Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7
pubmed:dateCreated
2001-6-25
pubmed:abstractText
In neonatal Wistar rats injected with streptozotocin (STZ) at birth (n0-STZ model), a recognized model of beta-cell regeneration, we investigated the capacity of early treatment with glucagon-like peptide 1 (GLP-1) or exendin-4 to promote beta-cell regeneration and thereby improve islet function in the long term, when animals become adults. To this end, n0-STZ rats were submitted to GLP-1 or exendin-4 from postnatal day 2 to day 6 only, and their beta-cell mass and pancreatic functions were tested on day 7 and at 2 months. On day 7, both treatments increased body weight, decreased basal plasma glucose, decreased insulinemia, and increased pancreatic insulin content in n0-STZ rats. At the same age, the beta-cell mass, measured by immunocytochemistry and morphometry methods, was strongly increased in n0-STZ/GLP-1 and n0-STZ/Ex rats compared with n0-STZ rats, representing 51 and 71%, respectively, of the beta-cell mass in Wistar rats, whereas n0-STZ beta-cell mass represented only 21% of the Wistar control value. Despite such early improved beta-cell mass, which is maintained at adult age, the basal and glucose-stimulated insulin secretion (in vivo after intravenous glucose load or in vitro using perfused pancreas) were not improved in the 2-month-old n0-STZ rats previously treated with GLP-1 or exendin-4 compared with untreated n0-STZ rats. However, both treated groups significantly exhibited a decreased basal plasma glucose level and an increased plasma glucose clearance rate compared with the 2-month-old untreated n0-STZ group at adult age. These findings in the n0-STZ model indicate for the first time that GLP-1 or exendin-4 applied during the neonatal diabetic period exert both short- and long-term beneficial effects on beta-cell mass recovery and glucose homeostasis. However, the increase in beta-cell mass, which is still present in the adult n0-STZ rats previously treated, contrasts with the poor beta-cell responsiveness to glucose. Further studies are needed to understand the dissociation between beta-cell regeneration and the lack of improvement in beta-cell function.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0012-1797
pubmed:author
pubmed:issnType
Print
pubmed:volume
50
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1562-70
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:11423477-Animals, pubmed-meshheading:11423477-Animals, Newborn, pubmed-meshheading:11423477-Apoptosis, pubmed-meshheading:11423477-Blood Glucose, pubmed-meshheading:11423477-Body Weight, pubmed-meshheading:11423477-Diabetes Mellitus, Experimental, pubmed-meshheading:11423477-Female, pubmed-meshheading:11423477-Glucagon, pubmed-meshheading:11423477-Glucagon-Like Peptide 1, pubmed-meshheading:11423477-Homeostasis, pubmed-meshheading:11423477-Immunohistochemistry, pubmed-meshheading:11423477-Insulin, pubmed-meshheading:11423477-Islets of Langerhans, pubmed-meshheading:11423477-Organ Size, pubmed-meshheading:11423477-Peptide Fragments, pubmed-meshheading:11423477-Peptides, pubmed-meshheading:11423477-Protein Precursors, pubmed-meshheading:11423477-Rats, pubmed-meshheading:11423477-Rats, Wistar, pubmed-meshheading:11423477-Venoms
pubmed:year
2001
pubmed:articleTitle
Glucagon-like peptide-1 and exendin-4 stimulate beta-cell neogenesis in streptozotocin-treated newborn rats resulting in persistently improved glucose homeostasis at adult age.
pubmed:affiliation
Laboratory of Physiopathology of Nutrition, Centre National de la Recherche Scientifique ESA 7059, Université Paris7/Denis Diderot, 2 place Jussieu, 75251 Paris Cedex 05, France. tourrel@paris7.jussieu.fr
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't