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Brain neuropeptide Y and CCK and peripheral adipokine receptors: temporal response in obesity induced by palatable diet.
Int J Obes (Lond). 2008 Feb; 32(2):249-58.IJ

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.

Authors+Show Affiliations

Department of Pharmacology, School of Medical Sciences, University of New South Wales, Sydney, New South Wales, Australia. m.morris@unsw.edu.auNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

17768423

Citation

Morris, M J., et al. "Brain Neuropeptide Y and CCK and Peripheral Adipokine Receptors: Temporal Response in Obesity Induced By Palatable Diet." International Journal of Obesity (2005), vol. 32, no. 2, 2008, pp. 249-58.
Morris MJ, Chen H, Watts R, et al. Brain neuropeptide Y and CCK and peripheral adipokine receptors: temporal response in obesity induced by palatable diet. Int J Obes (Lond). 2008;32(2):249-58.
Morris, M. J., Chen, H., Watts, R., Shulkes, A., & Cameron-Smith, D. (2008). Brain neuropeptide Y and CCK and peripheral adipokine receptors: temporal response in obesity induced by palatable diet. International Journal of Obesity (2005), 32(2), 249-58.
Morris MJ, et al. Brain Neuropeptide Y and CCK and Peripheral Adipokine Receptors: Temporal Response in Obesity Induced By Palatable Diet. Int J Obes (Lond). 2008;32(2):249-58. PubMed PMID: 17768423.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Brain neuropeptide Y and CCK and peripheral adipokine receptors: temporal response in obesity induced by palatable diet. AU - Morris,M J, AU - Chen,H, AU - Watts,R, AU - Shulkes,A, AU - Cameron-Smith,D, Y1 - 2007/09/04/ PY - 2007/9/5/pubmed PY - 2008/8/5/medline PY - 2007/9/5/entrez SP - 249 EP - 58 JF - International journal of obesity (2005) JO - Int J Obes (Lond) VL - 32 IS - 2 N2 - 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. SN - 1476-5497 UR - https://www.unboundmedicine.com/medline/citation/17768423/Brain_neuropeptide_Y_and_CCK_and_peripheral_adipokine_receptors:_temporal_response_in_obesity_induced_by_palatable_diet_ L2 - http://dx.doi.org/10.1038/sj.ijo.0803716 DB - PRIME DP - Unbound Medicine ER -