periphery and the central nervous system have evolved concomitantly with multicellular organisms to maintain whole‐body energy homeostasis and ensure the organism's adaptation to external cues.”
  • The paper relies on this without support.

    These interactions are altered in pathological conditions such as obesity and type 2 diabetes.

    “These interactions are altered in pathological conditions such as obesity and type 2 diabetes.”
  • The paper relies on this without support.

    Bioactive peptides and proteins, such as hormones and cytokines, produced by both peripheral organs and the central nervous system, are key messengers in inter-organ communication.

    “Bioactive peptides and proteins, such as hormones and cytokines, produced by both peripheral organs and the central nervous system, are key messengers in this inter‐organ communication.”
  • The paper relies on this without support.

    Inter-organ communication is altered in different pathologic conditions, for example, in conditions related to adipose tissue dysfunction, like obesity.

    “Inter‐organ communication is altered in different pathologic conditions, for example, in conditions related to adipose tissue dysfunction, like obesity.”
  • The paper relies on this without support.

    Alterations in hormones and cytokines contribute to the spectrum of obesity-associated pathologies.

    “As such, alterations in hormones and cytokines are currently known to notably contribute to the spectrum of obesity‐associated pathologies.”
  • The paper relies on this without support.

    Pharmacological interventions to modify the production of hormones/cytokines, or directly delivering recombinant hormones/cytokines, are promising approaches to treat obesity-related endocrine diseases.

    “Therefore, pharmacological interventions to modify the production of hormones/cytokines, or directly delivering recombinant hormones/cytokines, are currently being explored as promising approaches to treat a wide variety of obesity‐related endocrine diseases.”
6 of 6

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

Each contradiction between two passages listed here was confirmed by an independent check.

  • Myostatin deficiency has opposite reported effects on insulin resistance

    Minor

    The text says myostatin-deficient mice develop insulin resistance, but the title of its cited reference 148 says they exhibit reduced insulin resistance. This reverses the reported metabolic effect.

1 of 1

Citations

Cites

Flagged first, then by citations

2 of the 177 references couldn’t be matched to a known paper.

Research works printed but not linked: 1

  1. Bernard C (1853) Nouvelle fonction du foie considéré comme organe producteur de matière sucrée chez l'homme et les animaux. Paris: Baillère JB

Cited by

Sorted by citations

See all 178

Metadata

Authors
Castillo‐Armengol, J., Fajas, L., & Lopez‐Mejia, I. C.
Affiliations
University of Lausanne (CH)
Venue
The EMBO Reports
Published
2019-08-19
Volume
20
Issue
9
Pages
e47903-e47903
ISSN
  • 1469-221X (ISSN-L)
  • 1469-3178
OpenAlex
W2969433956
Cited by
178
References
177
Citations by year
2026: 24 · 2025: 29 · 2024: 35 · 2023: 28 · 2022: 29 · 2021: 19 · 2020: 13 · 2019: 1
FWCI
1.86
Type
journal article
Language
en
Open access
Locations
  • EMBO Reports (publishedVersion)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • SERVAL (Université de Lausanne) (publishedVersion, cc-by)
  • IRIS (submittedVersion, cc-by)
Funders
Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (168077)
Topics
  • Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
  • Health Sciences › Medicine › Reproductive Medicine › Hypothalamic control of reproductive hormones
Keywords
inter-organ communication, gut-brain axis, energy homeostasis, metabolic crosstalk, hormones, cytokines, bioactive peptides, obesity, type 2 diabetes, metabolic disorders, treatment options
MeSH terms
Animals, Diabetes Mellitus, Type 2, Energy Metabolism, Homeostasis, Humans, Models, Biological, Obesity

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

A language model drew the claims from the paper on 2026-10-10, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).

A second model labelled each claim on 2026-10-10 (model jev-1.13-20260917, definition revision gold-guideline-v0.2).

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review