Obesity and Diabetes

Weight is likely the most essential factor in the advancement of insulin obstruction; however, science's comprehension of the chain of occasions is as yet spotty. Now researchers have developed possible outcomes for obesity sets the stage for diabetes and why thin people can become insulin-resistant. ER (endoplasmic reticulum) stress is the condition which is induced by a high-fat diet and is overly activated in obese people, triggers aberrant glucose production in the liver, an important step on the path for insulin resistance.

In healthy people, a fasting switch possibly flips on glucose production when blood glucose levels run low during fasting. The existence of a second cellular cascade signalling—like an alternate route from A to B—that can modulate glucose production, shows the potential to distinguish new classes of medications that that may bring down glucose by disrupting this alternative pathway. It had been well established that obesity promotes insulin resistance through the inappropriate inactivation of a process called gluconeogenesis, where the liver creates glucose for fuel and which usually happens just during fasting. 

At the point when a cell begins to sense stress a red light goes on, which slows down the generation of proteins. This procedure, which is known as ER stress response, is abnormally active in livers of obese individuals, where it contributes to the development of high blood glucose levels or hyperglycemia. We asked whether chronic endoplasmic reticulum stress in obesity leads to abnormal activation of the fasting switch that usually controls glucose production in the liver. The endoplasmic reticulum, short for endoplasmic reticulum, is a protein factory within the cell. Endoplasmic reticulum stress can induce gluconeogenesis in lean mice. Glucose production is turned on by a transcriptional switch called CRTC2, which typically sits outside the nucleus waiting for the signal that allows it to slip inside and do its work. Once in the nucleus, it collaborates with a protein called CREB and together they switch on the genes necessary to increase glucose output. In insulin-resistant mice, however, the CRTC2 switch seems to get stuck in the "on" position and the cells begin producing glucose like sugar factories in overdrive.  

Contact details:
Alina Grace
Program Manager | Obesity Middle East 2019
Mail Id: obesityendo@mehealthevents.org