Adipokines-AMPK Cross-Talk in Avian Species: A Translational Model for Human Obesity

Alissa Piekarski-Welsher, Walter Bottje, Sami Dridi

Center of Excellence for Poultry Science, University of Arkansas, Fayetteville, AR 72701, USAUnited States

DOI: https://doi.org/10.17140/oroj-3-126 · Published 2016-09-02 · Licence: https://creativecommons.org/licenses/by/4.0 · © 2016 The Author(s)

Also available as PDF (figures and tables appear in the PDF).

Keywords: Adipocytokine; AMP-activated protein kinase (AMPK); Obesity; Chicken; Adipocytokine; AMP-activated protein kinase (AMPK); Obesity; Chicken

Article History th Received: August 26th, 2016 nd Adipocytokines, or adipokines, are circulating hormones mainly produced by adipose tissue Accepted: September 2 , 2016 nd and are key regulators of whole body metabolism and immune homeostasis. Due to a rise in Published: September 2 , 2016 human obesity-related diseases, pathways related to metabolism are being studied using sev- eral animal models to identify key molecular signatures for development of mechanism-based Citation therapeutic strategies. Previous work published in our laboratory has used chickens as a model Piekarski-Welsher A, Bottje W, for obesity because of its peculiarities that will be described in this article. In particular, recent Dridi S. Adipokines-AMPK cross- advances in our understanding of adipokine AMP-activated protein kinase (AMPK) interac- talk in avian species: A translational model for human obesity. Obes tions in the regulation of energy balance will be summarized as well as facilitating the discus- Res Open J. 2016; 3(2): 40-42. sion by asking new questions which may open new vistas for future research.

doi: 10.17140/OROJ-3-126 KEYWORDS: Adipocytokine; AMP-activated protein kinase (AMPK); Obesity; Chicken. ABBREVIATIONS: AMPK: AMP-activated protein kinase; ARC: Arcuate nucleus; PVN: Para- ventricular nucleus; GLUT4: Glucose transporter type 4; SOCS3: Suppressor of cytokine sig- naling 3; LDL: Low-density lipoprotein.

The relationship between adipocytokines and AMP-activated protein kinase (AMPK) in the regulation of several metabolic processes has been the subject of many studies. AMPK has been shown to be activated/deactivated by several adipokine-inducing cellular energy al- teration. The adipokines adiponectin, leptin, resistin and visfatin play pivotal roles in obesity, 1-6 insulin resistance and related inflammatory disorders.1-6 Adiponectin is involved in regulating glucose levels as well as fatty acid breakdown, with circulating levels varying in healthy adults but may be inversely correlated with body fat percentage.7 Leptin regulates energy balance through its anorexigenic effects in the hypothalamus. In obesity, leptin sensitivity decreases 8,9 although it has high circulating levels.8,9 Resistin is also known as adipose tissue-specific se- cretory factor (ADSF) and is secreted by immune and epithelial cells, playing a role in high levels of low-density lipoprotein (LDL) and serves endocrine functions involved in insulin resistance.10 Visfatin has been shown to activate insulin receptor and to have insulin-mimetic effects such as lowering blood glucose and improving insulin sensitivity.11 This cytokine is highly expressed in visceral fat and its serum levels is high in obese subjects.11 Studies detailing the control of hepatic glucose production by activated AMPK was demonstrated in resistin knockout mice and adiponectin treated rodents, and suggested that hepatic AMPK is a specific target of both adipocytokines with resistin inhibiting AMPK and Copyright 12,13 adiponectin activating AMPK. AMPK is expressed in feeding-related hypothalamic nuclei ©2016 Piekarski-Welsher A. This is an open access article distributed such as arcuate nucleus (ARC) and paraventricular nucleus (PVN) and has been shown to under the Creative Commons Attri- mediate the (an)orexigenic effects of adipocytokine. For instance, adiponectin increases food bution 4.0 International License (CC intake, but leptin decreases food intake through activating AMPK in the hypothalamus. These BY 4.0), which permits unrestricted results, along with others, show that food intake and nutrient metabolism are regulated by the use, distribution, and reproduction in any medium, provided the original AMPK pathway15 as shown in a fasting study that resulted inactivation of AMPK whereas work is properly cited. re-feeding inhibited AMPK activity in mice.16 Feed efficiency in poultry, (the ability of the animal to convert their feed into usable energy) is an important

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