Submitted on July 8, 2007
Accepted on October 14, 2007
Detrimental metabolic effects of combining long term cigarette smoke exposure and high-fat diet in mice
Hui Chen1, Michelle Joan Hansen2, Jessica E Jones3, Ross Vlahos3, Gary Anderson4, and Margaret J Morris5*
1 Pharmacology, University of New South Wales, Sydney, Victoria, Australia
2 Department of Pharmacology, The University of Melbourne, Melbourne, Victoria, Australia
3 Department of Pharmacology, The University of Melbourne, Melbourne, Victoria, Australia; CRC for Chronic Inflammatory Diseases, The University of Melbourne, Melbourne, Victoria, Australia
4 Medicine/Pharmacology, University of Melbourne, Parkville, Victoria, Australia; CRC for Chronic Inflammatory Diseases, The University of Melbourne, Melbourne, Victoria, Australia
5 Pharmacology, University of New South Wales, Sydney, New South Wales, Australia
* To whom correspondence should be addressed. E-mail: m.morris{at}unsw.edu.au.
Obesity and cigarette smoking are both important risk factors for insulin resistance, cardiovascular disease, and cancer. Smoking reduces appetite, which makes many people reluctant to quit. Few studies have documented the metabolic impact of combined smoke exposure (SE) and high-fat-diet (HFD). Neuropeptide Y (NPY) is a powerful hypothalamic feeding stimulator that promotes obesity. We investigated how chronic SE affects caloric intake, adiposity, plasma hormones, inflammatory mediators and hypothalamic NPY peptide in animals fed a palatable HFD.
Methods: Balb/c mice (5 weeks, male) were exposed to smoke (2 cigarettes, twice/day, 6 days/week, for 7 weeks) with or without HFD. Sham-exposed mice were handled similarly without SE. Plasma leptin, hypothalamic NPY, and adipose triglyceride lipase (ATGL) mRNA were measured.
Results: HFD induced a 2.3 fold increase in caloric intake, increased adiposity, and glucose in both sham and SE cohorts. SE decreased caloric intake by 23%, with reduced body weight in both dietary groups. Fat mass and glucose were only reduced by SE in the chow fed animals. ATGL mRNA was reduced by HFD in SE animals. Total hypothalamic NPY was reduced by HFD, but only in sham-exposed animals; SE increased arcuate NPY.
Conclusion: Although SE ameliorated hyperphagia and reversed the weight gain associated with HFD, it failed to reverse fat accumulation and hyperglycemia. The reduced ATGL mRNA expression induced by combined HFD and SE may contribute to fat retention. Our data support a powerful health message that smoking in the presence of an unhealthy western diet increases metabolic disorders and fat accumulation.
