Biology subjects

Koletzko, B.

Publications and source records attributed to Koletzko, B..

3 recordsLinked to original sources

bioRxiv2026

Neuro-metabolic pathways of high-protein meal reducing food craving

Across species, high-protein foods have been shown to reduce appetite throughout the day. Although higher protein intake alters multiple metabolic responses, the exact neuro-metabolic mechanisms underlying food craving remain unclear. Here, we investigated whether a protein-rich diet modulates plasma tyrosine dynamics, the precursor of dopamine, thereby altering dopaminergic brain activity and reducing food craving in humans. In this within-subject, cross-over study, 30 healthy participants (age, Mean=23.63, SD=3.23 years) were provided with either a high- or low-protein/carbohydrate breakfast. Three and a half hours after breakfast, participants viewed high-or low caloric food images while undergoing magnetic resonance imaging (MRI), and their subjective food craving was assessed using the validated Food Craving Questionnaire- State version. Through the experimental procedure, plasma tyrosine levels were continuously monitored. Our results show that the high-protein/carbohydrate breakfast significantly enhanced plasma tyrosine levels, which were negatively associated with subjective food craving several hours after meal intake. Importantly, we observed significantly stronger midbrain activity following the high-protein/carbohydrate breakfast, which was associated with greater reduction in subjective food craving. Furthermore, we analyzed brain gradients that characterize spatial patterns of large-scale neural activity, allowing us to examine the entire process underlying dietary choices at the whole-brain level. Compared with the low-protein/carbohydrate breakfast, the high-protein/carbohydrate breakfast reduced whole-brain functional reorganization, indicating lower neural sensitivity to high- versus low-caloric food stimuli. Notably, the degree of this high-protein/carbohydrate induced brain-state shift was related to the reduction in food craving. Together, these results provide strong evidence that high-protein/carbohydrate meals modulate dopaminergic mechanisms and large-scale whole-brain neural reorganization, contributing to reduced food craving throughout the day in humans.

neuroscience↗

bioRxiv2021

The epoxyeicosatrienoic pathway is intact in endothelial and smooth muscle cells exposed to aldosterone excess

ObjectivesEndothelial dysfunction (ED) is considered to be a major driver of the increased incidence of cardiovascular disease in primary aldosteronism (PA). Whether the epoxyeicosatrienoic acid (EET) pathway, involving the release of beneficial endothelium-derived lipid mediators, contributes to ED in PA is unknown. Preclinical evidence suggests this pathway to be relevant in the pathogenesis in various models of experimental hypertension. In addition, an orally available soluble epoxide hydrolase inhibitor, which halts the breakdown of EETs, has already passed a phase 1 clinical trial. We, therefore, exposed primary human coronary artery endothelial cells to 1 nM aldosterone. MethodsWe used qPCR to investigate changes in the expression levels of essential genes for the synthesis and degradation of EETs as well as mass spectrometry to determine endothelial synthetic capacity to release EETs upon stimulation. We also assessed primary human coronary artery smooth muscle cells for expression of putative EET receptor ion channels or downstream mediators as well as for the calcium response to EETs using calcium imaging. ResultsNo major aldosterone-related expression changes were detected on the endothelial as well as the smooth muscle side. Stimulated release of endothelial EETs was unaffected. Likewise, the smooth muscle calcium response was unchanged after aldosterone excess. ConclusionsThe EET pathway is not negatively affected by increased aldosterone concentrations as seen in PA. Modulating the EET pathway with therapeutic intent in patients with PA might therefore be assessed in future preclinical and clinical trials to address ED.

physiology↗

bioRxiv2020

Eating to dare - Nutrition impacts human risk decision and related brain function

Macronutrient composition modulates plasma amino acids that are precursors of neurotransmitters and can impact brain function and decisions. Neurotransmitter serotonin has been shown to regulate not only food intake, but also economic decisions. We investigated whether an acute nutrition-manipulation inducing plasma tryptophan fluctuation affects brain function, thereby affecting risky decisions. Breakfasts differing in carbohydrate/protein ratios were offered to test changes in risky decision making while metabolic and neural dynamics were tracked. We identified that a high-carbohydrate/protein meal increased plasma tryptophan which mapped to individual risk propensity changes. Moreover, the meal-driven fluctuation in tryptophan and risk propensity changes were modulated by individual difference in body fat mass. Using fMRI, we further identified activation in the parietal lobule during risk-processing, of which activities 1) were correlated with the risk propensity changes in decision making, 2) were sensitive to the tryptophan fluctuation, and 3) were modulated by individuals body fat mass. Furthermore, the activity in the parietal lobule positively mediated the tryptophan-fluctuation to risk-propensity-changes relationship. Our results provide evidence for a personalized nutrition-driven modulation on human risky decisions and its metabolic and neural mechanisms.

neuroscience↗