High fat diet altered the mechanism of energy homeostasis induced by nicotine and withdrawal in C57BL/6 mice

Young Na Hur, Gee Hyun Hong, Sang-Hyun Choi, Kyung-Ho Shin, Boe Gwun Chun

Research output: Contribution to journalArticle

18 Citations (Scopus)

Abstract

Nicotine treatment has known to produce an inverse relationship between body weight and food intake in rodents. Present study determined the effect of repeated treatment with nicotine and withdrawal in control and obese mice, on: (1) body weight, caloric intake and energy expenditure; (2) hypothalamic neuropeptides mRNA expression; and (3) serum leptin. 21-week-old C57BL/6 mice (n = 65) received nicotine (3.0 mg/kg/day; 2 weeks) and saline (1 ml/kg/day; 2 weeks) subcutaneously. Animals were given either a normal-fat (10% kcal from fat, NF) or a high-fat diet (45% kcal from fat, HF) from the 12 th week to 25 th week. While, nicotine treatment for 14 days induced an increase in hypothalamic agouti-related protein, cocaine- and amphetamine- regulated transcript, pro-opiomelanocortin mRNA expressions, nicotine also produced a reducing effect in body weight gain and leptin concentration in NF mice. High-fat diet induced obese mice showed a blunted hypothalamic and leptin response to nicotine. Remarkable weight loss in obese mice was mediated not just by decreasing caloric intake, but also by increasing total energy expenditure (EE). During nicotine withdrawal period, weight gain occurred in NF and HF groups, which was ascribed to a decrease in EE rather than changes in caloric intake. Hypothalamic AgRP might play a role for maintaining energy balance under the nicotine-induced negative energy status.

Original languageEnglish
Pages (from-to)219-226
Number of pages8
JournalMolecules and Cells
Volume30
Issue number3
DOIs
Publication statusPublished - 2010 Sep 1

Fingerprint

High Fat Diet
Nicotine
Inbred C57BL Mouse
Homeostasis
Obese Mice
Leptin
Energy Intake
Energy Metabolism
Fats
Body Weight
Weight Gain
Agouti-Related Protein
Pro-Opiomelanocortin
Messenger RNA
Amphetamine
Neuropeptides
Cocaine
Weight Loss
Rodentia
Eating

Keywords

  • body weight
  • food intake
  • hypothalamic neuropeptides
  • nicotine
  • obesity

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology

Cite this

High fat diet altered the mechanism of energy homeostasis induced by nicotine and withdrawal in C57BL/6 mice. / Hur, Young Na; Hong, Gee Hyun; Choi, Sang-Hyun; Shin, Kyung-Ho; Chun, Boe Gwun.

In: Molecules and Cells, Vol. 30, No. 3, 01.09.2010, p. 219-226.

Research output: Contribution to journalArticle

@article{846800051d4548f78618c8d00fe06540,
title = "High fat diet altered the mechanism of energy homeostasis induced by nicotine and withdrawal in C57BL/6 mice",
abstract = "Nicotine treatment has known to produce an inverse relationship between body weight and food intake in rodents. Present study determined the effect of repeated treatment with nicotine and withdrawal in control and obese mice, on: (1) body weight, caloric intake and energy expenditure; (2) hypothalamic neuropeptides mRNA expression; and (3) serum leptin. 21-week-old C57BL/6 mice (n = 65) received nicotine (3.0 mg/kg/day; 2 weeks) and saline (1 ml/kg/day; 2 weeks) subcutaneously. Animals were given either a normal-fat (10{\%} kcal from fat, NF) or a high-fat diet (45{\%} kcal from fat, HF) from the 12 th week to 25 th week. While, nicotine treatment for 14 days induced an increase in hypothalamic agouti-related protein, cocaine- and amphetamine- regulated transcript, pro-opiomelanocortin mRNA expressions, nicotine also produced a reducing effect in body weight gain and leptin concentration in NF mice. High-fat diet induced obese mice showed a blunted hypothalamic and leptin response to nicotine. Remarkable weight loss in obese mice was mediated not just by decreasing caloric intake, but also by increasing total energy expenditure (EE). During nicotine withdrawal period, weight gain occurred in NF and HF groups, which was ascribed to a decrease in EE rather than changes in caloric intake. Hypothalamic AgRP might play a role for maintaining energy balance under the nicotine-induced negative energy status.",
keywords = "body weight, food intake, hypothalamic neuropeptides, nicotine, obesity",
author = "Hur, {Young Na} and Hong, {Gee Hyun} and Sang-Hyun Choi and Kyung-Ho Shin and Chun, {Boe Gwun}",
year = "2010",
month = "9",
day = "1",
doi = "10.1007/s10059-010-0110-3",
language = "English",
volume = "30",
pages = "219--226",
journal = "Molecules and Cells",
issn = "1016-8478",
publisher = "Korean Society for Molecular and Cellular Biology",
number = "3",

