Background:
The National Institute of Diabetes and Digestive Kidney Disease reports 1 in every 3 adults in America are considered to be obese. This is a record number compared to any other country. The mechanism, of which obesity contributes to diabetes and heart failure, is yet to be completely understood. A system of multifunctional organelle, the endoplasmic reticulum poses a significant contribution to diabetes inducing heart failure in humans. A site for protein folding, lipid synthesis, calcium ion homeostasis, and some metabolic functions, these networks of membranous sacs are currently the center topic of discussion. In recent studies, research shows that obesity induces endoplasmic reticulum (ER) stress, which in …show more content…
Where exactly is this stress localized from in the cell? Gökhan S. Hotamisligil and his colleagues from various departments at Harvard University have identified the E.R to be responsible for cellular stress. To gain a deeper understanding of the two intertwined worlds of diabetes and cardiology, a variety of different research techniques were used. First, it was important for scientists to confirm if obesity really did induce E.R. stress. To do this, they used a series of mice. One set of mice had a regular diet (controlled). The second group of mice had a high fat diet. After a period of time, both sets of mice were tested for certain molecular markers known to increase with E.R stress. Among these markers were various forms of: PERK, eIF2α, and c-Jun N-terminal kinase (JNK).
Results:
The first experiment showed exactly what scientists had hypothesizedThrough experimental research with mice, scientists were able to gain a much deeper understanding of these two worlds. Results from the experiment showed