Evidence map›Paper›PMID 34716543›Full record

ReviewReviews in endocrine & metabolic disorders2022

Adipogenic progenitors in different organs: Pathophysiological implications.

Francesca Favaretto, Silvia Bettini, Luca Busetto, Gabriella Milan, Roberto Vettor

Open access · hybridAbstract readReview
In one paragraph

Review in Reviews in endocrine & metabolic disorders, 2022. 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
1.8field-weighted citation impact, top 15% 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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.

  1. Pooled it
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  5. Review
  6. Article
  7. Observational
  8. Article
  9. Review
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  11. Article
  12. Review
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  15. Obesity and Skeletal Fragility.The Journal of clinical endocrinology and metabolism · 2024
    Review
  16. Review
  17. Article
  18. Article
  19. Relevance of body composition in phenotyping the obesities.Reviews in endocrine & metabolic disorders · 2023
    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

5 authors at 1 institution in 1 country.

Francesca FavarettoDepartment of Medicine, Internal Medicine 3, University of Padua, via Giustiniani 2, 35128, Padua, Italy.ORCID 0000-0002-8219-0500
Silvia BettiniDepartment of Medicine, Internal Medicine 3, University of Padua, via Giustiniani 2, 35128, Padua, Italy.ORCID 0000-0002-6001-3335
Luca BusettoDepartment of Medicine, Internal Medicine 3, University of Padua, via Giustiniani 2, 35128, Padua, Italy.ORCID 0000-0003-4883-8980
Gabriella MilanDepartment of Medicine, Internal Medicine 3, University of Padua, via Giustiniani 2, 35128, Padua, Italy.ORCID 0000-0001-8987-5310
Roberto VettorDepartment of Medicine, Internal Medicine 3, University of Padua, via Giustiniani 2, 35128, Padua, Italy. roberto.vettor@unipd.it.ORCID 0000-0003-0625-6667
University of Padua · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In physiological conditions, the adipose organ resides in well-defined areas, where it acts providing an energy supply and as an endocrine organ involved in the control of whole-body energy metabolism. Adipose tissue adipokines connect the body's nutritional status to the regulation of energy balance. When it surrounds organs, it provides also for mechanical protection. Adipose tissue has a complex and heterogenous cellular composition that includes adipocytes, adipose tissue-derived stromal and stem cells (ASCs) which are mesenchymal stromal cells, and endothelial and immune cells, which signal to each other and to other tissues to maintain homeostasis. In obesity and in other nutrition related diseases, as well as in age-related diseases, biological and functional changes of adipose tissue give rise to several complications. Obesity triggers alterations of ASCs, impairing adipose tissue remodeling and adipose tissue function, which induces low-grade systemic inflammation, progressive insulin resistance and other metabolic disorders. Adipose tissue grows by hyperplasia recruiting new ASCs and by hypertrophy, up to its expandability limit. To overcome this limitation and to store the excess of nutrients, adipose tissue develops ectopically, involving organs such as muscle, bone marrow and the heart. The origin of ectopic adipose organ is not clearly elucidated, and a possible explanation lies in the stimulation of the adipogenic differentiation of mesenchymal precursor cells which normally differentiate toward a lineage specific for the organ in which they reside. The chronic exposition of these newly-formed adipose depots to the pathological environment, will confer to them all the phenotypic characteristics of a dysfunctional adipose tissue, perpetuating the organ alterations. Visceral fat, but also ectopic fat, either in the liver, muscle or heart, can increase the risk of developing insulin resistance, type 2 diabetes, and cardiovascular diseases. Being able to prevent and to target dysfunctional adipose tissue will avoid the progression towards the complications of obesity and other nutrition-related diseases. The aim of this review is to summarize some of the knowledge regarding the presence of adipose tissue in particular tissues (where it is not usually present), describing the composition of its adipogenic precursors, and the interactions responsible for the development of organ pathologies.

Indexed as

Diabetes Mellitus, Type 2AdipocytesAdipogenesisAdipokinesAdipose TissueHumansAdipokinesAdipose tissueAdipose tissue-derived stromal and stem cells (ASCs)AdiposopathyIntermuscular adipose tissue (IMAT)Mesenchymal stromal cells (MSCs)ObesitySignaling

Identifiers

PMID34716543
PMCPMC8873140
OpenAlexW3210565339

What Socratic holds

Textmetadata
LicenceCC BY
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.