Evidence map›Paper›PMID 37291473›Full record

ArticleDigestive diseases and sciences2023

Low LDL Cholesterol Is Not an Independent Risk Factor for Hepatic Steatosis.

Scott McHenry, Ameen Awad, Julia Kozlitina, Nathan O Stitziel, Nicholas O Davidson

Abstract read
PubMed Publisher
In one paragraph

Article in Digestive diseases and sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.4field-weighted citation impact, top 35% 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

0 citing papers in PubMed, 2 citations in OpenAlex.

No citing paper in PubMed yet.

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 2 institutions in 1 country.

Scott McHenryDivision of Gastroenterology, Department of Medicine, Washington University in Saint Louis, St. Louis, MO, 53110, USA. smchenry@wustl.edu.ORCID http://orcid.org/0000-0001-6786-0345
Ameen AwadDivision of Gastroenterology, Department of Medicine, Washington University in Saint Louis, St. Louis, MO, 53110, USA.
Julia KozlitinaEugene McDermott Center for Human Growth and Development, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Nathan O StitzielDivision of Gastroenterology, Department of Medicine, Washington University in Saint Louis, St. Louis, MO, 53110, USA.
Nicholas O DavidsonDivision of Gastroenterology, Department of Medicine, Washington University in Saint Louis, St. Louis, MO, 53110, USA.
Washington University in St. Louis · USSouthwestern Medical Center · US

Funding

Washington University Institute of Clinical and Translational Sciences (TL1)TL1TR002344 · NCATS · WASHINGTON UNIVERSITY · PI Jay F. Piccirillo · 2017 to 2026
$8.5M
Impaired VLDL secretion, progression and reversal of hepatic fibrogenesisR01DK119437 · NIDDK · WASHINGTON UNIVERSITY · PI Nicholas O. Davidson · 2019 to 2026
$3.8M
NCATS NIH HHS TL1 TR002344NIDDK NIH HHS R01 DK119437
6 · The paper itself

Abstract

backgroundGenetic mutations causing defective VLDL secretion and low LDL cholesterol are associated with hepatic steatosis and nonalcoholic fatty liver disease (NAFLD).

aimsDetermine if low LDL cholesterol (< 5th percentile) was an independent predictor of hepatic steatosis.

methodsSecondary data analysis of the Dallas Heart study (an urban, multiethnic, probability-based sample), we defined hepatic steatosis utilizing intrahepatic triglyceride (IHTG) analyzed using magnetic resonance spectroscopy in conjunction and available demographic, serological and genetic information. We exclude patients on lipid lowering medications.

resultsOf the 2094 subjects that met our exclusion criteria, 86 had a low LDL cholesterol, of whom 19 (22%) exhibited hepatic steatosis. After matching for age, sex, BMI, and alcohol consumption, low LDL cholesterol was not a risk factor for hepatic steatosis compared to those with normal (50-180 mg/dL) or high (> 180 mg/dL) LDL. When analyzed as a continuous variable, we observed lower IHTG in the low LDL group compared to the normal or high LDL groups (2.2%, 3.5%, 4.6%; all pairwise comparisons p < 0.001). Subjects with both hepatic steatosis and low LDL cholesterol exhibited a more favorable lipid profile but similar insulin resistance and hepatic fibrosis risk compared to other subjects with hepatic steatosis. The distribution of variant alleles associated with NAFLD, including PNPLA3, GCKR, and MTTP was indistinguishable between subjects with hepatic steatosis and low versus high LDL cholesterol.

conclusionThese findings suggest that low serum LDL levels are not a useful predictor of hepatic steatosis and NAFLD. Moreover, subjects with low LDL exhibit a more favorable lipid profile and lower IHTG.

Indexed as

Insulin ResistanceNon-alcoholic Fatty Liver DiseaseHumansLiverLiver CirrhosisRisk FactorsTriglyceridesTriglyceridesAlcoholAPOBMTTPNAFLD

Identifiers

PMID37291473
OpenAlexW4379876513

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.