The effects of leptin on REM sleep and slow wave delta in rats are reversed by food deprivation

Christopher M. Sinton, Thomas E. Fitch, Howard K. Gershenfeld

Research output: Contribution to journalArticle

98 Citations (Scopus)

Abstract

Leptin (ob protein) is an adipose tissue derived circulating hormone that acts at specific receptors in the hypothalamus to reduce food intake. The protein is also critically involved in energy balance and metabolic status. Here the effect of leptin on sleep architecture in rats was evaluated because food consumption and metabolic status are known to influence sleep. Sprague-Dawley rats were chronically implanted with electrodes for EEG and EMG recording and diurnal sleep parameters were quantified over 9-h periods following leptin administration. Murine recombinant leptin (rMuLep) was administered systemically to rats that either had undergone 18 h of prior food deprivation or had received food ad libitum. In the normally fed rats, leptin significantly decreased the duration of rapid eye movement sleep (REMS) by about 30% and increased the duration of slow wave sleep (SWS) by about 13%, the latter effect reflecting enhanced power in the delta frequency band. These results are consistent with studies that have linked changes in metabolic rate with effects on sleep. Leptin administration has previously been shown to alter neuroendocrine parameters that could have mediated these changes in sleep architecture. Unexpectedly, prior food deprivation negated the effect of leptin on both REMS and SWS, a result that emphasizes the significance of the apparent coupling between sleep parameters and energy status.

Original languageEnglish (US)
Pages (from-to)197-203
Number of pages7
JournalJournal of Sleep Research
Volume8
Issue number3
DOIs
StatePublished - 1999

Fingerprint

Food Deprivation
REM Sleep
Leptin
Sleep
Food
Implanted Electrodes
Hypothalamus
Sprague Dawley Rats
Adipose Tissue
Electroencephalography
Eating
Hormones

Keywords

  • CRF energy balance
  • HPA insulin
  • Metabolic status
  • Somatostatin

ASJC Scopus subject areas

  • Neuroscience(all)
  • Physiology

Cite this

The effects of leptin on REM sleep and slow wave delta in rats are reversed by food deprivation. / Sinton, Christopher M.; Fitch, Thomas E.; Gershenfeld, Howard K.

In: Journal of Sleep Research, Vol. 8, No. 3, 1999, p. 197-203.

Research output: Contribution to journalArticle

Sinton, Christopher M. ; Fitch, Thomas E. ; Gershenfeld, Howard K. / The effects of leptin on REM sleep and slow wave delta in rats are reversed by food deprivation. In: Journal of Sleep Research. 1999 ; Vol. 8, No. 3. pp. 197-203.
@article{92a71616bf6b4911a78cc41de97c5556,
title = "The effects of leptin on REM sleep and slow wave delta in rats are reversed by food deprivation",
abstract = "Leptin (ob protein) is an adipose tissue derived circulating hormone that acts at specific receptors in the hypothalamus to reduce food intake. The protein is also critically involved in energy balance and metabolic status. Here the effect of leptin on sleep architecture in rats was evaluated because food consumption and metabolic status are known to influence sleep. Sprague-Dawley rats were chronically implanted with electrodes for EEG and EMG recording and diurnal sleep parameters were quantified over 9-h periods following leptin administration. Murine recombinant leptin (rMuLep) was administered systemically to rats that either had undergone 18 h of prior food deprivation or had received food ad libitum. In the normally fed rats, leptin significantly decreased the duration of rapid eye movement sleep (REMS) by about 30{\%} and increased the duration of slow wave sleep (SWS) by about 13{\%}, the latter effect reflecting enhanced power in the delta frequency band. These results are consistent with studies that have linked changes in metabolic rate with effects on sleep. Leptin administration has previously been shown to alter neuroendocrine parameters that could have mediated these changes in sleep architecture. Unexpectedly, prior food deprivation negated the effect of leptin on both REMS and SWS, a result that emphasizes the significance of the apparent coupling between sleep parameters and energy status.",
keywords = "CRF energy balance, HPA insulin, Metabolic status, Somatostatin",
author = "Sinton, {Christopher M.} and Fitch, {Thomas E.} and Gershenfeld, {Howard K.}",
year = "1999",
doi = "10.1046/j.1365-2869.1999.00158.x",
language = "English (US)",
volume = "8",
pages = "197--203",
journal = "Journal of Sleep Research",
issn = "0962-1105",
publisher = "Wiley-Blackwell",
number = "3",

}

TY - JOUR

T1 - The effects of leptin on REM sleep and slow wave delta in rats are reversed by food deprivation

AU - Sinton, Christopher M.

AU - Fitch, Thomas E.

AU - Gershenfeld, Howard K.

PY - 1999

Y1 - 1999

N2 - Leptin (ob protein) is an adipose tissue derived circulating hormone that acts at specific receptors in the hypothalamus to reduce food intake. The protein is also critically involved in energy balance and metabolic status. Here the effect of leptin on sleep architecture in rats was evaluated because food consumption and metabolic status are known to influence sleep. Sprague-Dawley rats were chronically implanted with electrodes for EEG and EMG recording and diurnal sleep parameters were quantified over 9-h periods following leptin administration. Murine recombinant leptin (rMuLep) was administered systemically to rats that either had undergone 18 h of prior food deprivation or had received food ad libitum. In the normally fed rats, leptin significantly decreased the duration of rapid eye movement sleep (REMS) by about 30% and increased the duration of slow wave sleep (SWS) by about 13%, the latter effect reflecting enhanced power in the delta frequency band. These results are consistent with studies that have linked changes in metabolic rate with effects on sleep. Leptin administration has previously been shown to alter neuroendocrine parameters that could have mediated these changes in sleep architecture. Unexpectedly, prior food deprivation negated the effect of leptin on both REMS and SWS, a result that emphasizes the significance of the apparent coupling between sleep parameters and energy status.

AB - Leptin (ob protein) is an adipose tissue derived circulating hormone that acts at specific receptors in the hypothalamus to reduce food intake. The protein is also critically involved in energy balance and metabolic status. Here the effect of leptin on sleep architecture in rats was evaluated because food consumption and metabolic status are known to influence sleep. Sprague-Dawley rats were chronically implanted with electrodes for EEG and EMG recording and diurnal sleep parameters were quantified over 9-h periods following leptin administration. Murine recombinant leptin (rMuLep) was administered systemically to rats that either had undergone 18 h of prior food deprivation or had received food ad libitum. In the normally fed rats, leptin significantly decreased the duration of rapid eye movement sleep (REMS) by about 30% and increased the duration of slow wave sleep (SWS) by about 13%, the latter effect reflecting enhanced power in the delta frequency band. These results are consistent with studies that have linked changes in metabolic rate with effects on sleep. Leptin administration has previously been shown to alter neuroendocrine parameters that could have mediated these changes in sleep architecture. Unexpectedly, prior food deprivation negated the effect of leptin on both REMS and SWS, a result that emphasizes the significance of the apparent coupling between sleep parameters and energy status.

KW - CRF energy balance

KW - HPA insulin

KW - Metabolic status

KW - Somatostatin

UR - http://www.scopus.com/inward/record.url?scp=0032882796&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0032882796&partnerID=8YFLogxK

U2 - 10.1046/j.1365-2869.1999.00158.x

DO - 10.1046/j.1365-2869.1999.00158.x

M3 - Article

C2 - 10476006

AN - SCOPUS:0032882796

VL - 8

SP - 197

EP - 203

JO - Journal of Sleep Research

JF - Journal of Sleep Research

SN - 0962-1105

IS - 3

ER -