redOrbit Staff & Wire Reports – Your Universe Online
Changes in a person’s cellular metabolism, not genetic predisposition, may be the primary factor that causes a person to contract Type 2 diabetes, researchers from the University of California – Santa Barbara (UCSB) have discovered.
Building upon previous research at the university, which uncovered the identity of the molecular building blocks required to construct the four types of macromolecules found in all cells, the UCSB team behind the current study used computational systems biology modeling to discover a failure of beta cells in the pancreas to detect a rise in blood sugar and respond by secreting insulin to regulate the body’s blood glucose levels.
“The researchers identified a ‘tipping point,’ or metabolic threshold, that when crossed results in the failure of beta cells to adequately sense glucose in order to properly secrete insulin,” the university said in a statement on Friday. “Obesity has long been linked to Type 2 diabetes, but the cellular origin of the disease due to beta cell failure has not been described until now.”
“In obesity there’s a lot of fat in the system,” explained Jamey Marth, a professor in the UCSB Department of Molecular, Cellular, and Developmental Biology and the Biomolecular Science and Engineering Program. “When the cell is exposed to high levels of fat or lipids, this mechanism starts, and that’s how environment plays a role, among large segments of the population bearing ‘normal’ genetic variation. 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.”
According to the university, this research, which was published in the December 27 issue of the journal PLOS ONE, could ultimately lead to the development of new ways to treat, cure, or prevent Type 2 diabetes — a condition which the American Diabetes Association (ADA) says affects more than 8-percent of all Americans.
“Even in the post-genomic era, after the human genome has been sequenced, we’re beginning to realize that diseases aren’t always in our genes — that the environment is playing a major role in many of the common diseases,” Marth said. “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.”
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