Evidence map›Paper›PMID 19819977›Full record

ArticleEndocrinology2009

Impaired skeletal muscle beta-adrenergic activation and lipolysis are associated with whole-body insulin resistance in rats bred for low intrinsic exercise capacity.

Sarah J Lessard, Donato A Rivas, Zhi-Ping Chen, Bryce J van Denderen, Matthew J Watt, Lauren G Koch, Steven L Britton, Bruce E Kemp, John A Hawley

Open access · greenAbstract read
In one paragraph

Article in Endocrinology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
4.2field-weighted citation impact, top 6% 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

32 citing papers in PubMed, 56 citations in OpenAlex.

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  12. Beta2-adrenoceptor stimulation has no effect on skeletal muscle glucose uptake.Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2014
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  15. Leanness and heightened nonresting energy expenditure: role of skeletal muscle activity thermogenesis.American journal of physiology. Endocrinology and metabolism · 2014
    Article
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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

9 authors at 4 institutions in 2 countries.

Sarah J LessardJoslin Diabetes Center, 1 Joslin Place, Boston, Massachusetts 02215, USA. sarah.lessard@joslin.harvard.edu
Donato A Rivas
Zhi-Ping Chen
Bryce J van Denderen
Matthew J Watt
Lauren G Koch
Steven L Britton
Bruce E Kemp
John A Hawley
St Vincents Institute of Medical Research · AUUniversity of Michigan–Ann Arbor · USMonash University · AUUniversity of Melbourne · AU

Funding

RESOURCE FOR RAT GENETIC MODELS OF AEROBIC CAPACITYR24RR017718 · NCRR · UNIVERSITY OF TOLEDO HEALTH SCI CAMPUS · PI BRITTON, STEVEN LOYAL · 2003 to 2011
$4.0M
NCRR NIH HHS R24 RR017718NCRR NIH HHS R24 RR17718
6 · The paper itself

Abstract

Rats selectively bred for high endurance running capacity (HCR) have higher insulin sensitivity and improved metabolic health compared with those bred for low endurance capacity (LCR). We investigated several skeletal muscle characteristics, in vitro and in vivo, that could contribute to the metabolic phenotypes observed in sedentary LCR and HCR rats. After 16 generations of selective breeding, HCR had approximately 400% higher running capacity (P < 0.001), improved insulin sensitivity (P < 0.001), and lower fasting plasma glucose and triglycerides (P < 0.05) compared with LCR. Skeletal muscle ceramide and diacylglycerol content, basal AMP-activated protein kinase (AMPK) activity, and basal lipolysis were similar between LCR and HCR. However, the stimulation of lipolysis in response to 10 mum isoproterenol was 70% higher in HCR (P = 0.004). Impaired isoproterenol sensitivity in LCR was associated with lower basal triacylglycerol lipase activity, Ser660 phosphorylation of HSL, and beta2-adrenergic receptor protein content in skeletal muscle. Expression of the orphan nuclear receptor Nur77, which is induced by beta-adrenergic signaling and is associated with insulin sensitivity, was lower in LCR (P < 0.05). Muscle protein content of Nur77 target genes, including uncoupling protein 3, fatty acid translocase/CD36, and the AMPK gamma3 subunit were also lower in LCR (P < 0.05). Our investigation associates whole-body insulin resistance with impaired beta-adrenergic response and reduced expression of genes that are critical regulators of glucose and lipid metabolism in skeletal muscle. We identify impaired beta-adrenergic signal transduction as a potential mechanism for impaired metabolic health after artificial selection for low intrinsic exercise capacity.

Indexed as

ExerciseInsulin ResistanceLipolysisAdrenergic beta-AgonistsAnimalsDiabetes Mellitus, Type 2Disease Models, AnimalGene ExpressionHumansHybridization, GeneticIsoproterenolMaleMuscle, SkeletalPhysical EnduranceRatsReceptors, Adrenergic, beta-2Adrenergic beta-AgonistsIsoproterenolReceptors, Adrenergic, beta-2

Identifiers

PMID19819977
PMCPMC2775978
OpenAlexW1980446844

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.