Evidence map›Paper›PMID 28731034›Full record

ReviewNature reviews. Endocrinology2017

Regulation of hepatic glucose metabolism in health and disease.

Max C Petersen, Daniel F Vatner, Gerald I Shulman

Abstract readComparative StudyReview
In one paragraph

Review in Nature reviews. Endocrinology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 543 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
543citing papers in PubMed, 4 pooled it
32.6field-weighted citation impact, top 1% 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

543 citing papers in PubMed, 4 syntheses or guidelines pooled it, 1,081 citations in OpenAlex.

  1. Efficacy and mechanisms ofFrontiers in pharmacology · 2026
    Pooled it
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  8. Review
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  13. DietaryGenes · 2026
    Article
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  16. Review
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  19. Review
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483 more citing papers are in PubMed but not listed here.

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

3 authors at 1 institution in 1 country.

Max C PetersenDepartment of Internal Medicine, Yale School of Medicine.
Daniel F VatnerDepartment of Internal Medicine, Yale School of Medicine.
Gerald I ShulmanDepartment of Internal Medicine, Yale School of Medicine.
Yale University · US

Funding

Yale Clinical and Translational Science Award (U Component)UL1TR001863 · NCATS · YALE UNIVERSITY · PI John H. Krystal, LUCILA OHNO-MACHADO · 2016 to 2026
$102.9M
Yale Diabetes Research CenterP30DK045735 · NIDDK · YALE UNIVERSITY · PI Richard A Flavell · 1993 to 2026
$44.0M
MEDICAL SCIENTIST TRAINING PROGRAMT32GM007205 · NIGMS · YALE UNIVERSITY · PI KAZMIERCZAK, BARBARA I · 1985 to 2019
$42.9M
NMR STUDIES OF GLYCOGEN METABOLISM IN HUMANSR01DK049230 · NIDDK · YALE UNIVERSITY · PI SHULMAN, GERALD I · 1995 to 2014
$5.4M
Mechanisms of Lipid-Induced Hepatic Insulin ResistanceR01DK040936 · NIDDK · YALE UNIVERSITY · PI SHULMAN, GERALD I · 1989 to 2015
$5.1M
Effects of Hepatic Acetyl-CoA Carboxylase Inhibition on NAFLD and Hepatic Insulin ResistanceR01DK113984 · NIDDK · YALE UNIVERSITY · PI SHULMAN, GERALD I · 2017 to 2021
$3.7M
In vivo regulation of lipid flux in the etiology of NAFLD and Insulin ResistanceK23DK102874 · NIDDK · YALE UNIVERSITY · PI VATNER, DANIEL · 2015 to 2019
$776k
Novel mechanisms of insulin receptor inhibition in liver by nPKCs and MARCH1F30DK104596 · NIDDK · YALE UNIVERSITY · PI PETERSEN, MAX CHRISTIAN · 2015 to 2017
$124k
Howard Hughes Medical InstituteNCATS NIH HHS UL1 TR001863NIDDK NIH HHS F30 DK104596NIDDK NIH HHS K23 DK102874NIDDK NIH HHS P30 DK045735NIDDK NIH HHS R01 DK040936NIDDK NIH HHS R01 DK049230NIDDK NIH HHS R01 DK113984NIGMS NIH HHS T32 GM007205
6 · The paper itself

Abstract

The liver is crucial for the maintenance of normal glucose homeostasis - it produces glucose during fasting and stores glucose postprandially. However, these hepatic processes are dysregulated in type 1 and type 2 diabetes mellitus, and this imbalance contributes to hyperglycaemia in the fasted and postprandial states. Net hepatic glucose production is the summation of glucose fluxes from gluconeogenesis, glycogenolysis, glycogen synthesis, glycolysis and other pathways. In this Review, we discuss the in vivo regulation of these hepatic glucose fluxes. In particular, we highlight the importance of indirect (extrahepatic) control of hepatic gluconeogenesis and direct (hepatic) control of hepatic glycogen metabolism. We also propose a mechanism for the progression of subclinical hepatic insulin resistance to overt fasting hyperglycaemia in type 2 diabetes mellitus. Insights into the control of hepatic gluconeogenesis by metformin and insulin and into the role of lipid-induced hepatic insulin resistance in modifying gluconeogenic and net hepatic glycogen synthetic flux are also discussed. Finally, we consider the therapeutic potential of strategies that target hepatosteatosis, hyperglucagonaemia and adipose lipolysis.

Indexed as

Insulin ResistanceCase-Control StudiesDiabetes Mellitus, Type 2Fatty LiverFemaleGluconeogenesisGlucoseHumansLiverLiver GlycogenMaleReference ValuesGlucoseLiver Glycogen

Identifiers

PMID28731034
PMCPMC5777172
OpenAlexW2736390409

What OpenQuestion holds

Textmetadata
LicenceTDM
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.