Junk food inflames fatty tissue more than lard

UNC-CHAPEL HILL (US) — A diet based on US junk food may result in more obesity-induced inflammation than a diet high in animal fat, according to a new study.

The study analyzed inflammatory responses in rats fed different diets: control diets, a lard-based high-fat diet, and a “cafeteria junk-food” 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,” says Liza Makowski, assistant professor of nutrition at the University of North Carolina Gillings School of Global Public Health and the study’s senior author.

A junk-food 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.

While it has been known for some time that obesity can cause inflammation in fatty tissue, Makowski says, this study is one of the first to show that a junk-food diet may cause dramatic alterations in certain metabolites—molecular chemicals created when food is converted to energy.

These alterations may be responsible for obesity-induced inflammation and increased insulin resistance and 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.

The junk-food diet used in the study 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,” says Makowski. “This needs to be replicated in human studies; it could be highly useful in future diabetes research.”

Researchers from Duke University contributed to the study, which is published in PLoS ONE.

The study was funded by grants from the National Institutes of Health, Lineberger Comprehensive Cancer Center University Cancer Research Funds, and a Freedom to Discover Award from Bristol Meyers Squibb.

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