A Recent Discovery: Age-Related Diabetes

Posted by Jane Farrell

Diabetes is often the result of obesity and poor diet choices, but for some older adults the disease might simply be a consequence of aging. Researchers at the Salk Institute for Biological Science in La Jolla, California have discovered that diabetes — or insulin resistance –I n aged, lean mice has a different cellular cause than the diabetes that results from weight gain (type 2). The findings point toward a possible cure for what the co-leading scientists, Ronald Evans and Ye Zheng, are now calling a new kind of diabetes (type 4). The paper was published November 18th 2015 in Nature.

A release from the institute quotes senior author Evans, director of Salk’s Gene Expression Laboratory, as saying, “A lot of diabetes in the elderly goes undiagnosed because they don’t have the classical risk factors for type 2 diabetes, such as obesity. We hope our discovery not only leads to therapeutics, but to an increased recognition of type 4 diabetes as a distinct disease.”

The release explains that in healthy people, the pancreas produces the hormone insulin, which signals to cells to take sugar out of the blood after a meal. In people with diabetes, however, the cycle is broken: either insulin is not produced in response to a meal or the muscle and liver cells don’t respond to the insulin (also known as insulin resistance). In either case, sugar stays in the bloodstream for longer times, leading to a host of health issues ranging from loss of limbs to death.

Traditionally, diabetes has been grouped into the rarer type 1 disease, which most often appears in childhood when the pancreas stops producing insulin; and type 2, which is characterized by the body’s failure to respond to insulin and most often attributed to being overweight. Both forms of the disease lead to high blood sugar levels. A third type of diabetes results in symptoms mimicking Alzheimer’s. But Evans–after a thin, older family friend developed diabetes–wondered why some people developed the disease later in life without weight gain.

Evans, along with Zheng, an assistant professor in Salk’s Nomis Foundation Laboratories for Immunobiology and Microbial Pathogenesis, and colleagues, set out to compare the immune systems of healthy mice, those with obesity-related diabetes and those with age-related diabetes. The mice with age-related disease, they found, had abnormally high levels of immune cells called T regulatory cells (Tregs) inside their fat tissue. Mice with obesity-related diabetes, on the other hand, had normal levels of Tregs within the tissue, despite having more fat tissue.

“We created a census of immune cells in the fat of these mice,” says Sagar Bapat, a graduate student in the Evans and Zheng labs and first author of the new paper. “Simply by counting cell types, we immediately saw that there were more Tregs in the older mice with diabetes than any other group.”

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