The study, titled “Resting Metabolic Rate, Abdominal Fat Pad and Liver Metabolic Gene Expression in Female Rats Provided a Snacking Diet from Weaning to Adulthood,” was published in the Physiology & Behavior journal.

Carissa and other professionals are worried about the prevalence of obesity that continues to increase in the United States. “More than one-third of Americans and nearly one in five children are obese. Nearly 80% of obese children become obese adults.” Not only is obesity a public health concern, but it can also lead to long-term illnesses.

The study’s main objective was to determine some of the consequences snacking has on childhood obesity. Researchers investigated whether resting metabolic rate (RMR), the calories your body burns on a normal day at rest, alters in response to a snacking diet. “In previous studies, our lab has shown that snacking from weaning to adulthood in female rats causes weight gain, increased stomach fat, and other signs of metabolic syndrome, including high blood pressure and high blood sugar,” said Carissa. “These effects were seen in an absence of increased caloric intake, suggesting that snacking may change how energy is stored and used.”

The study proposed that a decrease in RMR in snacking rats might account for changes in energy storage. Researchers also looked at changes in genes relating to carbohydrate and lipid metabolism, which involves the synthesis of structural and functional lipids, such as those used in the formation of cell membranes, as well as the breakdown or storage of fats for energy.

In order to sustain a comparable mean body weight across the two diet groups, the rats for this study were randomly assigned to one of two groups, having 8 per group. The Control group received normal rat food ad libitum, or as desired. The Snacking group received snacks ad libitum that were high in fats, sugar, or both (e.g., Tostitos tortilla chips, Keebler’s Sandies and Reese’s peanut butter chips), in addition to normal rat food. Whenever a new snack was given, the previous snack was removed, and its intake was recorded as the difference between the amount given and the amount removed at the next snack feeding.

RMR was determined for both groups every two weeks by using metabolic chambers (where fresh air circulates into the room and as it leaves the room, it passes through a number of analyzers to determine the amount of carbon dioxide and oxygen present). “Stomach fat pads and liver tissues were collected at termination for gene expression analysis,” explained Carissa.

The results established that snacking causes a change in energy storage in female rats, as the snacking rats gain weight and deposit excess stomach fat with no increase in caloric intake. “However, our outcome of interest, RMR, was not significant, as it was not different between the snacking and control rats at any point in time,” said Carissa. “Rather, analysis of gene expression data showed a difference between metabolic outcomes in control and snacking rats in stomach fat pads and liver.”

Typically, there is excess carbohydrate storage (enhanced lipogenesis) in stomach fat, as well as excess fat storage (adipogenesis) in the liver. “Therefore, in our snacking rat model, it is constant energy intake, rather than excess energy intake, of snacks high in carbohydrates and fats that causes excess weight gain, excess abdominal fat storage, and signs of metabolic syndrome. Some of the effects of metabolic syndrome may be irreversible if not treated early,” explained Carissa.

Given that their model mimics human feeding behavior, researchers involved predict that a diet that includes continuous access to snacks would result in similar metabolic changes in humans.

Written by Deycha Torres Hernández

Published on September 27, 2022