Leptin and neuropeptide Y have opposing modulatory effects on nucleus of the solitary tract neurophysiological responses to gastric loads: Implications for the control of food intake

Gary J. Schwartz, Timothy H. Moran

Research output: Contribution to journalArticle

90 Citations (Scopus)

Abstract

Leptin is an adiposity hormone that modulates the activity of multiple hypothalamic signaling pathways involved in the control of food intake. The present experiments were designed to evaluate whether central administration of leptin or one of its downstream mediators, neuropeptide Y (NPY), could affect food intake by modulating the brain stem neurophysiological response to ascending meal-related feedback signals in the nucleus of the solitary tract (NTS) in anesthetized male Long-Evans rats. NTS neurons at the rostrocaudal level of the area postrema were dose-dependently activated by gastric loads ranging from 2-10 ml, and leptin and NPY had opposite modulatory effects on this load volume/activity relationship: leptin significantly increased NTS responses to gastric loads, whereas NPY reduced the potency and efficacy with which gastric loads activated NTS neurons. These effects were probably not mediated by peripheral effects of centrally administered peptides or by the gastrokinetic effects of central NPY or leptin, because the dose-response relationship between gastric load volume and neurophysiological firing rate was unchanged in gastric load-sensitive vagal afferent fibers. These data suggest a mechanistic framework for considering how feeding behavior occurring in meals is altered by challenges to energy homeostasis, such as fasting and overfeeding.

Original languageEnglish (US)
Pages (from-to)3779-3784
Number of pages6
JournalEndocrinology
Volume143
Issue number10
DOIs
StatePublished - Oct 1 2002
Externally publishedYes

Fingerprint

Solitary Nucleus
Neuropeptide Y
Leptin
Stomach
Eating
Meals
Area Postrema
Neurons
Long Evans Rats
Adiposity
Feeding Behavior
Brain Stem
Fasting
Homeostasis
Hormones
Peptides

ASJC Scopus subject areas

  • Endocrinology
  • Endocrinology, Diabetes and Metabolism

Cite this

@article{ce41b1c4a0064e3ab55bbfe8224c6766,
title = "Leptin and neuropeptide Y have opposing modulatory effects on nucleus of the solitary tract neurophysiological responses to gastric loads: Implications for the control of food intake",
abstract = "Leptin is an adiposity hormone that modulates the activity of multiple hypothalamic signaling pathways involved in the control of food intake. The present experiments were designed to evaluate whether central administration of leptin or one of its downstream mediators, neuropeptide Y (NPY), could affect food intake by modulating the brain stem neurophysiological response to ascending meal-related feedback signals in the nucleus of the solitary tract (NTS) in anesthetized male Long-Evans rats. NTS neurons at the rostrocaudal level of the area postrema were dose-dependently activated by gastric loads ranging from 2-10 ml, and leptin and NPY had opposite modulatory effects on this load volume/activity relationship: leptin significantly increased NTS responses to gastric loads, whereas NPY reduced the potency and efficacy with which gastric loads activated NTS neurons. These effects were probably not mediated by peripheral effects of centrally administered peptides or by the gastrokinetic effects of central NPY or leptin, because the dose-response relationship between gastric load volume and neurophysiological firing rate was unchanged in gastric load-sensitive vagal afferent fibers. These data suggest a mechanistic framework for considering how feeding behavior occurring in meals is altered by challenges to energy homeostasis, such as fasting and overfeeding.",
author = "Schwartz, {Gary J.} and Moran, {Timothy H.}",
year = "2002",
month = "10",
day = "1",
doi = "10.1210/en.2002-220352",
language = "English (US)",
volume = "143",
pages = "3779--3784",
journal = "Endocrinology",
issn = "0013-7227",
publisher = "The Endocrine Society",
number = "10",

}

TY - JOUR

T1 - Leptin and neuropeptide Y have opposing modulatory effects on nucleus of the solitary tract neurophysiological responses to gastric loads

T2 - Implications for the control of food intake

AU - Schwartz, Gary J.

AU - Moran, Timothy H.

PY - 2002/10/1

Y1 - 2002/10/1

N2 - Leptin is an adiposity hormone that modulates the activity of multiple hypothalamic signaling pathways involved in the control of food intake. The present experiments were designed to evaluate whether central administration of leptin or one of its downstream mediators, neuropeptide Y (NPY), could affect food intake by modulating the brain stem neurophysiological response to ascending meal-related feedback signals in the nucleus of the solitary tract (NTS) in anesthetized male Long-Evans rats. NTS neurons at the rostrocaudal level of the area postrema were dose-dependently activated by gastric loads ranging from 2-10 ml, and leptin and NPY had opposite modulatory effects on this load volume/activity relationship: leptin significantly increased NTS responses to gastric loads, whereas NPY reduced the potency and efficacy with which gastric loads activated NTS neurons. These effects were probably not mediated by peripheral effects of centrally administered peptides or by the gastrokinetic effects of central NPY or leptin, because the dose-response relationship between gastric load volume and neurophysiological firing rate was unchanged in gastric load-sensitive vagal afferent fibers. These data suggest a mechanistic framework for considering how feeding behavior occurring in meals is altered by challenges to energy homeostasis, such as fasting and overfeeding.

AB - Leptin is an adiposity hormone that modulates the activity of multiple hypothalamic signaling pathways involved in the control of food intake. The present experiments were designed to evaluate whether central administration of leptin or one of its downstream mediators, neuropeptide Y (NPY), could affect food intake by modulating the brain stem neurophysiological response to ascending meal-related feedback signals in the nucleus of the solitary tract (NTS) in anesthetized male Long-Evans rats. NTS neurons at the rostrocaudal level of the area postrema were dose-dependently activated by gastric loads ranging from 2-10 ml, and leptin and NPY had opposite modulatory effects on this load volume/activity relationship: leptin significantly increased NTS responses to gastric loads, whereas NPY reduced the potency and efficacy with which gastric loads activated NTS neurons. These effects were probably not mediated by peripheral effects of centrally administered peptides or by the gastrokinetic effects of central NPY or leptin, because the dose-response relationship between gastric load volume and neurophysiological firing rate was unchanged in gastric load-sensitive vagal afferent fibers. These data suggest a mechanistic framework for considering how feeding behavior occurring in meals is altered by challenges to energy homeostasis, such as fasting and overfeeding.

UR - http://www.scopus.com/inward/record.url?scp=0036773262&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0036773262&partnerID=8YFLogxK

U2 - 10.1210/en.2002-220352

DO - 10.1210/en.2002-220352

M3 - Article

C2 - 12239088

AN - SCOPUS:0036773262

VL - 143

SP - 3779

EP - 3784

JO - Endocrinology

JF - Endocrinology

SN - 0013-7227

IS - 10

ER -