Have Researchers Found the Right Angle to Tackle Diabetes?

When your wellness is compromised by diabetes, you are part of a large and growing segment of the human population, and, especially among the obese, the disease can lead to nerve loss, blindness, and even death. Many medical experts are researching how genes and genetic mutations affect your wellness, but a group of biomedical researchers at UC Santa Barbara is studying cell metabolism, and that of their surrounding tissue, to try and determine how certain diseases begin, and this approach can be applied to Type 2 diabetes, autoimmune diseases, and neurodegenerative diseases, among others.

The team at UCSB have found that changes in cellular metabolism could be the triggering factor for the disease, rather than any genetic predisposition you might have. The pioneering researchers predict that their discovery could become a basis for diabetes prevention, and even a cure for the disease.

They based their work on a major finding by UCSB’s Jamey Marth, a professor in the Department of Molecular, Cellular, and Developmental Biology and the Biomolecular Science and Engineering Program; holder of the John Carbon Chair in Biochemistry and Molecular Biology and the Duncan and Suzanne Mellichamp Chair in Systems Biology; and professor with the Sanford-Burnham Medical Research Institute in La Jolla.

Marth discovered the molecular building blocks you need to construct the four types of macromolecules of all your cells, and explained ‘By studying the four types of components that make up the cell, we can, for the first time, begin to understand what causes many of the common grievous diseases that exist in the absence of definable genetic variation, but, instead, are due to environmental and metabolic alterations of our cells’.

According to Marth, UCSB is currently the only institution studying these four types of molecules in the cells while also using computational modelling to determine their functions in health and disease. ‘We’re trying to understand what actually causes disease, which is defined as cellular dysfunction. Once we understand what causes disease we can make a difference by devising more rational and effective preventative and therapeutic approaches.’

Co-author Frank Doyle, associate dean for research of the College of Engineering; director of UCSB’s Institute for Collaborative Biotechnologies; professor of chemical engineering; and the Mellichamp Chair in Process Control, added ‘We are excited to bring our 20 years of expertise on Type 1 diabetes and systems biology methods to look at the networks responsible for the onset of Type 2 diabetes’.