Evidence map›Paper›PMID 30968756›Full record

ReviewPhysiology (Bethesda, Md.)2019

Hepatic Insulin Clearance: Mechanism and Physiology.

Sonia M Najjar, Germán Perdomo

Open access · bronzeAbstract readReview
In one paragraph

Review in Physiology (Bethesda, Md.), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 151 papers.

0numbers the graph read from it
0cells of the map it votes in
151citing papers in PubMed
30.7field-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

151 citing papers in PubMed, 235 citations in OpenAlex.

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91 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

2 authors at 2 institutions in 2 countries.

Sonia M NajjarDepartment of Biomedical Sciences, Ohio University , Athens, Ohio.
Germán PerdomoDepartamento de Ciencias de la Salud, Universidad de Burgos , Burgos , Spain.
Ohio University · USUniversidad de Burgos · ES

Funding

SUBSTRATES AND INSULIN RECEPTOR ENDOCYTOSISR01DK054254 · NIDDK · UNIVERSITY OF TOLEDO HEALTH SCI CAMPUS · PI NAJJAR, SONIA M. · 2000 to 2021
$5.8M
CEACAM1: A link between metabolic and cardiovascular diseasesR01HL112248 · NHLBI · UNIVERSITY OF TOLEDO HEALTH SCI CAMPUS · PI NAJJAR, SONIA M. · 2012 to 2016
$1.9M
Insulin resistance in the pathogenesis of NASHR01DK083850 · NIDDK · UNIVERSITY OF TOLEDO HEALTH SCI CAMPUS · PI NAJJAR, SONIA M. · 2009 to 2010
$749k
NHLBI NIH HHS R01 HL112248NIDDK NIH HHS R01 DK054254NIDDK NIH HHS R01 DK083850
6 · The paper itself

Abstract

Upon its secretion from pancreatic β-cells, insulin reaches the liver through the portal circulation to exert its action and eventually undergo clearance in the hepatocytes. In addition to insulin secretion, hepatic insulin clearance regulates the homeostatic level of insulin that is required to reach peripheral insulin target tissues to elicit proper insulin action. Receptor-mediated insulin uptake followed by its degradation constitutes the basic mechanism of insulin clearance. Upon its phosphorylation by the insulin receptor tyrosine kinase, carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1) takes part in the insulin-insulin receptor complex to increase the rate of its endocytosis and targeting to the degradation pathways. This review summarizes how this process is regulated and how it is associated with insulin-degrading enzyme in the liver. It also discusses the physiological implications of impaired hepatic insulin clearance: Whereas reduced insulin clearance cooperates with increased insulin secretion to compensate for insulin resistance, it can also cause hepatic insulin resistance. Because chronic hyperinsulinemia stimulates hepatic de novo lipogenesis, impaired insulin clearance also causes hepatic steatosis. Thus impaired insulin clearance can underlie the link between hepatic insulin resistance and hepatic steatosis. Delineating these regulatory pathways should lead to building more effective therapeutic strategies against metabolic syndrome.

Indexed as

AnimalsAntigens, CDCell Adhesion MoleculesEndocytosisHepatocytesHumansInsulinInsulysinLiverReceptor, InsulinSignal TransductionAntigens, CDCD66 antigensCell Adhesion MoleculesInsulinInsulysinReceptor, Insulin

Identifiers

PMID30968756
PMCPMC6734066
OpenAlexW2937552917

What Socratic 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 Socratic graph.