Evidence map›Paper›PMID 26269521›Full record

ArticleAmerican journal of physiology. Regulatory, integrative and comparative physiology2015

Aberrant REDD1-mTORC1 responses to insulin in skeletal muscle from Type 2 diabetics.

David L Williamson, Cory M Dungan, Abeer M Mahmoud, Jacob T Mey, Brian K Blackburn, Jacob M Haus

Abstract read
In one paragraph

Article in American journal of physiology. Regulatory, integrative and comparative physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

29 citing papers in PubMed, 37 citations in OpenAlex.

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  17. Role of mTOR in Glucose and Lipid Metabolism.International journal of molecular sciences · 2018
    Review
  18. Article
  19. Article
  20. Dicarbonyl stress and glyoxalase enzyme system regulation in human skeletal muscle.American journal of physiology. Regulatory, integrative and comparative physiology · 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

6 authors at 2 institutions in 1 country.

David L WilliamsonDepartment of Exercise and Nutrition Sciences, School of Public Health and Health Professions, University at Buffalo, Buffalo, New York; and davidwil@buffalo.edu.
Cory M DunganDepartment of Exercise and Nutrition Sciences, School of Public Health and Health Professions, University at Buffalo, Buffalo, New York; and.
Abeer M MahmoudDepartment of Kinesiology and Nutrition, University of Illinois at Chicago, Chicago, Illinois.
Jacob T MeyDepartment of Kinesiology and Nutrition, University of Illinois at Chicago, Chicago, Illinois.
Brian K BlackburnDepartment of Kinesiology and Nutrition, University of Illinois at Chicago, Chicago, Illinois.
Jacob M HausDepartment of Kinesiology and Nutrition, University of Illinois at Chicago, Chicago, Illinois.
University of Illinois Chicago · USUniversity at Buffalo, State University of New York · US

Funding

PHS HHS ULRR029879
6 · The paper itself

Abstract

The objective of this study was to establish whether alterations in the REDD1-mTOR axis underlie skeletal muscle insensitivity to insulin in Type 2 diabetic (T2D), obese individuals. Vastus lateralis muscle biopsies were obtained from lean, control and obese, T2D subjects under basal and after a 2-h hyperinsulinemic (40 mU·m(-2)·min(-1))-euglycemic (5 mM) clamp. Muscle lysates were examined for total REDD1, and phosphorylated Akt, S6 kinase 1 (S6K1), 4E-BP1, ERK1/2, and MEK1/2 via Western blot analysis. Under basal conditions [(-) insulin], T2D muscle exhibited higher S6K1 and ERK1/2 and lower 4E-BP1 phosphorylation (P < 0.05), as well as elevations in blood cortisol, glucose, insulin, glycosylated hemoglobin (P < 0.05) vs. lean controls. Following insulin infusion, whole body glucose disposal rates (GDR; mg/kg/min) were lower (P < 0.05) in the T2D vs. the control group. The basal-to-insulin percent change in REDD1 expression was higher (P < 0.05) in muscle from the T2D vs. the control group. Whereas, the basal-to-insulin percent change in muscle Akt, S6K1, ERK1/2, and MEK1/2 phosphorylation was significantly lower (P < 0.05) in the T2D vs. the control group. Findings from this study propose a REDD1-regulated mechanism in T2D skeletal muscle that may contribute to whole body insulin resistance and may be a target to improve insulin action in insulin-resistant individuals.

Indexed as

AdultCase-Control StudiesDiabetes Mellitus, Type 2FemaleHumansInsulinMaleMechanistic Target of Rapamycin Complex 1Middle AgedMultiprotein ComplexesMuscle, SkeletalTOR Serine-Threonine KinasesTranscription FactorsDDIT4 protein, humanInsulinMechanistic Target of Rapamycin Complex 1Multiprotein ComplexesTOR Serine-Threonine KinasesTranscription Factorsglucocorticoidinsulin resistancemTORsignaling

Identifiers

PMID26269521
PMCPMC4666944
OpenAlexW2179653083

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.