Reverse Feeding Suppresses the Activity of the GH Axis in Rats and Induces a Preobesogenic State
Journal article, 2011

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 gamma 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. (Endocrinology 152: 869-882, 2011)

deprived rats

growth-hormone-secretion

peripheral circadian oscillators

prolonged

dietary-protein

suprachiasmatic nucleus

daily rhythms

food-deprivation

neuropeptide-y

somatostatin

hypothalamic expression

Author

Camilla A M Glad

University of Gothenburg

E. E. J. Kitchen

Cardiff University

G. C. Russ

Cardiff University

S. M. Harris

Cardiff University

J. S. Davies

Swansea University

Cardiff University

E. F. Gevers

MRC National Institute for Medical Research

Britt Gabrielsson

Chalmers, Chemical and Biological Engineering, Life Sciences

T. Wells

Cardiff University

Endocrinology

0013-7227 (ISSN)

Vol. 152 3 869-882

Subject Categories

Endocrinology and Diabetes

Biochemistry and Molecular Biology

Physiology

Biomedical Laboratory Science/Technology

Areas of Advance

Life Science Engineering (2010-2018)

DOI

10.1210/en.2010-0713

More information

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9/6/2018 7