Evidence map›Paper›PMID 24907277›Full record

ReviewThe Journal of biological chemistry2014

Pathway-selective insulin resistance and metabolic disease: the importance of nutrient flux.

Yolanda F Otero, John M Stafford, Owen P McGuinness

Open access · hybridAbstract readReview
In one paragraph

Review in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed, 1 pooled it
4.1field-weighted citation impact, top 5% 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

48 citing papers in PubMed, 1 synthesis or guideline pooled it, 91 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Review
  15. Article
  16. Journal of diabetes and metabolic disorders · 2021
    Article
  17. Review
  18. Review
  19. Sex, Cells, and Asthma.Mayo Clinic proceedings · 2021
    Review
  20. Review
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 2 institutions in 2 countries.

Yolanda F Otero
John M Stafford
Owen P McGuinness
Institute of Molecular Biology and Biophysics · RUVanderbilt University · US

Funding

Vanderbilt Diabetes Research CenterP30DK020593 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI ALVIN C POWERS · 2012 to 2026
$29.3M
TRANSGENIC MOUSE/ ES CELL SHARES RESOURCESP60DK020593 · NIDDK · VANDERBILT UNIVERSITY · PI POWERS, ALVIN C · 1986 to 2011
$28.1M
Vanderbilt Mouse Metabolic Physiology CenterU24DK059637 · NIDDK · VANDERBILT UNIVERSITY · PI WASSERMAN, DAVID H · 2001 to 2015
$14.9M
NUTRITION, INFECTION AND HEPATIC CARBOHYDRATE METABOLISMR01DK043748 · NIDDK · VANDERBILT UNIVERSITY · PI MCGUINNESS, OWEN P · 1997 to 2018
$7.9M
Vanderbilt Mouse Metabolic Phenotyping CenterU2CDK059637 · NIDDK · VANDERBILT UNIVERSITY · PI WASSERMAN, DAVID H · 2016 to 2021
$6.3M
Impact of Inflammation on the Control of Muscle Glucose UptakeR01DK078188 · NIDDK · VANDERBILT UNIVERSITY · PI MCGUINNESS, OWEN P · 2009 to 2013
$1.7M
Nutrition Infection and Hepatic Carbohydrate MetabolismR56DK043748 · NIDDK · VANDERBILT UNIVERSITY · PI MCGUINNESS, OWEN P · 2009 to 2009
$500k
REGULATION OF HEPATIC GLUCOSE METABOLISM IN INFECTIONR29DK043748 · NIDDK · VANDERBILT UNIVERSITY · PI MCGUINNESS, OWEN P · 1992 to 1996
–
Cholesteryl ester transfer protein, a novel mediator of insulin sensitivityI01BX002223 · VA · VETERANS HEALTH ADMINISTRATION · PI STAFFORD, JOHN MICHAEL · 2014 to 2017
–
BLRD VA I01 BX002223NIDDK NIH HHS DK020593NIDDK NIH HHS DK043748NIDDK NIH HHS DK059637NIDDK NIH HHS DK078188NIDDK NIH HHS P30 DK020593NIDDK NIH HHS P60 DK020593NIDDK NIH HHS R01 DK043748NIDDK NIH HHS R01 DK078188NIDDK NIH HHS R56 DK043748NIDDK NIH HHS U24 DK059637
6 · The paper itself

Abstract

Hepatic glucose and lipid metabolism are altered in metabolic disease (e.g. obesity, metabolic syndrome, and Type 2 diabetes). Insulin-dependent regulation of glucose metabolism is impaired. In contrast, lipogenesis, hypertriglyceridemia, and hepatic steatosis are increased. Because insulin promotes lipogenesis and liver fat accumulation, to explain the elevation in plasma and tissue lipids, investigators have suggested the presence of pathway-selective insulin resistance. In this model, insulin signaling to glucose metabolism is impaired, but insulin signaling to lipid metabolism is intact. We discuss the evidence for the differential regulation of hepatic lipid and glucose metabolism. We suggest that the primary phenotypic driver is altered substrate delivery to the liver, as well as the repartitioning of hepatic nutrient handling. Specific alterations in insulin signaling serve to amplify the alterations in hepatic substrate metabolism. Thus, hyperinsulinemia and its resultant increased signaling may facilitate lipogenesis, but are not the major drivers of the phenotype of pathway-selective insulin resistance.

Indexed as

Insulin ResistanceAnimalsDiabetes Mellitus, Type 2Fatty LiverGlucoseHumansHypertriglyceridemiaInsulinLipogenesisLiverMetabolic SyndromeSignal TransductionGlucoseInsulin

Identifiers

PMID24907277
PMCPMC4110258
OpenAlexW2092608666

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.