Linked Life Data

16621895

Source:http://linkedlifedata.com/resource/pubmed/id/16621895

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2006-8-16
pubmed:abstractText
Growth hormone (GH), acting through its receptor (GHR), is essential for somatic growth and development and maintaining metabolic homeostasis. GHR gene-deficient (GHR(-/-)) mice exhibit drastically diminished insulin-like growth factor-I (IGF-I) levels, proportional growth retardation, elevated insulin sensitivity, and reduced islet beta-cell mass. Unlike the liver, which is mostly unaffected by changes in IGF-I level, skeletal muscles express high levels of IGF-I receptor (IGF-IR). The net result of a concurrent deficiency in the actions of both GH and IGF-I, which exert opposite influences on insulin responsiveness, has not been evaluated. We studied insulin-stimulated early responses in the insulin receptor (IR), insulin receptor substrate-1 (IRS-1), and p85 subunit of phosphatidylinositol 3-kinase. Upon in vivo insulin stimulation, skeletal muscles of GHR(-/-) mice exhibit transient delayed responses in IR and IRS-1 phosphorylation but normal levels of p85 association with IRS-1. This is in contrast to normal/elevated insulin responses in hepatocytes and indicates tissue-specific effects of GHR gene deficiency. In addition to stimulating normal islet cell growth, GH may participate in islet cell overgrowth, which compensates for insulin resistance induced by obesity. To determine whether the islet cell overgrowth is dependent on GH signaling, we studied the response of male GHR(-/-) mice to high-fat diet (HFD)-induced obesity. After 17 wk on a HFD, GHR(-/-) mice became more significantly obese than wild-type mice and exhibited increased beta-cell mass to a slightly higher extent. These data demonstrate that GH signaling is not required for compensatory islet growth. Thus, in both muscle insulin responsiveness and islet growth compensation, normal levels of GH signals do not seem to play a dominant role.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0193-1849
pubmed:author
pubmed:issnType
Print
pubmed:volume
291
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
E491-8
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:16621895-Adipose Tissue, pubmed-meshheading:16621895-Animals, pubmed-meshheading:16621895-Body Weight, pubmed-meshheading:16621895-Diet, pubmed-meshheading:16621895-Hyperplasia, pubmed-meshheading:16621895-Insulin, pubmed-meshheading:16621895-Insulin Receptor Substrate Proteins, pubmed-meshheading:16621895-Islets of Langerhans, pubmed-meshheading:16621895-Liver, pubmed-meshheading:16621895-Male, pubmed-meshheading:16621895-Mice, pubmed-meshheading:16621895-Mice, Inbred BALB C, pubmed-meshheading:16621895-Mice, Inbred C57BL, pubmed-meshheading:16621895-Mice, Knockout, pubmed-meshheading:16621895-Muscle, Skeletal, pubmed-meshheading:16621895-Obesity, pubmed-meshheading:16621895-Phosphatidylinositol 3-Kinases, pubmed-meshheading:16621895-Phosphoproteins, pubmed-meshheading:16621895-Phosphorylation, pubmed-meshheading:16621895-Receptor, Insulin, pubmed-meshheading:16621895-Receptors, Somatotropin
pubmed:year
2006
pubmed:articleTitle
Growth hormone receptor gene deficiency causes delayed insulin responsiveness in skeletal muscles without affecting compensatory islet cell overgrowth in obese mice.
pubmed:affiliation
Fraser Laboratories for Diabetic Research, Department of Medicine, McGill University Health Center, Montreal, QC, Canada.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't