Obesity Strongly Linked to Insulin Processing

Obesity, itself thought to be a major cause of insulin resistance, in fact appears to result from distinct insulin processing as well. A recent study has concluded that differences in insulin processing within cells are responsible for variations in how fat is stored within these cells, potentially leading to obesity.

This study conflicts with past research that has suggested “fat genes,” hereditary cells that store excessive amounts of fat, are greatly responsible for obesity. The current finding, that when insulin is processed within a cell faster, more fat is subsequently stored, suggests that the genetic links of obesity are less than previously imagined. Says researcher Dr. Thuc T. Le, “this work supports an emerging viewpoint that not all biological information in cells is encoded in the genetic blueprint.”

The researchers observed that fat storage could vary in genetically identical cells, if these cells had varying insulin mechanisms. More specifically, variations in “insulin-signaling pathways,” which are responsible for processing glucose from blood, appeared to be responsible for varying levels of fat storage.

A series of complex single cell profiles were preformed, which enabled the comparison of individual cells to each other. This form of analysis allows detailed measurements to be taken, such as insulin signaling and “gene expressions,” within individual cells. “By profiling multiple events in single cells, we found that variability in fat storage is due to varied rates of insulin processing among cells,” explains lead researcher Dr. Ji-Xen Cheng.

This study is a first step in a potentially new understanding of a major cause of obesity, and perhaps type 2 diabetes as well. More than one-third of Americans are obese, so these findings, if supported and developed further, through future research, could have profound implications for many individuals. Stresses Dr. Cheng, “Insights from our study also will be important for understanding the precise roles of insulin in obesity or Type II diabetes, and to the design of effective intervention strategies.”

Source: Defeat Diabetes Foundation: Cheng, Ji-Xen. Le, Thuc. Venere, Emil. Purdue University news release. April 2009.