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Allison B. Goldfine, M.D.

Dr. Goldfine is Head of the Section of Clinical, Behavioral & Outcomes Research at Joslin Diabetes Center and an Associate Professor of Medicine at Harvard Medical School. She received her medical degree from the University of Pennsylvania and did her postdoctoral training at the University of Massachusetts Medical Center, Harvard Medical School and Joslin. In 1999 and 2000, she received the Harvard Medical School Center of Excellence in Women’s Health Research Grant; in 2002, the Priscilla White Fellowship; and in 2006, a Career Development Award from the American Diabetes Association.

The desire to work more closely with patients while addressing the worldwide epidemic of type 2 diabetes drew Dr. Goldfine out of the basic science laboratory and into a career in clinical research. Dr. Goldfine has studied the ways in which risk factors—including genetic predisposition, obesity and lifestyle—interact in the development of diabetes and the cardiovascular complications of the disease. To identify the complex molecular pathways leading to disease, Dr. Goldfine’s laboratory evaluates early physiologic, molecular and genetic determinants of type 2 diabetes in individuals at risk of developing the disease, focusing specifically on obesity and a strong family history of diabetes as risk factors. For example, while insulin resistance appears to precede and predict the development of type 2 diabetes in people with a strong family history of the disease, Dr. Goldfine has shown it is a less reliable predictor in people without a family history of diabetes.

The common varieties of type 2 diabetes are characterized by both insulin resistance and disordered beta-cell function, most notably a defect in glucose-stimulated insulin secretion. Rohit Kulkarni, M.D., Ph.D., a colleague in the Section on Cellular and Molecular Physiology, has recently demonstrated that insulin receptors and insulin signaling proteins are found within the beta cells themselves and that the insulin signaling pathway is functionally important for glucose sensing in rodents and in cultured cells. However, the physiological and pathophysiological role of insulin signaling in normal and diabetic human beta cells is largely unknown. Dr. Goldfine is studying whether insulin might regulate the beta-cell function in people, and if so whether this effect would be different in patients with type 2 diabetes or at high risk of developing the disease, including those who are overweight or have a strong family history of diabetes. 

People with diabetes are at greater risk of vascular disease, including heart attack and stroke. Evidence suggests that inflammation might play an important role in the development of both diabetes and cardiovascular disease.  If so, then is it possible to use drugs that treat inflammation to treat or prevent diabetes and/or cardiovascular disease? Dr. Goldfine, in collaboration with Steven E. Shoelson, M.D., Ph.D., Head of the Section on Cellular and Molecular Physiology, has performed small studies to treat inflammation in order to reduce blood glucose in patients with diabetes using a drug that is related to aspirin and appears to have an excellent safety profile. They achieved success in the early clinical trials, where the drug was found to reduce inflammation, lower blood glucose and have positive effects on cholesterol profiles. Large clinical trials now are testing to determine if molecular targeting of inflammation is beneficial to treat or prevent diabetes and cardiovascular disease. Furthermore, the researchers want to learn how a doctor might identify patients who would be more likely to respond to this treatment.

Selected References
Goldfine AB, Crunkhorn S, Costello M, Gami H, Landaker EJ, Niinobe M,
Yoshikawa K, Lo D, Warren A, Jimenez-Chillaron J, Patti ME. Necdin and E2F4 are modulated by rosiglitazone therapy in diabetic human adipose and muscle tissue. Diabetes 55:640-650, 2006.

Patti ME, McMahon G, Mun EC, Bitton A, Holst JJ, Goldsmith J, Hanto DW,
Callery M, Arky R, Nose V, Bonner-Weir S, Goldfine AB. Severe hypoglycaemia post-gastric bypass requiring partial pancreatectomy: evidence for inappropriate insulin secretion and pancreatic islet hyperplasia. Diabetologia 48:2236-2240, 2005.

Halperin F, Beckman JA, Patti ME, Trujillo ME, Garvin M, Creager MA, Scherer
PE, Goldfine AB. The role of total and high-molecular-weight complex of adiponectin in vascular function in offspring whose parents both had type 2 diabetes. Diabetologia  48:2147-2154, 2005.

Aldhahi W, Armstrong J, Bouche C, Carr RD, Moses A, Goldfine AB. b-cell insulin secretory response to oral hypoglycemic agents is blunted in
humans in vivo during moderate hypoglycemia. J Clin Endocrinol Metab 89:4553-4557, 2004.

Goldfine AB, Bouche C, Parker RA, Kim C, Kerivan A, Soeldner JS, Martin BC,
Warram JH, Kahn CR. Insulin resistance is a poor predictor of type 2 diabetes in individuals with no family history of disease. Proc Natl Acad Sci U S A 100:2724-2729, 2003.

Beckman JA, Goldfine AB, Gordon MB, Garrett LA, Creager MA. Inhibition of protein kinase Cb prevents impaired endothelium-dependent vasodilation caused by hyperglycemia in humans. Circ Res 90:107-111, 2002.


Page last updated: October 21, 2014