Person: Calay, Ediz
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Calay
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Ediz
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Calay, Ediz
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Publication A hormone complex of FABP4 and nucleoside kinases regulates islet function(Springer Science and Business Media LLC, 2021-12-08) Prentice, Kacey J.; Saksi, Jani Pertti Kristian; Robertson, Lauren T.; Lee, Grace Y.; Inouye, Karen; Eguchi, Kosei; Lee, Alexandra; Cakici, Ozgur; Otterbeck, Emily; Cedillo, Paulina; Achenbach, Peter; Ziegler, Anette-Gabriele; Calay, Ediz; Engin, Feyza; Hotamisligil, Gökhan S.; Hotamisligil, GokhanLiberation of energy stores from adipocytes is critical to support survival in times of energy deficit, however, uncontrolled or chronic lipolysis associated with insulin resistance and/or insulin insufficiency, disrupts metabolic homeostasis. Coupled to lipolysis is the release of a recently identified hormone, fatty acid-binding protein 4 (FABP4). While circulating FABP4 levels have been strongly associated with cardiometabolic diseases in both preclinical models and humans, no mechanism of action has yet been described. Here, we show that hormonal FABP4 forms a novel functional hormone complex with Adenosine Kinase (ADK) and Nucleoside Diphosphate Kinase (NDPK) to regulate extracellular ATP and ADP levels. We identify a substantial impact of this hormone on beta-cells and given the central role of beta-cell function in both the control of lipolysis and development of diabetes, postulate that hormonal FABP4 is a key regulator of an adipose-beta-cell endocrine axis. Antibody-mediated targeting of this hormone complex improves metabolic outcomes, enhances beta-cell function, and preserves beta-cell integrity to prevent both type 1 and type 2 diabetes. Thus, the FABP4-ADK-NDPK complex, Fabtin, represents a previously unknown hormone and mechanism of action integrating energy status with the function of metabolic organs, representing a promising target against metabolic disease.Publication Cellular and Systemic Metabolic Adaptations to Energy Status(2014-06-06) Calay, Ediz; Hotamisligil, Gokhan S.; Kobzik, Lester; Saatcioglu, Fahri; Mitchell, James; Yuan, Zhi-Min; Puigserver, Pere; Lu, QuanMy thesis work has focused on physiological adaptations to nutrient stress; from genes, environment and hormonal perspective, and how failure of these systems result in common chronic diseases.Publication Dietary restriction protects against experimental cerebral malaria via leptin modulation and T cell mTORC1 suppression(2014) Mejia, Pedro; Treviño-Villarreal, J. Humberto; Hine, Christopher; Harputlugil, Eylul; Lang, Samantha; Calay, Ediz; Rogers, Rick; Wirth, Dyann; Duraisingh, Manoj; Mitchell, JamesHost nutrition can affect the outcome of parasitic diseases through metabolic effects on host immunity and/or the parasite. Here we show that modulation of mouse immunometabolism through brief restriction of food intake (dietary restriction, DR) prevents neuropathology in experimental cerebral malaria (ECM). While no effects are detected on parasite growth, DR reduces parasite accumulation in peripheral tissues including brain, and increases clearance in the spleen. Leptin, a host-derived adipokine linking appetite, energy balance and immune function, is required for ECM pathology and its levels are reduced upon DR. Recombinant leptin abrogates DR benefits, while pharmacological or genetic inhibition of leptin signaling protects against ECM. DR reduces mTORC1 activity in T cells, and this effect is abrogated upon leptin administration. Furthermore, mTORC1 inhibition with rapamycin prevents ECM pathology. Our results suggest that leptin and mTORC1 provide a novel mechanistic link between nutrition, immunometabolism and ECM pathology, with potential therapeutic implications for cerebral malaria.