Nicotine improves obesity and hepatic steatosis and ER stress in diet-induced obese male rats

Patricia Seoane-Collazo, Pablo Blanco Martinez De Morentin, Johan Ferno, Carlos Dieguez, Ruben Nogueiras, Miguel Lopez

Research output: Contribution to journalArticle

55 Citations (Scopus)

Abstract

Nicotine, the main addictive component of tobacco, promotes body weight reduction in humans and rodents. Recent evidence has suggested that nicotine acts in the central nervous system to modulate energy balance. Specifically, nicotine modulates hypothalamic AMP-activated protein kinase to decrease feeding and to increase brown adipose tissue thermogenesis through the sympathetic nervous system, leading to weight loss. Of note, most of this evidence has been obtained in animal models fed with normal diet or low-fat diet (LFD). However, its effectiveness in obese models remains elusive. Because obesity causes resistance towards many factors involved in energy homeostasis, the aim of this study has been to compare the effect of nicotine in a diet-induced obese (DIO) model, namely rats fed a high-fat diet, with rats fed a LFD. Our data show that chronic peripheral nicotine treatment reduced body weight by decreasing food intake and increasing brown adipose tissue thermogenesis in both LFD and DIO rats. This overall negative energy balance was associated to decreased activation of hypothalamic AMP-activated protein kinase in both models. Furthermore, nicotine improved serum lipid profile, decreased insulin serum levels, as well as reduced steatosis, inflammation, and endoplasmic reticulum stress in the liver of DIO rats but not in LFD rats. Overall, this evidence suggests that nicotine diminishes body weight and improves metabolic disorders linked to DIO and might offer a clear-cut strategy to develop new therapeutic approaches against obesity and its metabolic complications.

Original languageEnglish
Pages (from-to)1679-1689
Number of pages11
JournalEndocrinology
Volume155
Issue number5
Early online date11 Feb 2014
DOIs
Publication statusPublished - May 2014

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Nicotine
Obesity
Fat-Restricted Diet
Diet
Liver
AMP-Activated Protein Kinases
Brown Adipose Tissue
Thermogenesis
Body Weight
Weight Loss
Endoplasmic Reticulum Stress
Sympathetic Nervous System
High Fat Diet
Serum
Tobacco
Rodentia
Homeostasis
Central Nervous System
Animal Models
Eating

Keywords

  • AMP-Activated Protein Kinases
  • Adipose Tissue, Brown
  • Animals
  • Appetite Depressants
  • Appetite Regulation
  • Diet, Fat-Restricted
  • Diet, High-Fat
  • Dyslipidemias
  • Endoplasmic Reticulum Stress
  • Fatty Liver
  • Hyperinsulinism
  • Hypothalamus
  • Injections, Subcutaneous
  • Liver
  • Male
  • Nicotine
  • Nicotinic Agonists
  • Non-alcoholic Fatty Liver Disease
  • Obesity
  • Rats
  • Rats, Sprague-Dawley
  • Thermogenesis
  • Weight Loss

Cite this

Nicotine improves obesity and hepatic steatosis and ER stress in diet-induced obese male rats. / Seoane-Collazo, Patricia; Martinez De Morentin, Pablo Blanco; Ferno, Johan ; Dieguez, Carlos; Nogueiras, Ruben; Lopez, Miguel.

In: Endocrinology, Vol. 155, No. 5, 05.2014, p. 1679-1689.

Research output: Contribution to journalArticle

Seoane-Collazo, Patricia ; Martinez De Morentin, Pablo Blanco ; Ferno, Johan ; Dieguez, Carlos ; Nogueiras, Ruben ; Lopez, Miguel. / Nicotine improves obesity and hepatic steatosis and ER stress in diet-induced obese male rats. In: Endocrinology. 2014 ; Vol. 155, No. 5. pp. 1679-1689.
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