As obesity continues to grow across the world, better understanding of the disease, treatments, and outcomes becomes increasingly important. Animal models used to study these aspects of obesity have 3 phases: experimental (EXP), caloric restriction (CR), and weight regain (WR). For this study an ad libitum high-fat diet (HFD) was used to induce hyperphagia and weight gain in Sprague-Dawley rats in the experimental period. Rats then transitioned to a chow (CH) diet and energy intake (EI; kcal/day) was reduced 40-60% during the caloric restriction period. In weight regain, rats were given chow ad libitum. This protocol was run 3 times, once every academic school year (2017-2018, 2018-2019, and 2019-2020). Sample sizes listed in the order of high fat (HF) rats then chow (CH) rats for each year were as follows: 2017-2018 (n=11, n=8), 2018-2019 (n=12, n=8), 2019-2020 (n=14, n=10). Analysis of energy intake was performed on the first week of the experimental phase and the first week of the weight regain phase. <br/><br/>HF EXP rats showed hyperphagic average daily EIs compared to CH EXP rats for all 3 years (p<0.01-0.0001). HF WR rats were similar to CH WR rats in all applicable years in terms of average daily EI. However, both HF WR and CH WR rats were hyperphagic. HFD caused hyperphagia to be highest at the beginning of the first week of EXP and then EI decreased significantly as days went by. However, in WR, hyperphagia (HF WR and CH WR) was flat throughout the week. Obesity prone (OP) rats during EXP had similar EI behavior to obesity resistant (OR) rats during EXP within the same year. During WR though, OP rats had significantly greater average daily EI (p<0.05-0.001) compared to WR OR rats within the same year for 2 out of the 3 years. <br/><br/>These results suggest that HFD induces hyperphagia during weight gain. In weight regain, where HFD is absent, HF rats and CH rats are both hyperphagic. This suggests that WR induces hyperphagia in both rat groups. WR also induces a greater increase in EI for OP rats compared to OR rats. Therefore, hyperphagia seems to be driven by 2 mechanisms (HFD and WR). The profiles of the responses are different however. HFD induces hyperphagia that decreases over the first week and the level of hyperphagia is similar between OP and OR rats. WR induces hyperphagia that remains stable in the first week and is more pronounced in OP rats compared to OR rats.

Excessive weight gain, otherwise known as obesity, has become a pervasive medical condition throughout the world. Though caloric restriction (CR) results in weight reduction, this weight loss is often unsustainable in the long term. As such, the goal is to find a treatment that can maintain the results of restricted energy intake (EI). Studies have found that dietary menthol could be a possible treatment and preventative measure for excessive weight gain. While several studies have found that, as an agonist of TRPM8, dietary menthol increases the energy expenditure (EE) of the body without impacting EI, they have not studied the efficacy of dietary menthol in preventing weight regain (WR) following a period of CR. Methods used in this experiment include studying young Sprague-Dawley rats during 24-hour periods towards the end of the following three phases: (1) an experimental phase of 12 weeks, comprised of ad-libitum feeding of high fat diet (HFD) to 10 rats and chow diet to 4 rats, (2) a CR phase of 4-weeks with controlled feeding of the HFD rats with either a chow diet (n=4) or chow diet + 0.5% dietary menthol (n=6) and keeping the other rats on chow (n=4), and (3) a WR period of 4-weeks with ad libitum feeding of the same diets as in CR. EI and EE (via indirect calorimetry) were measured over 24-hour periods and were divided by the rat’s respective body weight (BW) on testing day to normalize the sample population. The energy gap (EG) was determined by subtracting EE from EI. The experimental and WR phase revealed a positive EG or energy balance (EI > EE) whereas CR yielded a negative EG or energy balance (EI