Evidence map›Paper›PMID 40675912›Full record

ArticleJournal of clinical lipidology

Lipoprotein profiles across a spectrum of insulin signaling.

Michael Hwang, Robert D Shamburek, Maureen Sampson, Brent S Abel, Marissa Lightbourne, Rebecca J Brown

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of clinical lipidology. 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. 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

6 authors.

Michael HwangNational Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, USA (Dr Hwang, Abel, Lightbourne, and Brown).
Robert D ShamburekNational Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA (Dr Shamburek).
Maureen SampsonDepartment of Laboratory Medicine, Clinical Center, National Institutes of Health, Bethesda, MD, USA (Dr Sampson).
Brent S AbelNational Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, USA (Dr Hwang, Abel, Lightbourne, and Brown).
Marissa LightbourneNational Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, USA (Dr Hwang, Abel, Lightbourne, and Brown).
Rebecca J BrownNational Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, USA (Dr Hwang, Abel, Lightbourne, and Brown). Electronic address: rebecca.brown@nih.gov.

Funding

Molecular and Clinical Studies of Insulin ResistanceZIADK047050 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI BROWN, REBECCA · 2009 to 2025
$6.1M
Intramural NIH HHS ZIA DK047050
6 · The paper itself

Abstract

backgroundObesity and type 2 diabetes (T2D) are associated with insulin resistance (IR), a risk factor for atherosclerotic cardiovascular disease (ASCVD). In these conditions, IR affects only a subset of insulin signaling pathways, with preserved insulin signaling in others (termed "pathway-selective IR"). Consequently, individuals with obesity and T2D develop both hypertriglyceridemia from excess insulin signaling and hyperglycemia from insufficient insulin signaling.

objectiveAs IR involves biology mediated by both increased and decreased insulin signaling, we created a conceptual rare disease model to better understand whether ASCVD risk in states of IR is predominantly driven by excessive insulin action, insufficient insulin action, or a combination of both.

methodsWe compared nuclear magnetic resonance lipoprotein profiles (markers of ASCVD risk) in 14 patients (86% female, age 39 ± 17 years) with type B IR (TBIR), a disorder where autoantibodies against the insulin receptor block all insulin signaling (low insulin signaling), which is restored in remission (normal insulin signaling). Age and sex-matched patients with lipodystrophy were included to represent high insulin signaling.

resultsAcross the spectrum of insulin signaling, from lowest (TBIR active) to intermediate (TBIR remission) to highest (lipodystrophy), there were increases in all triglyceride-rich lipoprotein parameters. We also observed a shift toward smaller high-density lipoprotein particles (HDL-Ps), with reciprocal decreases in large HDL-Ps and increases in small HDL-Ps across groups.

conclusionExcess insulin signaling contributes to a proatherogenic lipoprotein profile. Interventions that downregulate or rebalance insulin signaling may offer cardiovascular benefits for individuals with severe (lipodystrophy) and mild (obesity and T2D) forms of pathway-selective IR.

Indexed as

InsulinLipoproteinsSignal TransductionAdultDiabetes Mellitus, Type 2FemaleHumansInsulin ResistanceMaleMiddle AgedInsulinLipoproteinsAtherosclerosisInsulinInsulin resistanceInsulin signalingLipodystrophyLipoproteinsType B insulin resistance

Identifiers

PMID40675912
PMCPMC12320491

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Registered trials

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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.