The Influence of Heat on Appetite Regulating Hormones
Advisor Information
Dustin Slivka
Location
MBSC 201
Presentation Type
Poster
Start Date
6-3-2020 2:00 PM
End Date
6-3-2020 3:15 PM
Abstract
Leptin has been established as an energy-controlling hormone because of its role in activating the JAK-STAT3 pathway. Exercising in the heat (1-hour of cycling @60% VO2max in 33°C) has also induced reductions in leptin. However, in order to better understand the influence of environmental temperature, independent of exercise, a fasted resting investigation is needed. This investigation explored the impact of environmental temperature (33 vs. 20°C) on adipose-derived appetite-regulating hormones (leptin and adiponectin) and energy expenditure. Ten college-aged males (27±5y, 86±13kg, and 183±4cm) completed two randomized, resting trials in the Heat (HT, 33°C) and in Room Temperature (RT, 20°C). Blood draws were taken pre-intervention and 3 hr post-intervention for analysis of leptin and adiponectin. Oxygen consumption was measured at 1-, 2-, and 3-hr timepoints. HT trial temperatures were greater than RT for core (37.17±0.08 vs. 36.89±0.08°C, p=0.002) and skin (37.59±0.10 vs. 32.65±0.48°C; pnd (4.37±0.14 vs. 4.13±0.15 ml/kg/min, p=0.037) and 3rd (4.95±0.26 vs. 4.28±0.19 ml/kg/min, p=0.002) hours in RT. Fasting leptin concentrations in RT decreased to a greater extent than in HT (mean Δ±SEM; -2.05±0.83 vs. -0.89±0.74 ng/ml; p=0.032); however, after adjustment for plasma volume shifts (-7.5±4.2%) the interaction disappeared (mean Δ±SEM; -1.79±1.72 vs. -0.89±0.74 ng/ml; p=0.068). The addition of heat stress increased energy expenditure and attenuated the leptin reduction. These data may have implications for appetite control and weight management.
The Influence of Heat on Appetite Regulating Hormones
MBSC 201
Leptin has been established as an energy-controlling hormone because of its role in activating the JAK-STAT3 pathway. Exercising in the heat (1-hour of cycling @60% VO2max in 33°C) has also induced reductions in leptin. However, in order to better understand the influence of environmental temperature, independent of exercise, a fasted resting investigation is needed. This investigation explored the impact of environmental temperature (33 vs. 20°C) on adipose-derived appetite-regulating hormones (leptin and adiponectin) and energy expenditure. Ten college-aged males (27±5y, 86±13kg, and 183±4cm) completed two randomized, resting trials in the Heat (HT, 33°C) and in Room Temperature (RT, 20°C). Blood draws were taken pre-intervention and 3 hr post-intervention for analysis of leptin and adiponectin. Oxygen consumption was measured at 1-, 2-, and 3-hr timepoints. HT trial temperatures were greater than RT for core (37.17±0.08 vs. 36.89±0.08°C, p=0.002) and skin (37.59±0.10 vs. 32.65±0.48°C; pnd (4.37±0.14 vs. 4.13±0.15 ml/kg/min, p=0.037) and 3rd (4.95±0.26 vs. 4.28±0.19 ml/kg/min, p=0.002) hours in RT. Fasting leptin concentrations in RT decreased to a greater extent than in HT (mean Δ±SEM; -2.05±0.83 vs. -0.89±0.74 ng/ml; p=0.032); however, after adjustment for plasma volume shifts (-7.5±4.2%) the interaction disappeared (mean Δ±SEM; -1.79±1.72 vs. -0.89±0.74 ng/ml; p=0.068). The addition of heat stress increased energy expenditure and attenuated the leptin reduction. These data may have implications for appetite control and weight management.