Scientific Approach

How is Type 2 Diabetes Characterized?

Type 2 diabetes pathophysiology is characterized by a deregulation of the body's metabolic and cellular bioenergetics balances. This is linked to high food supply and low energy demand due to a sedentary lifestyle of diabetic patients and leads to mitochondrial dysfunction.

In diabetes pathophysiology, metabolic misbalance creates a pressure onto the mitochondria, which leads to their dysfunction, overproduction of reactive oxygen species (ROS), reduction of oxidative capacity, and subsequently to the accumulation of lipids in insulin-sensitive tissues and, lastly, to insulin resistance and diabetes.

What's Going on Inside the Body of a Type 2 Diabetes Patient?

Recent scientific investigations support the concept that type 2 diabetes is fundamentally tied to changes in mitochondrial content or oxidative capacity in insulin-sensitive tissues (liver, muscle, adipose tissue) and in the pancreas of insulin-resistant patients. Studies have demonstrated that this oxidation failure and inappropriate lipid storage in the tissues can be correlated with a decline in both insulin sensitivity and metabolic flexibility, due to a defect in insulin signaling.

The Foundation of Our Approach

Therapeutic interventions aiming at restoring the cellular bioenergetics balance are promising approaches to treat type 2 diabetes. We have focused our research strategy onto two targets, both of which are important in the regulation of the cellular bioenergetics:

  • The mitochondria
  • The AMP-activated protein kinase (AMPK)

Our Target: Mitochondria

Mitochondria play an essential role in the pathophysiology of diabetes. They are the power stations of the body's cells, contributing to the regulation of energy balance and metabolism. The principal role of mitochondria is to produce energy in the form of an adenosine tri-phosphate (ATP) molecule by oxidizing nutrients such as glucose and fatty acids from food. In diabetes pathophysiology, metabolic misbalance creates a pressure onto the mitochondria, which leads to their dysfunction, reduction of oxidative capacity, and subsequently to the accumulation of lipids in insulin-sensitive tissues and, lastly, to insulin resistance and diabetes.

Our Target: The AMPK Enzyme

The AMPK enzyme is an energy sensor whose role is to maintain cellular energy homeostasis. Depending on the cellular bioenergetics status, AMPK activation enhances catabolic processes and down-regulates anabolic pathways. In the context of diabetes pathophysiology, AMPK activation leads to fatty acid oxidation, decrease of lipogenesis, decrease of lipid storage, decrease of glucose production, and stimulation of glucose consumption. All these phenomena contribute to hyperglycemia and dyslipidemia regulation, decrease in liver steatosis and finally to insulin sensitivity restoration.