Evidence map›Paper›PMID 27748389›Full record

ReviewNature reviews. Nephrology2016

The impact of insulin resistance on the kidney and vasculature.

Ferruh Artunc, Erwin Schleicher, Cora Weigert, Andreas Fritsche, Norbert Stefan, Hans-Ulrich Häring

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Nephrology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 279 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
279citing papers in PubMed, 4 pooled it
12.4field-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

279 citing papers in PubMed, 4 syntheses or guidelines pooled it, 441 citations in OpenAlex.

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  18. Insulin receptorNature communications · 2026
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219 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

6 authors at 1 institution in 1 country.

Ferruh ArtuncDepartment of Internal Medicine IV, Division of Endocrinology, Diabetology, Vascular Disease, Nephrology and Clinical Chemistry, University Hospital Tübingen, Otfried-Mueller-Strasse 10, 72076 Tübingen, Germany.
Erwin SchleicherDepartment of Internal Medicine IV, Division of Endocrinology, Diabetology, Vascular Disease, Nephrology and Clinical Chemistry, University Hospital Tübingen, Otfried-Mueller-Strasse 10, 72076 Tübingen, Germany.
Cora WeigertDepartment of Internal Medicine IV, Division of Endocrinology, Diabetology, Vascular Disease, Nephrology and Clinical Chemistry, University Hospital Tübingen, Otfried-Mueller-Strasse 10, 72076 Tübingen, Germany.
Andreas FritscheDepartment of Internal Medicine IV, Division of Endocrinology, Diabetology, Vascular Disease, Nephrology and Clinical Chemistry, University Hospital Tübingen, Otfried-Mueller-Strasse 10, 72076 Tübingen, Germany.
Norbert StefanDepartment of Internal Medicine IV, Division of Endocrinology, Diabetology, Vascular Disease, Nephrology and Clinical Chemistry, University Hospital Tübingen, Otfried-Mueller-Strasse 10, 72076 Tübingen, Germany.
Hans-Ulrich HäringDepartment of Internal Medicine IV, Division of Endocrinology, Diabetology, Vascular Disease, Nephrology and Clinical Chemistry, University Hospital Tübingen, Otfried-Mueller-Strasse 10, 72076 Tübingen, Germany.
University of Tübingen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Insulin resistance is a systemic disorder that affects many organs and insulin-regulated pathways. The disorder is characterized by a reduced action of insulin despite increased insulin concentrations (hyperinsulinaemia). The effects of insulin on the kidney and vasculature differ in part from the effects on classical insulin target organs. Insulin causes vasodilation by enhancing endothelial nitric oxide production through activation of the phosphatidylinositol 3-kinase pathway. In insulin-resistant states, this pathway is impaired and the mitogen-activated protein kinase pathway stimulates vasoconstriction. The action of insulin on perivascular fat tissue and the subsequent effects on the vascular wall are not fully understood, but the hepatokine fetuin-A, which is released by fatty liver, might promote the proinflammatory effects of perivascular fat. The strong association of salt-sensitive arterial hypertension with insulin resistance indicates an involvement of the kidney in the insulin resistance syndrome. The insulin receptor is expressed on renal tubular cells and podocytes and insulin signalling has important roles in podocyte viability and tubular function. Renal sodium transport is preserved in insulin resistance and contributes to the salt-sensitivity of blood pressure in hyperinsulinaemia. Therapeutically, renal and vascular insulin resistance can be improved by an integrated holistic approach aimed at restoring overall insulin sensitivity and improving insulin signalling.

Indexed as

Insulin ResistanceAdipose TissueAnimalsDisease Models, AnimalEndotheliumHumansKidneyKidney TubulesMetabolic SyndromeReceptor Cross-TalkSignal TransductionSodium Chloride, DietarySodium Chloride, Dietary

Identifiers

PMID27748389
OpenAlexW2536523837

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.