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Kenny Walter is an editor with HCPLive. Prior to joining MJH Life Sciences in 2019, he worked as a digital reporter covering nanotechnology, life sciences, material science and more with R&D Magazine. He graduated with a degree in journalism from Temple University in 2008 and began his career as a local reporter for a chain of weekly newspapers based on the Jersey shore. When not working, he enjoys going to the beach and enjoying the shore in the summer and watching North Carolina Tar Heel basketball in the winter.
By addressing insulin resistance, researchers believe they can reduce the comorbidities associated with type 2 diabetes.
Insulin resistance has long been known as a critical factor in the pathogenesis of type 2 diabetes.
However, it might not entirely be known what the particular role of diacylglycerol and acetyl-CoAin play in insulin resistance.
During the 18th World Congress of Insulin Resistance Diabetes & Cardiovascular (WCIRDC) Online CME Conference presented by the Metabolic Institute of America (TMIOA), Gerald Shulman, MD, PhD, George R. Cowgill Professor of Medicine and Cellular & Molecular Physiology at Yale, explained how this can be a beneficial therapeutic target to reduce the amount of obese patients with insulin resistance.
The researchers believe these lipids explain insulin resistance concept because fat will build up where it does not belong, triggering insulin resistance.
This could also explain why certain drugs are able to reduce the fat in certain organs and reverses insulin resistance. Fat is not, however, the causal agent of insulin resistance, leading to the hypothesis that it is another lipid species that causes insulin resistance.
Recent studies show it is diacylglycerol that trigger PKC activation, leading to blocks to insulin signaling and insulin action.
Shulman also explained how fixing insulin resistance could have an impact at reducing some of the cardiovascular and kidney comorbidities commonly associated with type 2 diabetes.