Investigations in the Banks lab focus on understanding the mechanisms linking obesity with insulin resistance. The goal of this work is to provide new insights that may lead to novel therapeutic interventions. Approaches used in our work include pharmacologic and genetic approaches in mice and in human cells to mechanistically model aspects of human metabolic disease.
Dr. Banks studied chemistry at Brandeis University in Waltham, Massachusetts. He then worked with Dr. Martin Myers at the Joslin Diabetes Center as a research assistant on the signaling cascades downstream of the leptin receptor, an essential mediator of hunger and food intake. An interest in signal transduction led to a Ph.D. dissertation focused on a novel inhibitor of beta-cell insulin receptor and cytokine receptor signaling in the lab of Dr. Paul Rothman at Columbia University. Studies of this inhibitory molecule and an accompanying knock-out mouse were an excellent starting point for understanding metabolic physiology. This project identified Socs7 as a gene highly expressed in pancreatic islets and capable of regulating postnatal beta-cell growth and function.
Dr. Banks’ postdoctoral research was performed in labs focused on hepatic and adipose biology, respectively. In the lab of Dr. Domenico Accili at Columbia University, he found that glucose homeostasis can be controlled by protein acetylation. They identified the actions of the protein deacetylase Sirt1 on protein substrates to increase hepatic insulin sensitivity and the effects of acetylated Foxo1 as a transcriptional regulator of the rate-limiting steps controlling glucose production. These projects were significant for their use of mouse molecular genetics to clarify the mechanistic basis of disease pathology.
Dr. Banks’ postdoctoral research in the lab of Dr. Bruce Spiegelman at the Dana-Farber Cancer Institute and Harvard Medical School focused on adipose tissue biology. Obesity-induced in mice by high-fat feeding activates protein kinases in adipose tissues. This results in phosphorylation and altered functionality of the nuclear receptor PPARg, a dominant regulator of adipogenesis and fat cell gene expression. This work strongly suggests that phosphorylation of PPARg may be involved in the pathogenesis of insulin resistance and further presents an opportunity for the development of an improved generation of anti-diabetic drugs through specific modulation of PPARg.
In 2018 the Banks lab moved to Beth Israel Deaconess Medical Center at Harvard Medical School in the Division of Endocrinology from the Brigham and Women’s Hospital at Harvard Medical School. Dr. Banks is an Assistant Professor of Medicine. He is also the director of the Energy Balance Core Facility which measures metabolic rates in laboratory animals.
All the links: Harvard Catalyst Profile, Pubmed, ORCID, Google Scholar