Fasting hypometabolism and refeeding hyperphagia in rats: Effects of capsaicin desensitization of the abdominal vagus

András Garami, M. Balaskó, M. Székely, Margit Solymár, Erika Pétervári

Research output: Contribution to journalArticle

14 Citations (Scopus)

Abstract

Capsaicin-sensitive abdominal vagal fibers contribute to postprandial satiety and hypermetabolism. We hypothesized that the hypometabolic adaptation to fasting involves similar mechanisms and that blockade of such signals might enhance loss of body weight upon fasting. A low dosage of capsaicin (5. mg/kg) administered intraperitoneally desensitizes the local afferent vagal nerve endings for approximately three weeks without causing systemic desensitization or damaging the efferent fibers. Following such desensitization, male Wistar rats deprived of food for 120. h lost significantly (18.9 ± 0.4% vs. 15.8 ± 1.0%), i.e. 20% more weight than the controls. Based on the present results, this can only be explained by the demonstrated defective hypometabolic adaptation in desensitized animals. Other mechanisms do not seem to make up for this defective function. Upon refeeding following a period of fasting, in the first 0.5-3. h the food intake was significantly greater in capsaicin pretreated compared to the control group, demonstrating blockade of satiety as a sign of desensitization. The delayed gastrointestinal passage supported that vagal afferent nerve endings were in a desensitized state in these rats. In conclusion, local desensitization of the abdominal capsaicin-sensitive fibers attenuates the hypometabolic adaptation to food deprivation and the lack of fasting-induced activation of these fibers cannot be substituted by other fasting-dependent mechanisms. It is suggested that reports of low body weight in mice lacking the transient receptor potential vanilloid-1 channel and in rats with systemic capsaicin desensitization might be explained by a lasting absence of similar (vagus-mediated) hypometabolic processes, preventing weight gain or obesity.

Original languageEnglish
Pages (from-to)61-66
Number of pages6
JournalEuropean Journal of Pharmacology
Volume644
Issue number1-3
DOIs
Publication statusPublished - Oct 2010

Fingerprint

Hyperphagia
Capsaicin
Fasting
Nerve Endings
Body Weight
Food Deprivation
Weight Gain
Wistar Rats
Obesity
Eating
Psychologic Desensitization
Weights and Measures
Food
Control Groups

Keywords

  • Body weight
  • Capsaicin
  • Fasting hypometabolism
  • Food intake
  • TRPV1
  • Vagus

ASJC Scopus subject areas

  • Pharmacology

Cite this

Fasting hypometabolism and refeeding hyperphagia in rats : Effects of capsaicin desensitization of the abdominal vagus. / Garami, András; Balaskó, M.; Székely, M.; Solymár, Margit; Pétervári, Erika.

In: European Journal of Pharmacology, Vol. 644, No. 1-3, 10.2010, p. 61-66.

Research output: Contribution to journalArticle

@article{d1162ee626b146a68a4c22b0d3d68e68,
title = "Fasting hypometabolism and refeeding hyperphagia in rats: Effects of capsaicin desensitization of the abdominal vagus",
abstract = "Capsaicin-sensitive abdominal vagal fibers contribute to postprandial satiety and hypermetabolism. We hypothesized that the hypometabolic adaptation to fasting involves similar mechanisms and that blockade of such signals might enhance loss of body weight upon fasting. A low dosage of capsaicin (5. mg/kg) administered intraperitoneally desensitizes the local afferent vagal nerve endings for approximately three weeks without causing systemic desensitization or damaging the efferent fibers. Following such desensitization, male Wistar rats deprived of food for 120. h lost significantly (18.9 ± 0.4{\%} vs. 15.8 ± 1.0{\%}), i.e. 20{\%} more weight than the controls. Based on the present results, this can only be explained by the demonstrated defective hypometabolic adaptation in desensitized animals. Other mechanisms do not seem to make up for this defective function. Upon refeeding following a period of fasting, in the first 0.5-3. h the food intake was significantly greater in capsaicin pretreated compared to the control group, demonstrating blockade of satiety as a sign of desensitization. The delayed gastrointestinal passage supported that vagal afferent nerve endings were in a desensitized state in these rats. In conclusion, local desensitization of the abdominal capsaicin-sensitive fibers attenuates the hypometabolic adaptation to food deprivation and the lack of fasting-induced activation of these fibers cannot be substituted by other fasting-dependent mechanisms. It is suggested that reports of low body weight in mice lacking the transient receptor potential vanilloid-1 channel and in rats with systemic capsaicin desensitization might be explained by a lasting absence of similar (vagus-mediated) hypometabolic processes, preventing weight gain or obesity.",
keywords = "Body weight, Capsaicin, Fasting hypometabolism, Food intake, TRPV1, Vagus",
author = "Andr{\'a}s Garami and M. Balask{\'o} and M. Sz{\'e}kely and Margit Solym{\'a}r and Erika P{\'e}terv{\'a}ri",
year = "2010",
month = "10",
doi = "10.1016/j.ejphar.2010.07.002",
language = "English",
volume = "644",
pages = "61--66",
journal = "European Journal of Pharmacology",
issn = "0014-2999",
publisher = "Elsevier",
number = "1-3",

