Linked Life Data

19323985

Source:http://linkedlifedata.com/resource/pubmed/id/19323985

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-3
pubmed:dateCreated
2009-4-3
pubmed:abstractText
Urotensin II (UII) is a somatostatin-like peptide recently identified to be involved in metabolic regulation and to play a significant role in diabetes and its complications. In the present study, we investigated the expression of UII and its receptor UT in the soleus muscle of male diabetic KK/upj-AY/J mice (2DM group) and the effects of UII on glucose uptake by the skeletal muscle to explore the role of skeletal muscle-derived UII in the pathogenesis of insulin resistance and diabetes. Radioimmunoassay, RT-PCR, immunohistochemistry and radio-ligand binding assay were used in this study. Compared with C57BL/6J mice (control group), 2DM mice showed increased UII content, by 34.0% in plasma, 15.4% in skeletal muscle tissue and 30.6% in medium containing UII from muscle (all P<0.05 or P<0.01). UII protein and UT mRNA expression were significantly enhanced in the skeletal muscle of 2DM mice. On [(125)I]UII binding to muscle sarcolemma, UT binding exhibited a saturable single-component characteristic in a specific and time-dependent manner. Scatchard plot analysis showed higher maximal number of specific binding sites (Bmax) in skeletal muscle, by 42.9% (P<0.01), and a lower dissociation constant (Kd), by 26.4% (P<0.01), in the 2DM group than in controls. On in vitro tissue pre-incubation with UII (10(-9), 10(-8) and 10(-7) mol/L), the insulin-stimulated [(3)H]-2-DG uptake by split soleus muscle was lower, by 9.5%, 33.4% and 39.7% (all P<0.01), respectively, than without UII incubation. UII/UT upregulated in skeletal muscle of 2DM mice suggests that UII derived from skeletal muscle might induce the pathogenesis of skeletal muscle insulin resistance as an autocrine factor.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0167-0115
pubmed:author
pubmed:issnType
Print
pubmed:day
10
pubmed:volume
154
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
85-90
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:19323985-Animals, pubmed-meshheading:19323985-Blood Glucose, pubmed-meshheading:19323985-Diabetes Mellitus, Type 2, pubmed-meshheading:19323985-Gene Expression Regulation, pubmed-meshheading:19323985-Hypoglycemic Agents, pubmed-meshheading:19323985-Immunohistochemistry, pubmed-meshheading:19323985-Insulin, pubmed-meshheading:19323985-Insulin Resistance, pubmed-meshheading:19323985-Male, pubmed-meshheading:19323985-Mice, pubmed-meshheading:19323985-Mice, Inbred C57BL, pubmed-meshheading:19323985-Mice, Inbred Strains, pubmed-meshheading:19323985-Muscle, Skeletal, pubmed-meshheading:19323985-Muscle Proteins, pubmed-meshheading:19323985-RNA, Messenger, pubmed-meshheading:19323985-Radioligand Assay, pubmed-meshheading:19323985-Receptors, G-Protein-Coupled, pubmed-meshheading:19323985-Urotensins
pubmed:year
2009
pubmed:articleTitle
Elevated expression of urotensin II and its receptor in skeletal muscle of diabetic mouse.
pubmed:affiliation
Department of Pathophysiology, Capital Medical University, Beijing 100069, China.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't