Brain neuropeptide Y and CCK and peripheral adipokine receptors : temporal response in obesity induced by palatable diet

Morris, M. J., Chen, H., Watts, R., Shulkes, A. and Cameron-Smith, David 2008, Brain neuropeptide Y and CCK and peripheral adipokine receptors : temporal response in obesity induced by palatable diet, International journal of obesity, vol. 32, pp. 249-258, doi: 10.1038/sj.ijo.0803716.

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Title Brain neuropeptide Y and CCK and peripheral adipokine receptors : temporal response in obesity induced by palatable diet
Author(s) Morris, M. J.
Chen, H.
Watts, R.
Shulkes, A.
Cameron-Smith, David
Journal name International journal of obesity
Volume number 32
Start page 249
End page 258
Publisher Nature Publishing Group
Place of publication London, England
Publication date 2008
ISSN 0307-0565
Keyword(s) hyperphagia
adiponectin receptor 1
leptin receptor
Summary Objective:
Palatable food disrupts normal appetite regulation, which may contribute to the etiology of obesity. Neuropeptide Y (NPY) and cholecystokinin play critical roles in the regulation of food intake and energy homeostasis, while adiponectin and carnitine palmitoyltransferase (CPT) are important for insulin sensitivity and fatty acid oxidation. This study examined the impact of short- and long-term consumption of palatable high-fat diet (HFD) on these critical metabolic regulators.

Male C57BL/6 mice were exposed to laboratory chow (12% fat), or cafeteria-style palatable HFD (32% fat) for 2 or 10 weeks. Body weight and food intake were monitored throughout. Plasma leptin, hypothalamic NPY and cholecystokinin, and mRNA expression of leptin, adiponectin, their receptors and CPT-1, in fat and muscles were measured.

Caloric intake of the palatable HFD group was 2–3 times greater than control, resulting in a 37% higher body weight. Fat mass was already increased at 2 weeks; plasma leptin concentrations were 2.4 and 9 times higher than control at 2 and 10 weeks, respectively. Plasma adiponectin was increased at 10 weeks. Muscle adiponectin receptor 1 was increased at 2 weeks, while CPT-1 mRNA was markedly upregulated by HFD at both time points. Hypothalamic NPY and cholecystokinin content were significantly decreased at 10 weeks.

Palatable HFD induced hyperphagia, fat accumulation, increased adiponectin, leptin and muscle fatty acid oxidation, and reduced hypothalamic NPY and cholecystokinin. Our data suggest that the adaptive changes in hypothalamic NPY and muscle fatty acid oxidation are insufficient to reverse the progress of obesity and metabolic consequences induced by a palatable HFD.
Language eng
DOI 10.1038/sj.ijo.0803716
Field of Research 111601 Cell Physiology
Socio Economic Objective 970111 Expanding Knowledge in the Medical and Health Sciences
HERDC Research category C1 Refereed article in a scholarly journal
ERA Research output type C Journal article
HERDC collection year 2008
Copyright notice ©2008, Nature Publishing Group
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Document type: Journal Article
Collection: School of Exercise and Nutrition Sciences
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