Evidence map›Paper›PMID 29160303›Full record

Trial reportThe pharmacogenomics journal2018

The PNPLA3 I148M variant is associated with transaminase elevations in type 2 diabetes patients treated with basal insulin peglispro.

S Pillai, S Duvvuru, P Bhatnagar, W Foster, M Farmen, S Shankar, C Harris, E Bastyr, B Hoogwerf, A Haupt

Abstract readClinical Trial, Phase IIIRandomized Controlled Trial
PubMed Publisher
In one paragraph

Trial report in The pharmacogenomics journal, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 2 pooled it
1.2field-weighted citation impact, top 20% 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

9 citing papers in PubMed, 2 syntheses or guidelines pooled it, 19 citations in OpenAlex.

  1. Impact of PNPLA3 I148M on Drug-Induced Hepatocellular Liver Injury: A Systematic Review and Meta-Analysis.Liver international : official journal of the International Association for the Study of the Liver · 2025
    Pooled it
  2. Guideline
  3. Review
  4. Review
  5. Review
  6. Review
  7. Novel Insights into the Genetic Landscape of Nonalcoholic Fatty Liver Disease.International journal of environmental research and public health · 2019
    Review
  8. Article
  9. Coding variants inHepatology communications · 2018
    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

10 authors at 2 institutions in 1 country.

S PillaiEli Lilly and Company, Indianapolis, IN, USA.
S DuvvuruEli Lilly and Company, Indianapolis, IN, USA.
P BhatnagarEli Lilly and Company, Indianapolis, IN, USA.
W FosterEli Lilly and Company, Indianapolis, IN, USA.
M FarmenEli Lilly and Company, Indianapolis, IN, USA.
S ShankarEli Lilly and Company, Indianapolis, IN, USA.
C HarrisEli Lilly and Company, Indianapolis, IN, USA.
E BastyrDivision of Endocrinology and Metabolism, Indiana University School of Medicine, Indianapolis, IN, USA.
B HoogwerfEli Lilly and Company, Indianapolis, IN, USA.
A HauptEli Lilly and Company, Indianapolis, IN, USA.
Eli Lilly (United States) · USIndiana University School of Medicine

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Basal insulin peglispro (BIL) is a novel insulin with hepato-preferential action. In phase 3 trials, BIL showed significantly improved glycemic control but higher levels of transaminases (alanine aminotransferase (ALT) and aspartate aminotransferase (AST)), triglycerides (TGs) and liver fat content (LFC) compared with insulin glargine (GL). As variants in PNPLA3 (I148M) and TM6SF2 (E167K) are associated with nonalcoholic fatty liver disease, we assessed these variants in type 2 diabetes (T2D) patients randomized to receive BIL (n=1822) or GL (n=1270) in three phase 3 trials. Magnetic resonance imaging assessments of LFC were conducted in a subset of patients (n=296). Analyses showed α-corrected significant increases in change from baseline in AST (P=0.0004) and nominal increases in ALT (P=0.019), and LFC (P=0.035) for PNPLA3 (148M/M) genotypes in the BIL arm at 26 weeks but no significant associations in GL. PNPLA3 (148M/M) was also associated with increases in total cholesterol (P=0.014) and low-density lipoprotein cholesterol (P=0.005) but not with hemoglobin A1c or TG. T2D patients with the PNPLA3 (148M/M) genotype treated with BIL may be more susceptible to increased liver fat deposition. The current data provide further insights into the biological role of PNPLA3 in lipid metabolism.

Indexed as

AcyltransferasesAdultAlanine TransaminaseAspartate AminotransferasesBlood GlucoseCholesterol, LDLDiabetes Mellitus, Type 2FemaleGenotypeHumansHypoglycemic AgentsInsulin LisproLipaseLipid MetabolismLiverMagnetic Resonance ImagingAcyltransferasesAlanine TransaminaseAspartate Aminotransferasesbasal insulin peglisproBlood GlucoseCholesterol, LDLHypoglycemic AgentsInsulin LisproLipaseMembrane ProteinsPhospholipases A2, Calcium-IndependentPNPLA3 protein, humanPolyethylene GlycolsTriglycerides

Identifiers

PMID29160303
OpenAlexW2768431995

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.