}

TY - JOUR

T1 - Fasting hypometabolism and refeeding hyperphagia in rats

T2 - Effects of capsaicin desensitization of the abdominal vagus

AU - Garami, András

AU - Balaskó, M.

AU - Székely, M.

AU - Solymár, Margit

AU - Pétervári, Erika

PY - 2010/10

Y1 - 2010/10

N2 - Capsaicin-sensitive abdominal vagal fibers contribute to postprandial satiety and hypermetabolism. We hypothesized that the hypometabolic adaptation to fasting involves similar mechanisms and that blockade of such signals might enhance loss of body weight upon fasting. A low dosage of capsaicin (5. mg/kg) administered intraperitoneally desensitizes the local afferent vagal nerve endings for approximately three weeks without causing systemic desensitization or damaging the efferent fibers. Following such desensitization, male Wistar rats deprived of food for 120. h lost significantly (18.9 ± 0.4% vs. 15.8 ± 1.0%), i.e. 20% more weight than the controls. Based on the present results, this can only be explained by the demonstrated defective hypometabolic adaptation in desensitized animals. Other mechanisms do not seem to make up for this defective function. Upon refeeding following a period of fasting, in the first 0.5-3. h the food intake was significantly greater in capsaicin pretreated compared to the control group, demonstrating blockade of satiety as a sign of desensitization. The delayed gastrointestinal passage supported that vagal afferent nerve endings were in a desensitized state in these rats. In conclusion, local desensitization of the abdominal capsaicin-sensitive fibers attenuates the hypometabolic adaptation to food deprivation and the lack of fasting-induced activation of these fibers cannot be substituted by other fasting-dependent mechanisms. It is suggested that reports of low body weight in mice lacking the transient receptor potential vanilloid-1 channel and in rats with systemic capsaicin desensitization might be explained by a lasting absence of similar (vagus-mediated) hypometabolic processes, preventing weight gain or obesity.

AB - Capsaicin-sensitive abdominal vagal fibers contribute to postprandial satiety and hypermetabolism. We hypothesized that the hypometabolic adaptation to fasting involves similar mechanisms and that blockade of such signals might enhance loss of body weight upon fasting. A low dosage of capsaicin (5. mg/kg) administered intraperitoneally desensitizes the local afferent vagal nerve endings for approximately three weeks without causing systemic desensitization or damaging the efferent fibers. Following such desensitization, male Wistar rats deprived of food for 120. h lost significantly (18.9 ± 0.4% vs. 15.8 ± 1.0%), i.e. 20% more weight than the controls. Based on the present results, this can only be explained by the demonstrated defective hypometabolic adaptation in desensitized animals. Other mechanisms do not seem to make up for this defective function. Upon refeeding following a period of fasting, in the first 0.5-3. h the food intake was significantly greater in capsaicin pretreated compared to the control group, demonstrating blockade of satiety as a sign of desensitization. The delayed gastrointestinal passage supported that vagal afferent nerve endings were in a desensitized state in these rats. In conclusion, local desensitization of the abdominal capsaicin-sensitive fibers attenuates the hypometabolic adaptation to food deprivation and the lack of fasting-induced activation of these fibers cannot be substituted by other fasting-dependent mechanisms. It is suggested that reports of low body weight in mice lacking the transient receptor potential vanilloid-1 channel and in rats with systemic capsaicin desensitization might be explained by a lasting absence of similar (vagus-mediated) hypometabolic processes, preventing weight gain or obesity.

KW - Body weight

KW - Capsaicin

KW - Fasting hypometabolism

KW - Food intake

KW - TRPV1

KW - Vagus

UR - http://www.scopus.com/inward/record.url?scp=77955772583&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=77955772583&partnerID=8YFLogxK

U2 - 10.1016/j.ejphar.2010.07.002

DO - 10.1016/j.ejphar.2010.07.002

M3 - Article

C2 - 20637192

AN - SCOPUS:77955772583

VL - 644

SP - 61

EP - 66

JO - European Journal of Pharmacology

JF - European Journal of Pharmacology

SN - 0014-2999

IS - 1-3

ER -