Evidence map›Paper›PMID 27581061›Full record

ArticleScientific reports2016

Myostatin inhibition therapy for insulin-deficient type 1 diabetes.

Samantha K Coleman, Irena A Rebalka, Donna M D'Souza, Namita Deodhare, Eric M Desjardins, Thomas J Hawke

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.2field-weighted citation impact, top 19% 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

20 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Myostatin deficiency not only prevents muscle wasting but also improves survival in septic mice.American journal of physiology. Endocrinology and metabolism · 2021
    Article
  17. Article
  18. Article
  19. Article
  20. 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 1 institution in 1 country.

Samantha K ColemanMcMaster University, Department of Pathology and Molecular Medicine, Hamilton, ON, L8S 4L8, Canada.
Irena A RebalkaMcMaster University, Department of Pathology and Molecular Medicine, Hamilton, ON, L8S 4L8, Canada.
Donna M D'SouzaMcMaster University, Department of Pathology and Molecular Medicine, Hamilton, ON, L8S 4L8, Canada.
Namita DeodhareMcMaster University, Department of Pathology and Molecular Medicine, Hamilton, ON, L8S 4L8, Canada.
Eric M DesjardinsMcMaster University, Department of Pathology and Molecular Medicine, Hamilton, ON, L8S 4L8, Canada.
Thomas J HawkeMcMaster University, Department of Pathology and Molecular Medicine, Hamilton, ON, L8S 4L8, Canada.
McMaster University · CA

Funding

CIHR
6 · The paper itself

Abstract

While Type 1 Diabetes Mellitus (T1DM) is characterized by hypoinsulinemia and hyperglycemia, persons with T1DM also develop insulin resistance. Recent studies have demonstrated that insulin resistance in T1DM is a primary mediator of the micro and macrovascular complications that invariably develop in this chronic disease. Myostatin acts to attenuate muscle growth and has been demonstrated to be elevated in streptozotocin-induced diabetic models. We hypothesized that a reduction in mRNA expression of myostatin within a genetic T1DM mouse model would improve skeletal muscle health, resulting in a larger, more insulin sensitive muscle mass. To that end, Akita diabetic mice were crossed with Myostatin(Ln/Ln) mice to ultimately generate a novel mouse line. Our data support the hypothesis that decreased skeletal muscle expression of myostatin mRNA prevented the loss of muscle mass observed in T1DM. Furthermore, reductions in myostatin mRNA increased Glut1 and Glut4 protein expression and glucose uptake in response to an insulin tolerance test (ITT). These positive changes lead to significant reductions in resting blood glucose levels as well as pronounced reductions in associated diabetic symptoms, even in the absence of exogenous insulin. Taken together, this study provides a foundation for considering myostatin inhibition as an adjuvant therapy in T1DM as a means to improve insulin sensitivity and blood glucose management.

Indexed as

AnimalsCrosses, GeneticDiabetes Mellitus, ExperimentalDiabetes Mellitus, Type 1Founder EffectGene Expression RegulationGenetic TherapyGlucoseGlucose Transporter Type 1Glucose Transporter Type 4HyperglycemiaInsulinInsulin ResistanceMiceMice, Inbred C57BLMice, KnockoutGlucoseGlucose Transporter Type 1Glucose Transporter Type 4InsulinMstn protein, mouseMyostatinRNA, MessengerSlc2a1 protein, mouseSlc2a4 protein, mouse

Identifiers

PMID27581061
PMCPMC5007491
OpenAlexW2514241645

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.