Linked Life Data

9322935

Source:http://linkedlifedata.com/resource/pubmed/id/9322935

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
10
pubmed:dateCreated
1997-10-23
pubmed:databankReference
pubmed:abstractText
New Zealand Obese (NZO) mice exhibit a polygenic syndrome of hyperphagia, obesity, hyperinsulinemia, and hyperglycemia similar to that observed in young diabetes mutant mice on the C57BLKS/J background (C57BLKS/J-Lepr(db)/Lepr(db)). Here we show that in NZO this syndrome is accompanied by a marked elevation of the leptin protein in adipose tissue and serum. The promoter region and the complementary DNA of the ob gene of NZO mice, including its 5'-untranslated region, are identical with the wild-type sequence (C57BL, BALB/c), except that the transcription start is located 5 bp upstream of the reported site. In contrast to C57BLKS/J+/+ and C57BL/6J-Lep(ob)/Lep(ob) mice, NZO mice failed to respond to recombinant leptin (7.2 microg/g) with a reduction of food intake. Leptin receptor messenger RNA as detected by PCR appears as abundant in hypothalamic tissue of NZO mice as in tissue from lean mice. Ten nucleotide polymorphisms are found in the complementary DNA of the leptin receptor, resulting in two conservative substitutions (V541I and V651I) in the extracellular part of the receptor and one nonconservative substitution (T1044I) in the intracellular domain between the presumed Jak and STAT binding boxes. However, these mutations are also present in the related lean New Zealand Black strain (body fat at 9 weeks: New Zealand Black, 6.2 +/- 1.3%; NZO, 17.0 +/- 1.7%). Thus, the polymorphic leptin receptor seems to play only a minor, if any, role in the obesity and hyperleptinemia of the NZO mouse. It is suggested that the main defect in NZO is located distal from the leptin receptor or at the level of leptin transport into the central nervous system.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0013-7227
pubmed:author
pubmed:issnType
Print
pubmed:volume
138
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
4234-9
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:9322935-Adipose Tissue, pubmed-meshheading:9322935-Animals, pubmed-meshheading:9322935-Base Sequence, pubmed-meshheading:9322935-Blotting, Northern, pubmed-meshheading:9322935-Body Weight, pubmed-meshheading:9322935-Carrier Proteins, pubmed-meshheading:9322935-DNA, Complementary, pubmed-meshheading:9322935-Disease Models, Animal, pubmed-meshheading:9322935-Eating, pubmed-meshheading:9322935-Hyperglycemia, pubmed-meshheading:9322935-Hyperinsulinism, pubmed-meshheading:9322935-Hypothalamus, pubmed-meshheading:9322935-Leptin, pubmed-meshheading:9322935-Mice, pubmed-meshheading:9322935-Mice, Inbred C57BL, pubmed-meshheading:9322935-Mice, Obese, pubmed-meshheading:9322935-Molecular Sequence Data, pubmed-meshheading:9322935-Obesity, pubmed-meshheading:9322935-Polymerase Chain Reaction, pubmed-meshheading:9322935-Polymorphism, Genetic, pubmed-meshheading:9322935-Precipitin Tests, pubmed-meshheading:9322935-Promoter Regions, Genetic, pubmed-meshheading:9322935-Proteins, pubmed-meshheading:9322935-RNA, Messenger, pubmed-meshheading:9322935-Receptors, Cell Surface, pubmed-meshheading:9322935-Receptors, Leptin, pubmed-meshheading:9322935-Recombinant Proteins
pubmed:year
1997
pubmed:articleTitle
Hyperleptinemia, leptin resistance, and polymorphic leptin receptor in the New Zealand obese mouse.
pubmed:affiliation
Institut für Pharmakologie und Toxikologie der RWTH, Aachen, Germany.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't