Using the same simple description of sickness as it applies to the body as a whole - that when it doesn’t work correctly, it’s sick - researchers at Temple University School of Medicine conclude the fat cells of patients suffering from obesity are, by that definition, sicker than a lean person’s fat cells.  They just don’t quite work right. 

Furthermore, the research team suggests it’s the malfunctioning of these fat cells that forms or strengthens the bond between obesity and increased risk of developing life-threatening, chronic diseases such as cardiovascular disease and diabetes.

Guenther Boden, MD, led the Temple study that involved the university’s biochemistry, endocrinology, and surgery departments.  Boden is a professor of medicine and chief of the university’s endocrinology department.  The team analyzed fat cells taken from the thighs of 12 people, half of whom were obese while the other half was lean.

Describing significant differences on a cellular basis, Boden says the fat cells in the obese study participants were deficient in multiple ways.  The fat tissue itself was more inflamed in the obese fat samples than in the lean fat samples, with a significant degree of stress observed in the endoplasmic reticulum (ER).

A part of every cell, ER helps the cell produce proteins and it determines how those proteins are folded.  Boden’s team identified evidence of stress in the ER of fat cells taken from obese people that affects the production and folding of certain proteins in a way that leads, ultimately, to insulin resistance.  Insulin resistance is an underlying condition thought to play a key role in the development of obesity-related medical diagnoses and it contributes to the progression of these medical conditions as well.

Height and weight are frequently addressed as body mass index (BMI), a measurement the National Institutes of Health (NIH) uses as standard of health.  The larger a person is, the higher his or her BMI.  When BMI climbs higher than 25, each point in increased BMI value indicates an increase of 25% for the risk of developing diabetes and a 10% increase in the risk of developing heart disease.

One way to reduce the amount of stress to the ER is to lose weight.  Losing weight lowers the risk for developing insulin resistance, thereby reducing the risk for developing related conditions, too.

The Boden research team is currently exploring the connection between free fatty acids and ER stress.  Full details of its comparison of the health status of fat cells in obese and lean people are available in the September issue of Diabetes, a publication of the American Diabetes Association, which helped fund the Boden study, along with the Groff Foundation and NIH.

Source: Temple University