Background The question of whether there is daytime time variation in diet-induced thermogenesis (DIT) has not been clearly answered. Moreover, it is unclear whether a potential diurnal variation in DIT is preserved during hypocaloric nutrition. Objective We hypothesized that DIT varies depending on the time of day and explored whether this physiological regulation is preserved after low-calorie compared with high-calorie intake. Design Under blinded conditions, 16 normal-weight men twice underwent a 3-day in-laboratory, randomized, crossover study. Volunteers consumed a predetermined low-calorie breakfast (11% of individual daily kilocalorie requirement) and high-calorie dinner (69%) in one condition and vice versa in the other. DIT was measured by indirect calorimetry, parameters of glucose metabolism were determined, and hunger and appetite for sweets were rated on a scale. Results Identical calorie consumption led to a 2.5-times higher DIT increase in the morning than in the evening after high-calorie and low-calorie meals (P < .001). The food-induced increase of blood glucose and insulin concentrations was diminished after breakfast compared with dinner (P < .001). Low-calorie breakfast increased feelings of hunger (P < .001), specifically appetite for sweets (P = .007), in the course of the day. Conclusions DIT is clearly higher in the morning than in the evening, irrespective of the consumed calorie amount; that is, this physiological rhythmicity is preserved during hypocaloric nutrition. Extensive breakfasting should therefore be preferred over large dinner meals to prevent obesity and high blood glucose peaks even under conditions of a hypocaloric diet.
A special characteristic of the brain is the usage of lactate as alternative fuel instead of glucose to preserve its energy homeostasis. This physiological function is valid for sufficient cerebral glucose supply, as well as presumably during hypoglycemia, given that exogenous lactate infusion suppresses hormonal counterregulation. However, it is not yet clarified whether this effect is mediated by the use of lactate as an alternative cerebral energy substrate or any other mechanism. We hypothesized that under conditions of limited access to glucose (ie, during experimental hypoglycemia) lactate infusion would prevent hypoglycemia‐induced neuroenergetic deficits in a neuroprotective way. In a randomized, double‐blind, crossover study, lactate vs placebo infusion was compared during hyperinsulinemic‐hypoglycemic clamps in 16 healthy young men. We measured the cerebral high‐energy phosphate content — ie, adenosine triphosphate (ATP), phosphocreatine (PCr) and inorganic phosphate (Pi) levels — by 31P‐magnetic resonance spectroscopy as well as the neuroendocrine stress response. During euglycemia, lactate infusion increased ATP/Pi as well as PCr/Pi ratios compared with baseline values and placebo infusion. During hypoglycemia, there were no differences between the lactate and the placebo condition in both ratios. Hormonal counterregulation was significantly diminished upon lactate infusion. Our data demonstrate an elevated cerebral high‐energy phosphate content upon lactate infusion during euglycemia, whereas there was no such effect during experimental hypoglycemia. Nevertheless, lactate infusion suppressed hypoglycemic hormonal counterregulation. Lactate thus adds to cerebral energy provision during euglycemia and may contribute to an increase in ATP reserves, which in turn protects the brain against neuroglucopenia under recurrent hypopglycemic conditions, eg, in diabetic patients.
Purpose Satiety is a crucial factor in the attempt to reduce food intake for long-term body weight loss. Since there is evidence for a negative correlation between cerebral energy levels and food intake, the provision of the primary energy substrate glucose to the brain through oral ingestion of carbohydrates could trigger feelings of satiety. Therefore, we hypothesized that a low-calorie saccharide preload would increase satiety, reduce subsequent food intake, and thereby decrease overall calorie consumption. Methods In a randomized single-blind crossover study, 17 healthy young normal-weight men received saccharide (26 kcal in total) or placebo capsules 30 min before a standardized breakfast buffet. We analysed food intake from the test buffet as well as plasma glucose and serum insulin levels. Results The saccharide preload reduced food intake from the buffet by 168 (± 34) kcal (p < 0.001) compared to control. This corresponds to a net reduction in total calorie consumption by 142 (± 34) kcal (p < 0.001) or 9.3% due to saccharide capsules. Conclusion A very low-calorie saccharide preload considerably reduces subsequent food intake leading to decreased overall calorie consumption. A saccharide preload before meals could, therefore, be a promising support for reducing caloric intake. German Clinical Trials Register DRKS00010281 (date of registration: 11.04.2016)
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