Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2011-2-22
pubmed:abstractText
Reversed feeding (RF) is known to disrupt hormone rhythmicity and metabolism. Although these effects may be mediated in part by phase inversion of glucocorticoid secretion, the precise mechanism is incompletely characterized. In this study, we demonstrate that acute nocturnal food deprivation in male rats suppressed the amplitude of spontaneous GH secretion during the dark phase by 62% (P < 0.001), without affecting baseline secretion. Prolonged RF, which reduced pituitary weight (by 22%; P < 0.05), also suppressed GH pulse height sufficiently to reduce skeletal growth (by 4-5%; P < 0.01) and terminal liver weight (by 11%; P < 0.001). Despite this suppression of the GH axis, proportionate adiposity was not elevated, probably due to the accompanying 16% reduction in cumulative food intake (P < 0.01). We demonstrate that RF also resulted in phase inversion of core clock gene expression in liver, abdominal white adipose tissue (WAT) and skeletal muscle, without affecting their expression patterns in the suprachiasmatic nucleus. In addition, RF resulted in phase inversion of hepatic peroxisome proliferator-activated receptor ?2 mRNA expression, a 3- to 5-fold elevation in fatty acid synthase mRNA in WAT in both light- and dark-phase samples (P < 0.01) and an elevation in muscle uncoupling protein 3 mRNA expression at the beginning of the light phase (P < 0.01). Consumption of a high-fat diet increased inguinal (by 36%; P < 0.05) and retroperitoneal WAT weight (by 72%; P < 0.01) only in RF-maintained rats, doubling the efficiency of lipid accumulation (P < 0.05). Thus, RF not only desynchronizes central and peripheral circadian clocks, and suppresses nocturnal GH secretion, but induces a preobesogenic state.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
1945-7170
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
152
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
869-82
pubmed:meshHeading
pubmed-meshheading:21209022-Adipose Tissue, pubmed-meshheading:21209022-Animals, pubmed-meshheading:21209022-CLOCK Proteins, pubmed-meshheading:21209022-Circadian Rhythm, pubmed-meshheading:21209022-Food Deprivation, pubmed-meshheading:21209022-Gene Expression Regulation, pubmed-meshheading:21209022-Ghrelin, pubmed-meshheading:21209022-Growth Hormone, pubmed-meshheading:21209022-Growth Hormone-Releasing Hormone, pubmed-meshheading:21209022-Hypothalamus, pubmed-meshheading:21209022-Kidney, pubmed-meshheading:21209022-Liver, pubmed-meshheading:21209022-Male, pubmed-meshheading:21209022-Muscle, Skeletal, pubmed-meshheading:21209022-Organ Size, pubmed-meshheading:21209022-Pituitary Gland, pubmed-meshheading:21209022-Rats, pubmed-meshheading:21209022-Rats, Sprague-Dawley, pubmed-meshheading:21209022-Tibia, pubmed-meshheading:21209022-Time Factors, pubmed-meshheading:21209022-Weight Gain
pubmed:year
2011
pubmed:articleTitle
Reverse feeding suppresses the activity of the GH axis in rats and induces a preobesogenic state.
pubmed:affiliation
Department of Endocrinology, Institute of Medicine, The Sahlgrenska Academy at the University of Gothenburg, SE-413 45 Göteborg, Sweden.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't