Michael M Meguid, M.D.

Professor, Surgery
M.D.: 1968, University of London, UK
Research Associate: 1972, Harvard Medical School
Ph.D.: 1981, Massachusetts Institute of Technology

8708 University Hospital
Upstate Medical University
750 East Adams Street
Syracuse, NY 13210
(315) 464-6277

Research Program and Department Affiliations

Biomedical Sciences Program
Neuroscience Program
Surgery

Research Interests

Neurophysiological regulation of food intake.

Michael M. Meguid attended University College, London and University College Hospital Medical School graduating with a (MB BS) MD degree in 1969, when he became an anatomy prosector in the Department of Anatomy, University College, London. He did his surgical residency at Peter Bent Brigham Hospital, Harvard Medical School and Boston University Hospital Boston, MA from 1970 until 1976 during which he also spent two years as a Research Fellow in the Harvard Surgical Labs studying Surgical Metabolism with Dr. Francis D. Moore. In 1976 he assumed the position as Assistant Professor at Boston University Hospital where he started his active surgical career in Surgical Oncology and Nutrition until 1979., From 1978 until 1981 he pursued his graduate studies in the Department Human Nutrition, MIT, Cambridge, MA, graduating with a PhD in Nutritional Biochemistry and Metabolism.

In 1979 he was recruited by the Division of Surgery at the City of Hope National Medical Center, Duarte, California and UCLA Medical School, in Los Angeles for the position of Associate Surgeon where he directed the Department of Nutrition in the Division of Surgery at the City of Hope. In 1984 he returned to the east coast when he was recruited by the Department of Surgery, University Hospital, Upstate Medical University, Syracuse, New York. He is a tenured Professor of Surgery, Vice-Chair for Surgical Research, and Director of Surgical Metabolism and Nutrition Laboratory, and a Professor of Neuroscience and Physiology, Graduate Program, Upstate Medical University and Director of the Nutritional Support Services at University Hospital. In addition to his clinical practice in surgery and research in patient-related nutrition support and metabolic issues, Meguid’s research interests include examining the interaction between the peripheral and central mechanisms of appetite regulation in the anorexia of diseases such as cancer, inflammatory diseases, and more recently the hyperphagia of obesity.

An active surgical practitioner in oncology and general surgery, his clinical and benchmark research studies from his Surgical Metabolism and Nutrition Lab have led to charter memberships in numerous surgical, neuroscience, nutrition and physiologic societies. , Meguid’s research has been funded continuously since 1977, primarily by NIH (DK), but also by the National Cancer Institute. He has also been funded by non-government organizations including the American Society Bariatric Surgery and the American Diabetes Association, as well as industry which has resulted in the successful filing of several patents and licenses. Meguid - has published over 300 papers in peer-reviewed journals. He is a recipient of the: “Joseph B. Goldberger Award in Clinical Nutrition” from the American Medical Association and is a member of numerous Editorial Boards, and scientific societies. Dr. Meguid is a frequent keynote speaker and guest lecturer at national and international conferences. He is the founder and Editor-in-Chief of Nutrition, The International Journal for Basic and Applied Nutritional Sciences, published by Elsevier Science.

The principal focus of Michael Meguid’s research team is to study the two most prevailing diseases he has encountered in his clinical practice as a byproduct of developing societies: cancer and obesity (with its associated type 2 diabetes mellitus). In both diseases there is an abnormality of food intake control and energy homeostasis, which are closely related to the inflammatory processes. In cancer patients the onset of anorexia reduces food intake, leading to catabolism of muscle and fat mass and organ and immune system integrity, both contributing to cachexia and delaying recuperation after surgery and adjuvant chemotherapy. The ongoing research is summarized in two recent publications: (Laviano A, Meguid MM, Inui A, Muscaritoli M, Rossi-Fanelli F. Therapy insight: cancer anorexia-cachexia syndrome: when all you can eat is yourself. Nature Clinical Practice, Oncology 2005; 2: 1-8) and (Guijarro A, Laviano A, Meguid MM. Hypothalamic integration of immune function and metabolism (Prog Brain Res 2006; 153: Chapter 22).

The opposite occurs in obese patients who have hyperphagia and in whom a proportion become morbidly obese. These processes are complex, but like cancer involve the interplay between the periphery (adipocyte and gut) and the brain (discrete hypothalamic nuclei and the memory system) that interact to maintain energy homeostasis and food intake. When this system fails, alterations in food intake and energy control result in eating disorders, including obesity.

