A new study's findings suggest insulin imbalance may not be the only cause of the onset of diabetes in obese individuals. Researchers of the study have found the liver has the ability to produce a large amount of glucose by an external and not hormonal signal.
Obesity is on the rise and a major risk factor for diabetes. University of Geneva (UNIGE) have found patients with excess liver fat and the overproduction of glucose could cause them to develop type 2 diabetes.
Two antagonistic hormones - insulin and glucagon - are responsible for managing blood sugar levels. One lowers it, while the other increases these levels. The liver also has an important role to play when it comes to regulating blood glucose levels. The liver producing and redistributing glucose depending on the influence of insulin and glucagon. That is why people who are obese are at risk of developing two serious conditions - type 2 diabetes and "fatty liver" syndrome, which is the accumulation of fat in liver cells. When there is an accumulation of lipids it causes changes in the morphology, as well as the structure of mitochondria.
"Do these alterations have an effect on mitochondrial function? Is there a link between liver cell mitochondria, obesity and diabetes? To find out, we focused on a protein called OPA1 which, in its "long" form, in other words its non-degraded form, has the function of maintaining the structure of mitochondria," lead author of the study Pierre Maechler, professor at the Department of Cell Physiology and Metabolism and at the Diabetes Faculty Centre of the UNIGE Faculty of Medicine, told a news portal.
To understand the function of mitochondria, the team inactivated the OPA1 function. "The liver of mice that do not have the long form of OPA1 loses its ability to produce sugar in just a few weeks," first author of the study Lingzi Li, a doctoral student in Professor Maechler's laboratory, told a news portal. Adding, "Liver cell mitochondria then show an altered morphology, confirming their importance in sugar metabolism."
They also reintroduced the functional OPA1 protein for further examination. "And the mitochondria have regained their normal morphology, but not their activity," the authors of the study told a news portal. Adding, "In this area too, shape does not dictate function! It is not enough for mitochondria to appear normal for them to function properly."
However, what they found next was surprising."By observing controls, i.e. healthy mice in which OPA1 had been introduced in its long form, we discovered that, when equipped with these "super-mitochondria," they generated more glucose than necessary, and their liver produced sugar without any hormonal call," Pierre Maechler told a news portal.
This is the first study to observe glucose production by the liver by an external signal. The findings could be explain why patients with "fatty liver" syndrome develop diabetes. Further research is needed to further understand this link.
The study's findings were originally published in the Journal of Biological Chemistry.
Picture Courtesy: Google Images