Evidence map›Paper›PMID 30168804›Full record

ReviewThe Journal of clinical investigation2018

Altered mitochondrial function in insulin-deficient and insulin-resistant states.

Gregory N Ruegsegger, Ana L Creo, Tiffany M Cortes, Surendra Dasari, K Sreekumaran Nair

Open access · bronzeAbstract readReview
In one paragraph

Review in The Journal of clinical investigation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 113 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
113citing papers in PubMed, 2 pooled it
8.6field-weighted citation impact, top 2% 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

113 citing papers in PubMed, 2 syntheses or guidelines pooled it, 192 citations in OpenAlex.

  1. Pooled it
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  9. CRISPR/Cas9-DrivenInternational journal of medical sciences · 2026
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53 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

5 authors at 1 institution in 1 country.

Gregory N Ruegsegger
Ana L Creo
Tiffany M Cortes
Surendra Dasari
K Sreekumaran Nair
Mayo Clinic · US

Funding

TECHNOLOGY NMR SPECTROSCOPYU24DK100469 · NIDDK · MAYO CLINIC ROCHESTER · PI NAIR, K SREEKUMARAN · 2013 to 2017
$9.0M
The Impact of Insulin Therapy on Protein Turnover in Pre-Diabetic CF PatientsR01DK101402 · NIDDK · UNIVERSITY OF MINNESOTA · PI MORAN, ANTOINETTE M. · 2015 to 2019
$3.5M
Postdoctoral Training Program for Research on AgingT32AG049672 · NIA · MAYO CLINIC ROCHESTER · PI PASSOS, JOAO · 2016 to 2022
$1.3M
NIA NIH HHS T32 AG049672NIDDK NIH HHS R01 DK101402NIDDK NIH HHS U24 DK100469
6 · The paper itself

Abstract

Diabetes profoundly alters fuel metabolism; both insulin deficiency and insulin resistance are characterized by inefficient mitochondrial coupling and excessive production of reactive oxygen species (ROS) despite their association with normal to high oxygen consumption. Altered mitochondrial function in diabetes can be traced to insulin's pivotal role in maintaining mitochondrial proteome abundance and quality by enhancing mitochondrial biogenesis and preventing proteome damage and degradation, respectively. Although insulin enhances gene transcription, it also induces decreases in amino acids. Thus, if amino acid depletion is not corrected, increased transcription will not result in enhanced translation of transcripts to proteins. Mitochondrial biology varies among tissues, and although most studies in humans are performed in skeletal muscle, abnormalities have been reported in multiple organs in preclinical models of diabetes. Nutrient excess, especially fat excess, alters mitochondrial physiology by driving excess ROS emission that impairs insulin action. Excessive ROS irreversibly damages DNA and proteome with adverse effects on cellular functions. In insulin-resistant people, aerobic exercise stimulates both mitochondrial biogenesis and efficiency concurrent with enhancement of insulin action. This Review discusses the association between both insulin-deficient and insulin-resistant diabetes and alterations in mitochondrial proteome homeostasis and function that adversely affect cellular functions, likely contributing to many diabetic complications.

Indexed as

Amino AcidsAnimalsDiabetes MellitusDNA DamageFemaleHumansInsulinInsulin ResistanceMaleMiceMitochondriaMitochondria, LiverMitochondria, MuscleModels, BiologicalOxygen ConsumptionProteomeAmino AcidsInsulinProteomeReactive Oxygen Species

Identifiers

PMID30168804
PMCPMC6118582
OpenAlexW2889183927

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.