Obese people are prone to a range of ailments owing to their physical condition. But the nexus between obesity and type 2 diabetes is of particular relevance in the American society. The gravity of the situation can be understood from the fact that government had to declare these two disorders as national epidemics last year 2009. This article tries to understand what scientific research has to say on the relation between obesity and insulin resistance.
What is Insulin Resistance?
We get energy from the food we eat. Insulin is the carrier of glucose or energy of our body to the building blocks of life, cells. The cells use this energy for carrying out vital functions in our body and store some of the energy as fat for later use.
In type 2 diabetes patients, the cells which produce insulin (the beta cells) are targeted by cells of the immune system. It is the natural protection system of our body. Why cells of our own body turn hostile and attack the beta cells is unclear. This makes diabetes an auto-immune disorder.
The consequence is the insulin produced by these impaired beta cells being less effective in its basic task. It cannot inhibit the rise of glucose levels as the body itself refuses to recognize this hormone. This undesirable condition is insulin resistance.
How Obese People are Prone to Insulin Resistance (IR)?
Researchers from the Salt Institute for Biological Studies discovered the relation between obesity and IR last year. The results of their findings were published in the online edition of the journal Nature in June 2009. The study was funded by the National Institutes of Health.
They found that a process called ER (endoplasmic reticulum) stress is overly active in obese people leading to IR. ER stress is caused by consumption of high fat diet.
Whenever the body is in short of energy, the liver initiates excess production of glucose. This process is called gluconeogenesis. The ER is the protein factory inside the cells. When gluconeogenesis is underway, protein production is stopped for a while. This situation is called ER stress.
But in obese people, both the processes are abnormally active. This leads to uncontrolled production of glucose once the process begins.
Mechanism of Abnormal Gluconeogenesis in Obese People:
Cells follow chemical instructions called genes to carry out their routine functions. The genes get activated when they receive appropriate signals from what are known as the signaling molecules. Two molecules CRTC2 and CREB, instruct the genes for glucose production.
The molecule CRTC2 is generally present outside a cell. On receiving appropriate signal, it enters inside the cell and binds with CREB. This development instructs the genes to initiate glucose production.
Research carried out on experimental mice suffering from insulin resistance has revealed that in these mice, CRTC2 remains stuck in the “ON” state, and this is how abnormal gluconeogenesis takes place. The findings can be extended on humans too.
In this way, abnormality in ER stress and gluconeogenesis processes, cause obese people be at higher risks of developing insulin resistance (or type 2 diabetes).
