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UC San Francisco researchers have discovered a new biological pathway in fat cells that could explain why some people with obesity are at high risk for metabolic diseases such as type 2 diabetes. The new findings — demonstrated initially in mice and supported by data from human patients — could lead to new biomarkers to predict who is at risk and guide treatments to reduce the medical burden of obesity.
More than one third of adults in the US are considered clinically obese and the number of people with extreme obesity (BMI over 40) has doubled in the past two decades, according to data from the Centers for Disease Control and Prevention (CDC). Obesity has been linked to many dangerous health conditions, including type 2 diabetes. However, recent research has revealed that only a minority of people with obesity are actually at higher risk of diabetes than the general population.
“It turns out that only about 30 percent of people with obesity are really high risk. The problem is that fundamentally we don’t know why some people with obesity go on to develop diabetes and others don’t,” said Suneil Koliwad, MD, PhD, assistant professor in the UCSF Diabetes Center and one of the new study’s two senior authors.
The new findings, published January 9, 2018 in Cell Metabolism, suggest that the link between obesity and diabetes may depend on fat cells’ ability to control adipose fibrosis — an accumulation of collagen in fat tissue that cause it to become stiff and inflexible — which is known to be linked to increased inflammation and metabolic dysfunction.
The research was initiated by the lab of Shingo Kajimura, PhD, an associate professor of cell and tissue biology in UCSF’s School of Dentistry, member of the UCSF Diabetes Center and the paper’s other senior author. Kajimura is known for discovering that human fat cells can shift between two states — …