ArticleEuropean journal of histochemistry : EJH2014
Skeletal muscle cellularity and glycogen distribution in the hypermuscular Compact mice.
Article in European journal of histochemistry : EJH, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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.
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Who cites it
3 citing papers in PubMed, 9 citations in OpenAlex.
- Is there still room for novelty, in histochemical papers?European journal of histochemistry : EJH · 2016Review
- Modulating effects of exercise training regimen on skeletal muscle properties in female polo ponies.BMC veterinary research · 2016Article
- Histochemistry in biology and medicine: a message from the citing journals.European journal of histochemistry : EJH · 2015Review
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
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Abstract
The TGF-beta member myostatin acts as a negative regulator of skeletal muscle mass. The Compact mice were selected for high protein content and hypermuscularity, and carry a naturally occurring 12-bp deletion in the propeptide region of the myostatin precursor. We aimed to investigate the cellular characteristics and the glycogen distribution of the Compact tibialis anterior (TA) muscle by quantitative histochemistry and spectrophotometry. We have found that the deficiency in myostatin resulted in significantly increased weight of the investigated hindlimb muscles compared to wild type. Although the average glycogen content of the individual fibers kept unchanged, the total amount of glycogen in the Compact TA muscle increased two-fold, which can be explained by the presence of more fibers in Compact compared to wild type muscle. Moreover, the ratio of the most glycolytic IIB fibers significantly increased in the Compact TA muscle, of which glycogen content was the highest among the fast fibers. In summary, myostatin deficiency caused elevated amount of glycogen in the TA muscle but did not increase the glycogen content of the individual fibers despite the marked glycolytic shift observed in Compact mice.
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