Evidence mapPaperPMID 41961206Full record

ReviewCurrent diabetes reports2026

Lipolysis in Health and Disease: Pathways, Regulation, and Metabolic Consequences.

Courtney L Bordelon, Jacqueline M Stephens

Abstract readReview
In one paragraph

Review in Current diabetes reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
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

1 citing paper in PubMed.

  1. 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

2 authors.

Courtney L BordelonPennington Biomedical Research Center, Louisiana State University, 6400 Perkins Road, Baton Rouge, LA, 70808, USA.ORCID http://orcid.org/0009-0004-4595-4235
Jacqueline M StephensPennington Biomedical Research Center, Louisiana State University, 6400 Perkins Road, Baton Rouge, LA, 70808, USA. jsteph1@lsu.edu.ORCID http://orcid.org/0000-0002-3796-9531

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purpose of reviewLipolysis regulates lipid distribution, energy availability, and metabolic homeostasis in organisms that store triacylglycerols. In multicellular organisms, adipose tissue evolved as a specialized organ that centralizes lipid storage and release, buffers nutrient fluctuations, and protects non-adipose tissues from lipid overload. Dysregulated adipocyte lipolysis occurs across diverse metabolic conditions, including obesity, diabetes, lipodystrophy, and inflammatory states. This review synthesizes evidence that defective suppression of basal lipolysis and impaired responsiveness to physiological stimuli disrupt lipid partitioning, promote insulin resistance, and drive ectopic lipid accumulation. RECENT

findingsResearch shows that metabolic dysfunction arises in both obese and non-obese settings and correlates more closely with impaired control of fatty acid flux than with adiposity itself. Higher expression of lipolytic receptors, including those targeted by weight-loss medications, together with genes that regulate lipolysis through insulin signaling, is associated with greater weight loss and improved systemic metabolic health. In this review, we highlight canonical and noncanonical mechanisms governing lipolytic regulation and contrast pathological lipolysis with the tightly controlled lipolysis observed during weight loss. Together, these findings reframe lipolysis as a central determinant of metabolic health and a therapeutic target when precisely regulated.

Indexed as

LipolysisMetabolic DiseasesObesityAdipocytesAdipose TissueAnimalsHumansInsulin ResistanceSignal TransductionAdipocyteLipolysisMetabolic disease

Identifiers

PMID41961206
PMCPMC13068693

What Socratic holds

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LicenceCC BY
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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.