Johanna Klement1, Britta Kubera2, Jonas Eggeling2, Christin Rädel2, Christin Wagner2, Soyoung Q Park3, Achim Peters2. 1. Department of Internal Medicine 1, University of Lübeck, Lübeck, Germany. Electronic address: johanna.klement@uksh.de. 2. Department of Internal Medicine 1, University of Lübeck, Lübeck, Germany. 3. Department of Psychology, Social Psychology & Decision Neuroscience, University of Lübeck, Lübeck, Germany.
Abstract
BACKGROUND:Delay discounting as a measure of impulsivity has been shown to be higher in obesity with an association of increased food intake. Moreover, obese humans showed a higher wanting for high-calorie food than lean men when blood glucose concentrations were low. First studies linking blood glucose levels to delay discounting yielded mixed results. We hypothesized that obese people - in comparison to lean men - have a relative lack of energy, especially when blood glucose levels are low, that results in higher levels of delay discounting, food intake and hormonal counterregulation. METHODS: We investigated 20 lean and 20 obese healthy young men in a single-blind balanced cross-over design. With a standardized glucose clamp technique, subjects underwent a hypoglycemic state in one condition and a euglycemic state in the control condition. Regularly, blood was sampled for assessment of hormonal status, and questionnaires were filled out to assess delay discounting and symptom awareness. After normalizing blood glucose concentrations, subjects were free to eat from a standardized test buffet, followed by a snack test. RESULTS:Delay discounting was higher in obese than in lean men throughout experiments (p < 0.03). However, we did not observe significant discounting differences between glucose conditions (p > 0.1). Furthermore, the discounting performance did not correlate with food intake from the test buffet or snack test (p > 0.3). As a response to hypoglycemia, hormonal counterregulation was pronounced in both weight groups (p < 0.03), but responses of ACTH, norepinephrine and glucagon were stronger in obese compared to lean men (p < 0.03). Also, intake from the high-calorie buffet after hypoglycemia compared to euglycemia was higher in obese subjects (p < 0.02) but comparable in lean men (p > 0.5). CONCLUSIONS: Our data suggest that augmented delay discounting is a robust feature in obesity that is not linked to glucose levels or actual food intake. With our systematically controlled approach, combining performance in delay discounting with regard to distinct blood glucose levels, different weight groups, counterregulatory behavior and food intake, our results imply that delay discounting is not susceptible to fluctuations of blood glucose and do not support the assumption that a low body's energy content leads to increased impulsivity. Further replications including women and larger sample sizes are needed to corroborate our data.
RCT Entities:
BACKGROUND: Delay discounting as a measure of impulsivity has been shown to be higher in obesity with an association of increased food intake. Moreover, obesehumans showed a higher wanting for high-calorie food than lean men when blood glucose concentrations were low. First studies linking blood glucose levels to delay discounting yielded mixed results. We hypothesized that obesepeople - in comparison to lean men - have a relative lack of energy, especially when blood glucose levels are low, that results in higher levels of delay discounting, food intake and hormonal counterregulation. METHODS: We investigated 20 lean and 20 obese healthy young men in a single-blind balanced cross-over design. With a standardized glucose clamp technique, subjects underwent a hypoglycemic state in one condition and a euglycemic state in the control condition. Regularly, blood was sampled for assessment of hormonal status, and questionnaires were filled out to assess delay discounting and symptom awareness. After normalizing blood glucose concentrations, subjects were free to eat from a standardized test buffet, followed by a snack test. RESULTS: Delay discounting was higher in obese than in lean men throughout experiments (p < 0.03). However, we did not observe significant discounting differences between glucose conditions (p > 0.1). Furthermore, the discounting performance did not correlate with food intake from the test buffet or snack test (p > 0.3). As a response to hypoglycemia, hormonal counterregulation was pronounced in both weight groups (p < 0.03), but responses of ACTH, norepinephrine and glucagon were stronger in obese compared to lean men (p < 0.03). Also, intake from the high-calorie buffet after hypoglycemia compared to euglycemia was higher in obese subjects (p < 0.02) but comparable in lean men (p > 0.5). CONCLUSIONS: Our data suggest that augmented delay discounting is a robust feature in obesity that is not linked to glucose levels or actual food intake. With our systematically controlled approach, combining performance in delay discounting with regard to distinct blood glucose levels, different weight groups, counterregulatory behavior and food intake, our results imply that delay discounting is not susceptible to fluctuations of blood glucose and do not support the assumption that a low body's energy content leads to increased impulsivity. Further replications including women and larger sample sizes are needed to corroborate our data.
Authors: Martin H Lundqvist; Kristina Almby; Urban Wiklund; Niclas Abrahamsson; Prasad G Kamble; Maria J Pereira; Jan W Eriksson Journal: Diabetologia Date: 2020-11-26 Impact factor: 10.122