To investigate these biological problems, Dr. Meguid’s lab uses two different rat models, the MCA-sarcoma and the diet-induced obese. The well-established MCA-sarcoma (methylcholanthrene) rat model is used to initiate anorexia and cachexia as the tumor grows. The sum of our data supports the concept that immune cell-derived cytokines are closely related with the regulation of metabolism and have both central and peripheral actions. The mechanism involves inducing anorexia via hypothalamic anorectic factors, serotonin and dopamine and inhibiting neuropeptide Y, and a host of cytokines that lead to a reduction in food intake and body weight. These data emphasize the interconnection of the immune and neuroendocrine systems in regulating metabolism which are elegantly summarized in the following references: Suzuki S, Goncalves CG, Meguid MM. Catabolic outcome from non-GI malignancy related malabsorption leading to malnutrition and weight loss. Curr Opin Clin Nutr Metab Care 2005;8:419-27, and in Turrin NP, Illyin SE, Gayle D, Plata-Salaman CR, Ramos EJB, Laviano A, Das UN, Inui A, Meguid MM. Interleukin- b system activation in anorectic catabolic tumor bearing rats. Curr Opin Clin Nutr Metab Care 2004;7:419-426.

Dr Meguid’s interest in hyperphagia in relation to the hypothalamus and morbid obesity with its linked Metabolic Syndrome, led him and his research team to develop the second animal model: This is a clinically applicable robust standardized Roux-en-Y gastric bypass (RYGB) animal model in diet-induced obese Sprague Dawley rats that parallels the temporal pattern of human weight loss including its ‘failure rate’ (‘ inadequate weight loss or failures to maintain weight loss’ i.e., weight regain after surgery). (Meguid MM, Ramos EJB, Suzuki S, Xu Y, George Z, Das UN, Hughes K, Quinn R, Chen C, Marx W, Cunningham PRG. A surgical rat model of human Roux-en-Y gastric bypass. J Gastro Surg 2004; 8:621-30). In this model, not only are ~10-13 rat days equal to 1 human year which allows for long term follow-up, but it also permits pair feeding studies, drug intervention studies, and the obtaining of brain tissues, thereby discovering the interaction of anatomical, metabolic and genetic factors in the mechanism of gastric bypass-induced weight loss. Lastly, it facilitates the study of genetic markers of weight regulation (Xu Y, Ramos EJ, Middleton F, Romanova I, Quinn R, Chen C, Das U, Inui A, Meguid MM. Gene expression profiles post Roux-en-Y gastric bypass. Surgery 2004; 136:246-52; Romanova IV, Ramos EJB, Xu Y, Quinn R, Chen C, George ZM, Inui A, Das U, Meguid MM. Neurobiological changes in the hypothalamus associated with weight loss after gastric bypass. JACS 2004; 199:887-95; and Guijarro A, Kirchner H, Meguid MM. Catabolic effects of gastric bypass in a diet induced obese rat model. Curr Opin Clin Nutr Metab Care , 2006; 9:403).

The Surgical Metabolism and Nutrition Laboratory is goal-oriented. Dr. Meguid strongly supports and engages in institutional, national and international collaboration, as reflected by his numerous co-authors. During the past 22 years he has trained 40 research fellows, graduate and PhD students from numerous countries, facilitating Masters and PhD degrees. Most of these have continued their research endeavors, frequently becoming collaborators and advancing to positions of professor, academic chairs and thought leaders in their respective academic world, internationally. His current lab team consists of Karen Hughes BA (Senior Technician), Hua Fang MD (Surgeon from China), Ana Guijarro PhD (Postdoc from Spain) and Henriette Kirchner MS (PhD-Student from Germany). Particularly interesting are the numerous medical students, with their unique prospective and backgrounds, who have spent time working with the team. He has had the honor of ‘hooding’ several during their graduation ceremony.

Honors and Awards

Ongoing Research Projects

Hypothalamic role in reversing obesity related type 2 diabetes mellitus: This study investigates the changes in hypothalamic neuropeptides and neurotransmitters contributing to the amelioration and reversal of obesity related type 2 diabetes mellitus (T2DM) induced by Roux-en-Y gastric bypass operation.

Changes in insulin signaling ameliorate obesity-related type 2 diabetes mellitus after Roux-en-Y gastric bypass: The goal of this project is to study the molecular mechanisms involved in the reversion of T2DM after Roux-en-Y Gastric Bypass in diet-induced obese rats.

Role of endocannabinoid system after Roux-en-Y gastric bypass in reversing type 2 diabetes mellitus in a robust rat model: The major aim of this project is to determine the role of the endocannabinoid system in ameliorating T2DM after Roux-en-Y gastric bypass in diet-induced obese rats and how these changes affect insulin signaling pathway.

Publications

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This profile was last updated on 09/29/2008

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