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

Journal article


Morris, N. J., Watts, Rani, 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. 32, pp. 249 - 258. https://doi.org/10.1038/sj.ijo.0803716
AuthorsMorris, N. J., Watts, Rani, Shulkes, A. and Cameron-Smith, David
Abstract

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. Methods: 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. Results: 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. Conclusion: 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.

Keywordshyperphagia; adiponectin; adiponectin receptor 1; CPT-1; leptin receptor
Year2008
JournalInternational Journal of Obesity
Journal citation32, pp. 249 - 258
PublisherInternational Journal of Obesity
ISSN0307-0565
Digital Object Identifier (DOI)https://doi.org/10.1038/sj.ijo.0803716
Page range249 - 258
Research GroupSports Performance, Recovery, Injury and New Technologies (SPRINT) Research Centre
Place of publicationUnited Kingdom
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