Junk-food diets spur inflammation more than saturated fats alone
|June 25, 2012|
A diet based on American junk food could lead to more obesity-induced inflammation than a diet high in animal fat, according to a new study published June 12 in the Public Library of Science One (PLoS ONE).
The study analyzed inflammatory responses in rats fed different diets: control diets, a lard-based high-fat diet and a “cafeteria junk-food” (CAF) diet consisting of nutrient-poor snacks such as salami, chocolate, cookies and chips.
“The diet that consisted of human junk food caused the most inflammation and dramatic metabolic changes,” said Liza Makowski, PhD, assistant professor of nutrition at UNC’s Gillings School of Global Public Health and the study’s senior author.
A CAF diet contains many ingredients associated with increased risk for coronary artery disease, stroke and Type 2 diabetes, including saturated fat, trans-fats, sodium and cholesterol. The diet also is low in protective nutrients such as fiber.
Makowski said that while it has been known for some time that obesity can cause inflammation in fatty tissue, this study is one of the first to show that the CAF diet may cause dramatic alterations in certain metabolites – molecular chemicals created when food is converted to energy.
These alterations, specifically in the metabolite lauroyl carnitine, may be responsible for obesity-induced inflammation and increased insulin resistance.
“We found evidence of diet-induced stress in the tissue,” Makowski said. “Lauroyl carnitine showed that it caused a pro-inflammatory response in white blood cells.”
This pro-inflammatory response could be a major contributing factor to metabolic syndrome, the cluster of factors that increase a person’s risk for coronary artery disease, stroke and Type 2 diabetes. As obesity and disability rates continue to rise in the United States, understanding the hows and whys of fat tissue inflammation is vital.
To understand the mechanism of inflammation in the study, Makowski and colleagues used a biochemical technique called metabolomics to look at many different metabolites at one time. This provides a virtual snapshot of a cell’s biology that helps scientists understand which metabolic pathways went awry.
The CAF diet, while not traditionally utilized in research, may be superior to high-fat diets for modeling modern human obesity trends, including exposure to energy-dense and nutrient-poor diets, early and rapid obesity development, and elevated markers of metabolic syndrome and inflammation.
“Biomarkers revealed in our study could be useful in future studies,” said Makowski. “This needs to be replicated in human studies; it could be highly useful in future diabetes research.”
Study co-authors from UNC are Brante P. Sampey, PhD (formerly a UNC postdoctoral fellow in nutrition, now at Metabolon Inc.); Jimmy Zhang, a UNC undergraduate beginning this fall; Alex J. Freemerman, PhD, nutrition research associate; Pei-Fen Kuan, PhD, research assistant professor of biostatistics; Heather A. Brauer, PhD, postdoctoral research associate in epidemiology; and Melissa A. Troester, PhD, research assistant professor of epidemiology, all from the UNC Gillings School of Global Public Health; and Joseph A. Galanko, PhD, research assistant professor of medicine, in the School of Medicine. Makowski, Kuan and Troester also are affiliated with the UNC Lineberger Comprehensive Cancer Center.
Other co-authors are Thomas M. O’Connell, PhD, senior director of assay research and development at LipoScience Inc., in Raleigh, N.C., formerly a faculty member in UNC’s pharmacy school; and research scientist Olga R. Ilkayeva, PhD, laboratory director Michael J. Muehlbauer, PhD, senior scientist and laboratory technical director Robert D. Stevens, PhD, and center director Christopher B. Newgard, PhD, all of the Sarah W. Stedman Nutrition and Metabolism Center at Duke University Medical Center, in Durham, N.C. Newgard also is a distinguished professor in Duke University Medical Center’s Department of Pharmacology and Cancer Biology.