Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2003-4-4
pubmed:abstractText
We examined the long-term effect of in utero exposure to streptozotocin-induced maternal diabetes on the progeny that postnatally received either ad libitum access to milk by being fed by control mothers (CM/DP) or were subjected to relative nutrient restriction by being fed by diabetic mothers (DM/DP) compared with the control progeny fed by control mothers (CM/CP). There was increased food intake, glucose intolerance, and obesity in the CM/DP group and diminished food intake, glucose tolerance, and postnatal growth restriction in the DM/DP group, persisting in the adult. These changes were associated with aberrations in hormonal and metabolic profiles and alterations in hypothalamic neuropeptide Y concentrations. By use of subfractionation and Western blot analysis techniques, the CM/DP group demonstrated a higher skeletal muscle sarcolemma-associated (days 1 and 60) and white adipose tissue plasma membrane-associated (day 60) GLUT4 in the basal state with a lack of insulin-induced translocation. The DM/DP group demonstrated a partial amelioration of this change observed in the CM/DP group. We conclude that the offspring of a diabetic mother with ad libitum postnatal nutrition demonstrates increased food intake and resistance to insulin-induced translocation of GLUT4 in skeletal muscle and white adipose tissue. This in turn leads to glucose intolerance and obesity at a later stage (day 180). Postnatal nutrient restriction results in reversal of this adult phenotype, thereby explaining the phenotypic heterogeneity that exists in this population.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0193-1849
pubmed:author
pubmed:issnType
Print
pubmed:volume
284
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
E901-14
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:12540375-Adipose Tissue, pubmed-meshheading:12540375-Animals, pubmed-meshheading:12540375-Animals, Newborn, pubmed-meshheading:12540375-Biological Transport, pubmed-meshheading:12540375-Diabetes Mellitus, Experimental, pubmed-meshheading:12540375-Drinking, pubmed-meshheading:12540375-Female, pubmed-meshheading:12540375-Forecasting, pubmed-meshheading:12540375-Glucose Intolerance, pubmed-meshheading:12540375-Glucose Transporter Type 4, pubmed-meshheading:12540375-Growth Disorders, pubmed-meshheading:12540375-Insulin, pubmed-meshheading:12540375-Lactation, pubmed-meshheading:12540375-Monosaccharide Transport Proteins, pubmed-meshheading:12540375-Muscle, Skeletal, pubmed-meshheading:12540375-Muscle Proteins, pubmed-meshheading:12540375-Obesity, pubmed-meshheading:12540375-Pregnancy, pubmed-meshheading:12540375-Pregnancy in Diabetics, pubmed-meshheading:12540375-Rats, pubmed-meshheading:12540375-Rats, Sprague-Dawley, pubmed-meshheading:12540375-Sarcolemma
pubmed:year
2003
pubmed:articleTitle
Aberrant insulin-induced GLUT4 translocation predicts glucose intolerance in the offspring of a diabetic mother.
pubmed:affiliation
Division of Neonatology and Developmental Biology, Department of Pediatrics, David Geffen School of Medicine, University of California, Los Angeles, CA 90095-1752, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.