}

TY - JOUR

T1 - High fat diet altered the mechanism of energy homeostasis induced by nicotine and withdrawal in C57BL/6 mice

AU - Hur, Young Na

AU - Hong, Gee Hyun

AU - Choi, Sang-Hyun

AU - Shin, Kyung-Ho

AU - Chun, Boe Gwun

PY - 2010/9/1

Y1 - 2010/9/1

N2 - Nicotine treatment has known to produce an inverse relationship between body weight and food intake in rodents. Present study determined the effect of repeated treatment with nicotine and withdrawal in control and obese mice, on: (1) body weight, caloric intake and energy expenditure; (2) hypothalamic neuropeptides mRNA expression; and (3) serum leptin. 21-week-old C57BL/6 mice (n = 65) received nicotine (3.0 mg/kg/day; 2 weeks) and saline (1 ml/kg/day; 2 weeks) subcutaneously. Animals were given either a normal-fat (10% kcal from fat, NF) or a high-fat diet (45% kcal from fat, HF) from the 12 th week to 25 th week. While, nicotine treatment for 14 days induced an increase in hypothalamic agouti-related protein, cocaine- and amphetamine- regulated transcript, pro-opiomelanocortin mRNA expressions, nicotine also produced a reducing effect in body weight gain and leptin concentration in NF mice. High-fat diet induced obese mice showed a blunted hypothalamic and leptin response to nicotine. Remarkable weight loss in obese mice was mediated not just by decreasing caloric intake, but also by increasing total energy expenditure (EE). During nicotine withdrawal period, weight gain occurred in NF and HF groups, which was ascribed to a decrease in EE rather than changes in caloric intake. Hypothalamic AgRP might play a role for maintaining energy balance under the nicotine-induced negative energy status.

AB - Nicotine treatment has known to produce an inverse relationship between body weight and food intake in rodents. Present study determined the effect of repeated treatment with nicotine and withdrawal in control and obese mice, on: (1) body weight, caloric intake and energy expenditure; (2) hypothalamic neuropeptides mRNA expression; and (3) serum leptin. 21-week-old C57BL/6 mice (n = 65) received nicotine (3.0 mg/kg/day; 2 weeks) and saline (1 ml/kg/day; 2 weeks) subcutaneously. Animals were given either a normal-fat (10% kcal from fat, NF) or a high-fat diet (45% kcal from fat, HF) from the 12 th week to 25 th week. While, nicotine treatment for 14 days induced an increase in hypothalamic agouti-related protein, cocaine- and amphetamine- regulated transcript, pro-opiomelanocortin mRNA expressions, nicotine also produced a reducing effect in body weight gain and leptin concentration in NF mice. High-fat diet induced obese mice showed a blunted hypothalamic and leptin response to nicotine. Remarkable weight loss in obese mice was mediated not just by decreasing caloric intake, but also by increasing total energy expenditure (EE). During nicotine withdrawal period, weight gain occurred in NF and HF groups, which was ascribed to a decrease in EE rather than changes in caloric intake. Hypothalamic AgRP might play a role for maintaining energy balance under the nicotine-induced negative energy status.

KW - body weight

KW - food intake

KW - hypothalamic neuropeptides

KW - nicotine

KW - obesity

UR - http://www.scopus.com/inward/record.url?scp=78049242867&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=78049242867&partnerID=8YFLogxK

U2 - 10.1007/s10059-010-0110-3

DO - 10.1007/s10059-010-0110-3

M3 - Article

VL - 30

SP - 219

EP - 226

JO - Molecules and Cells

JF - Molecules and Cells

SN - 1016-8478

IS - 3

ER -