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High Fat Diet Altered the Mechanism of Energy Homeostasis Induced by Nicotine and Withdrawal in C57BL/6 Mice

Authors
Hur, Young-NaHong, Gee-HyunChoi, Sang-HyunShin, Kyung-HoChun, Boe-Gwun
Issue Date
Sep-2010
Publisher
KOREAN SOC MOLECULAR & CELLULAR BIOLOGY
Keywords
body weight; food intake; hypothalamic neuropeptides; nicotine; obesity
Citation
MOLECULES AND CELLS, v.30, no.3, pp.219 - 226
Indexed
SCIE
SCOPUS
KCI
Journal Title
MOLECULES AND CELLS
Volume
30
Number
3
Start Page
219
End Page
226
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/115818
DOI
10.1007/s10059-010-0110-3
ISSN
1016-8478
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.
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