Abstract
Amylin can evoke insulin resistance by antagonizing insulin in a non-competitive manner. Here, we investigated the glycogenolytic effect of amylin in isolated skeletal muscle and compared it to the effects of a calcitonin gene-related peptide (CGRP). Amylin alone had no statistically significant effect on glucose transport. However, amylin decreased insulin-stimulated glucose transport by about 30%. The involvement of cAMP could not be detected at the concentrations shown to promote glycogenolysis. Previously, it has been shown that increased glycogen synthase kinase 3 (GSK3) activity plays a role in insulin resistance. Here, the ratio of GSK3 α:β isoforms in rat soleus was found to be 1.2:1. We found that amylin increased GSK3α activity, which in turn led to increased phosphorylation of glycogen synthase and decreased glycogen synthesis de novo.
| Original language | English |
|---|---|
| Pages (from-to) | 2119-2125 |
| Number of pages | 7 |
| Journal | Peptides |
| Volume | 25 |
| Issue number | 12 |
| DOIs | |
| State | Published - Dec 1 2004 |
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Keywords
- 2-deoxy-glucose
- cAMP
- CGRP
- Glycogen
ASJC Scopus subject areas
- Biochemistry
- Endocrinology
- Physiology
- Cellular and Molecular Neuroscience
Cite this
GSK3 involvement in amylin signaling in isolated rat soleus muscle. / Abaffy, Tatjana; Cooper, Garth J S.
In: Peptides, Vol. 25, No. 12, 01.12.2004, p. 2119-2125.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - GSK3 involvement in amylin signaling in isolated rat soleus muscle
AU - Abaffy, Tatjana
AU - Cooper, Garth J S
PY - 2004/12/1
Y1 - 2004/12/1
N2 - Amylin can evoke insulin resistance by antagonizing insulin in a non-competitive manner. Here, we investigated the glycogenolytic effect of amylin in isolated skeletal muscle and compared it to the effects of a calcitonin gene-related peptide (CGRP). Amylin alone had no statistically significant effect on glucose transport. However, amylin decreased insulin-stimulated glucose transport by about 30%. The involvement of cAMP could not be detected at the concentrations shown to promote glycogenolysis. Previously, it has been shown that increased glycogen synthase kinase 3 (GSK3) activity plays a role in insulin resistance. Here, the ratio of GSK3 α:β isoforms in rat soleus was found to be 1.2:1. We found that amylin increased GSK3α activity, which in turn led to increased phosphorylation of glycogen synthase and decreased glycogen synthesis de novo.
AB - Amylin can evoke insulin resistance by antagonizing insulin in a non-competitive manner. Here, we investigated the glycogenolytic effect of amylin in isolated skeletal muscle and compared it to the effects of a calcitonin gene-related peptide (CGRP). Amylin alone had no statistically significant effect on glucose transport. However, amylin decreased insulin-stimulated glucose transport by about 30%. The involvement of cAMP could not be detected at the concentrations shown to promote glycogenolysis. Previously, it has been shown that increased glycogen synthase kinase 3 (GSK3) activity plays a role in insulin resistance. Here, the ratio of GSK3 α:β isoforms in rat soleus was found to be 1.2:1. We found that amylin increased GSK3α activity, which in turn led to increased phosphorylation of glycogen synthase and decreased glycogen synthesis de novo.
KW - 2-deoxy-glucose
KW - cAMP
KW - CGRP
KW - Glycogen
UR - http://www.scopus.com/inward/record.url?scp=9644275576&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=9644275576&partnerID=8YFLogxK
U2 - 10.1016/j.peptides.2004.08.016
DO - 10.1016/j.peptides.2004.08.016
M3 - Article
C2 - 15572200
AN - SCOPUS:9644275576
VL - 25
SP - 2119
EP - 2125
JO - Peptides
JF - Peptides
SN - 0196-9781
IS - 12
ER -