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Name:	Nana A. Gletsu Miller
Position:	Assistant Professor of Surgery Assistant Professor of School of Public Health, Global Health
Degree:	Ph.D., University of Alberta, 1998
Programs:	NHS, Associate Member
Phone:	404 712-2033
Address:	Emory Hospital, Suite H-130, 1364 Clifton Rd NE, 1600-002-1AA
Email:	ngletsu@emory.edu
Website:	http://www.surgery.emory.edu/gen_surgery/fac_gletsu.htm
Research Descriptions:
Short:	The role of adipose tissue-induced inflammation and oxidative stress on obesity-related insulin resistance and other metabolic diseases.
Long:	My work is focused on human and animal studies in obesity. Although it is well recognized that an excess of adipose tissue plays a causal role in the development of several diseases, the mechanisms that link obesity to comorbidities such as insulin resistance and type 2 diabetes are not well understood. I have been involved in this field since my graduate studies and I feel that the increased attention given to obesity prevention and treatment is well warranted given the current, world wide, co-epidemics of obesity and diabetes. I currently use a translational approach in my research studies. Specifically, a combination of molecular and biochemical techniques are used to analyze patient biomaterial in the laboratory in order to better explain clinical data obtained from patients. The following is a brief summary of some of the data that is relevant to the lines of research that I would like to pursue. The links between excess body weight and obesity-related diseases are not yet understood, but it is becoming clear that adipose tissue is an important source of hormonal and inflammatory metabolic factors. Adipose tissue-derived factors have been associated with oxidative stress, inflammation and insulin resistance ¿ disorders that are thought to be critical to the development of metabolic diseases. How changes in adipose tissue and its products affect disease risk needs to be determined. Putative mediators of insulin resistance may be factors that are released in excess by large amounts of adipose tissue. Plasma concentrations of such factors termed adipocytokines, e.g. interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF- ), leptin, resistin and adiponectin have been shown to be altered in states of insulin resistance and may have a direct effect on glucose metabolism and insulin action. Also, the relative roles of visceral versus subcutaneous fat in the pathophysiology of insulin action are not yet clear. In our studies using severely obese women undergoing surgically-induced or medically-induced weight loss, we employ state-of-the-art techniques to determine relationships between measures of adiposity such as total fat mass, volumes of visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT) and systemic measures of adipocytokines. These longitudinal studies represent an excellent opportunity to determine associations between adipocytokines and insulin action. Also, this data will help elucidate which of the fat depots contribute more to systemic adipocytokine concentrations. In our studies we have shown that the etiology of insulin resistance and beta-cell function is strongly related to the localization and function of specific adipose depots, rather than generalized obesity. We have found that most severely obese patients are insulin resistant but have intact beta-cell function and that both parameters can be improved with weight loss. We demonstrated that following weight loss, improvements in insulin sensitivity were correlated to decreases in systemic concentrations of C-reactive protein, which suggests a link between insulin sensitivity and inflammatory stress. Also, we have shown that adiponectin, the anti-inflammatory and anti-diabetogenic cytokine, is increased during weight loss and this increase is associated with improvement in hepatic insulin resistance. Current research is focused on the molecular changes in adipose tissue that modulate adipocytokine concentrations and influence systemic inflammation and oxidative stress in both human and animal studies.