Study finds inadequacies in insulin production lead to obesity

Obesity increases the chance of a sugar metabolism imbalance and potentially diabetes. A study group at the University of Basel has recently demonstrated that the contrary is also true: inadequacies in the body’s insulin production contribute to obesity.

Poor nutrition, too little movement and too many pounds on the scale — lifestyle influences the risk of metabolic diseases like diabetes. But the relationship works the other way round as well, as a research group led by Dr. Daniel Zeman-Meier of the university’s Department of Biomedicine and the University Hospital of Basel reports. If insulin production is compromised, as is the case in the early stages of type 2 diabetes, this can contribute to overweight. The findings of the study were published in the journal Nature Communications.
When hormone activation goes awry

The research team focused on protease PC1/3, a key enzyme in the body that transforms various inactive hormone precursors into the final, active forms. If this enzyme isn’t functioning properly in a person, the result can be severe endocrine disorders. The consequences include a feeling of uncontrollable hunger and severe overweight.

“Until now, it was assumed that this dysregulation is caused by a lack of activation of satiety hormones,” explains the study’s leader, Dr. Zeman-Meier. “But when we turned off PC1/3 in the brains of mice, the animals’ body weight did not change significantly.” The researchers concluded from this that something other than a brain malfunction must be responsible.
Incorrect activation of insulin leads to hunger and overweight

In their next step, they tested whether overweight could be caused by incorrect activation of other hormones. PC1/3 activates insulin, among other things. Insulin plays a key role in the regulation of blood sugar and fat metabolism. “Investigating the role of insulin production as a cause of overweight was obvious,” says Dr. Zeman-Meier. The researchers shut off PC1/3 specifically in the insulin-producing beta cells of the pancreas in mice. The animals consumed significantly more calories and soon became overweight and diabetic.
An important mechanism in humans