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.

Obesity has reached epidemic proportions all around the world, and it has doubled in prevalence in both adults and children in over 70 countries from 1980 to 2015 (Afshin et al., 2017). Excessive weight gain in this proportion has been shown to negatively affect human cognition, reward neurocircuitry, stress responsiveness, and quality of life (Morris et al., 2015). Obesity is an example of a complex interaction between the environment (i.e., high-fat diets) and heredity (i.e., polygenic patterns of inheritance). The overconsumption of a high-fat diet (HFD) is an environmental factor that commonly induces weight gain (Hariri & Thibault, 2010). Two dietary-induced phenotypes have been observed in rats as a bimodal distribution of weight gain: obesity-prone (OP) and obesity-resistant (OR). Levin et al. (1997) investigated male and female HFD-fed Sprague-Dawley rats designated as OR when their weight gains were less than the heaviest chow-fed controls, and OP when their weight gains were greater than the heaviest chow-fed controls. OP rats showed greater weight gain, similar energy intake (EI), and similar feed efficiency (FE) compared to OR rats. Pagliassotti et al. (1997) designated male HFD-fed Wistar rats as OP and OR based on upper and lower tertiles of weight gain. OP rats displayed greater weight gain and EI than OR rats. These investigations highlight a predicament regarding rodent research in obesity: independent variables such as rat age, gender, strain, distribution of dietary macronutrients, and fatty acid composition of HFD and chow vary considerably, making it challenging to generalize data. Our experiment utilized outbred male Sprague-Dawley rats (5-6 weeks) administered a chow diet (19% energy from fat; 3.1 kcal/g) and a lard-based HFD (60% energy from fat; 5.24 kcal/g) over eight weeks. Separate rat populations were examined over three consecutive years (2017-2020), and independent obesogenic environmental variables were controlled. We investigated the persistence of weight gain, EI, and FE in HFD-fed rats inclusive of a population of designated OP and OR rats based on tertiles of weight gain. We define persistence as being p > 0.05. We hypothesize that the profiles (periodic data) of the dependent variables (weight gain, EI, FE) will be similar and persistent throughout the three separate years, but the magnitudes (cumulative data) of the dependent variables will differ. Our findings demonstrate that HFD, OP, and OR groups were persistent for periodic and cumulative weight gain, along with FE across the three consecutive independent years. Our findings also demonstrate impersistence for periodic EI in all groups, along with impersistence in cumulative EI for CHOW, OP, and OR groups. Therefore, our results allude to an inconsistent relationship between EI and weight gain, indicating that EI does not completely explain weight gain. Thus, the weakness between EI and weight gain relationship may be attributed to a polygenic pattern of inheritance, possibly signaling a weight setpoint regardless of EI.

Obesity has reached epidemic proportions all around the world, and it has doubled in prevalence in both adults and children in over 70 countries from 1980 to 2015 (Afshin et al., 2017). Excessive weight gain in this proportion has been shown to negatively affect human cognition, reward neurocircuitry, stress responsiveness, and quality of life (Morris et al., 2015). Obesity is an example of a complex interaction between the environment (i.e., high fat diets) and heredity (i.e., polygenic patterns of inheritance). The overconsumption of a high-fat diet (HFD) is an environmental factor that commonly induces weight gain (Hariri & Thibault, 2010). Two dietary-induced phenotypes have been observed in rats as a bimodal distribution of weight gain: obesity-prone (OP) and obesity-resistant (OR). Levin et al. (1997) investigated male and female HFD-fed Sprague-Dawley rats designated as OR when their weight gains were less than the heaviest chow-fed controls, and OP when their weight gains were greater than the heaviest chow-fed controls. OP rats showed greater weight gain, similar energy intake (EI), and similar feed efficiency (FE) compared to OR rats. Pagliassotti et al. (1997) designated male HFD-fed Wistar rats as OP and OR based on upper and lower tertiles of weight gain. OP rats displayed greater weight gain and EI than OR rats. These investigations highlight a predicament regarding rodent research in obesity: independent variables such as rat age, gender, strain, distribution of dietary macronutrients, and fatty acid composition of HFD and chow vary considerably, making it challenging to generalize data. Our experiment utilized outbred male Sprague-Dawley rats (5-6 weeks) administered a chow diet (19% energy from fat; 3.1 kcal/g) and a lard-based HFD (60% energy from fat; 5.24 kcal/g) over eight weeks. Separate rat populations were examined over three consecutive years (2017-2020), and independent obesogenic environmental variables were controlled. We investigated the persistence of weight gain, EI, and FE in HFD-fed rats inclusive of a population of designated OP and OR rats based on tertiles of weight gain. We define persistence as being p > 0.05. We hypothesize that the profiles (periodic data) of the dependent variables (weight gain, EI, FE) will be similar and persistent throughout the three separate years, but the magnitudes (cumulative data) of the dependent variables will differ. Our findings demonstrate that HFD, OP, and OR groups were persistent for periodic and cumulative weight gain, along with FE across the three consecutive independent years. Our findings also demonstrate impersistence for periodic EI in all groups, along with impersistence in cumulative EI for CHOW, OP, and OR groups. Therefore, our results allude to an inconsistent relationship between EI and weight gain, indicating that EI does not completely explain weight gain. Thus, the weakness between EI and weight gain relationship may be attributed to a polygenic pattern of inheritance, possibly signaling a weight setpoint regardless of EI.