The Insulin Action/Molecular Metabolism track at the 77th Scientific Sessions includes more than a dozen sessions on the hottest topics in the field.
The generation of vast data sets (big data) has become extremely common in diabetes research, according to Brian N. Finck, PhD, who helped plan the sessions in the Insulin Action/Molecular Metabolism track. The rise of omic-based approaches to quantify whole genomes, specific gene expressions, or entire classes of biologically active molecules such as lipids is generating immense troves of new data.
“Even though we are generating these massive data sets, it’s not always clear what we need to do with them to advance the field,” said Dr. Finck, Associate Professor in Geriatrics and Nutritional Science at Washington University.
A session on Friday, June 9, titled Big Data and Generating Novel Hypotheses (2:00 p.m.–4:00 p.m.) will bring together four of the leading researchers gathering these data troves and using them to tease apart novel mechanisms. Attendees will learn about the genetic architecture of obesity and diabetes, redox activity in insulin resistance biomarkers, and the use of metabolomics to identify new biomarkers.
On Saturday, June 10, four experts will discuss the links between cancer, obesity, and diabetes during a two-hour session (8:00 a.m.–10:00 a.m.) titled Mechanistic Links Between Cancer, Obesity, and Diabetes.
“We know there are links between the development of obesity and the incidence of cancer, but the mechanisms by which that happens are pretty unclear,” said Shawn C. Burgess, PhD, Associate Professor of Pharmacology and Head of the Advanced Imaging Research Center at the University of Texas Southwestern Medical Center. “We will explore the idea that signaling pathways that are disrupted in obesity might make an individual predisposed to developing certain types of cancers.”
Saturday afternoon brings another session that Dr. Finck recommended, Insulin Action and Cellular Metabolism (1:45 p.m.–3:45 p.m.).
“A lot of sessions are focused on the complications of diabetes,” he said. “Dealing with complications is vitally important, but if we can focus on the root cause of diabetes, all of those complications could be headed off. It would be a huge leap forward if we could expand on this research and find ways to prevent insulin resistance and diabetes from developing in the first place.”
Dr. Burgess recommended a session on Sunday, June 11, titled Cell Signaling in the Central Nervous System as Mediator of Disease (2:15 p.m.–4:15 p.m.). A growing body of evidence points to mechanisms at the neuron level in the brain that affect obesity and diabetes, he said. Several of the ADA’s Banting and Outstanding Scientific Achievement Awards for Scientific Achievement have honored research linking the CNS to obesity and diabetes.
“This symposium is a bit different in that we are emphasizing cell signaling pathways in the brain,” Dr. Burgess said. “Speakers will be looking at AMPK signaling, mTOR pathways, endoplasmic reticulum stress, and links between insulin resistance in the brain and cognitive decline. Mechanisms that link insulin resistance and neurodegenerative diseases have not received a lot of attention until recently, including at the ADA.”
A noteworthy symposium on molecular metabolism, Cellular Energy Balance as a Basis for Metabolic (Dys)Regulation, will be presented on Monday, June 12 (8:00 a.m.–10:00 a.m.). The session is an attempt to understand how different factors within the cell that either control or respond to energy metabolism might interact with the development of dysfunction mediated by insulin resistance.
“We have a huge variety of topics, from cellular redox circuits that could lead to metabolic dysfunction to glucose sensing in the brain that could affect whole-body metabolism and the effects of exercise on the liver,” Dr. Burgess said. “Exercise can activate intracellular pathways in the liver that improve substrate metabolism. Perhaps you can think of physical exercise as an indirect way of exercising your liver.”
Another Monday session, Immunity and Inflammation as Mediators of Insulin Resistance (4:30 p.m.– 6:30 p.m.), will examine how low-level inflammation is involved in obesity and insulin resistance.
“There are potential roles for low-level inflammation to interact with insulin resistance and these need to understood,” Dr. Burgess said. “One example is mechanisms by which lipid signaling inside immune cells can trigger inflammatory processes that might impair insulin signaling. The idea that low-level inflammation can interact with insulin resistance is an important one.”