Biology subjects

Wilms, B.

Publications and source records attributed to Wilms, 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↗

bioRxiv2025

Single-base m6A epitranscriptomics reveals novel HIV-1 host interaction targets in primary CD4+ T cells

N6-methyladenosine (m6A) is the most prevalent cellular mRNA modification and plays a critical role in regulating RNA stability, localization, and gene expression. m6A modification plays a vital role in modulating the expression of viral and cellular genes during HIV-1 infection. HIV-1 infection increases cellular RNA m6A levels in many cell types, which facilitates HIV-1 replication and infectivity in target cells. However, the function of m6A modification in regulating HIV-1 infection of primary CD4+ T cells remains unclear. Here, we demonstrate that HIV-1 infection of Jurkat CD4+ T cells and primary CD4+ T cells promotes the interaction between the m6A writer complex subunits methyltransferase-like 3 and 14 (METTL3/METTL14). Using single-base m6A-specific RNA sequencing, we identified several differentially m6A-modified cellular mRNAs, including perilipin 3 (PLIN3), during HIV-1 infection in primary CD4+ T cells. Interestingly, HIV-1 infection increased PLIN3 mRNA level by enhancing its stability, but PLIN3 protein level was decreased. Knocking down PLIN3 in primary CD4+ T cells reduced HIV-1 production but enhanced virion infectivity. In contrast, in Jurkat cells, PLIN3 mRNA and protein expression levels were unaffected by HIV-1 infection, and knocking out PLIN3 did not impact HIV-1 production or infectivity. These results indicate that the interplay between HIV-1 and PLIN3 is cell-type specific and only observed in primary CD4+ T cells. Overall, our results highlight the importance of m6A RNA modification in HIV-1-infected primary CD4+ T cells and suggest its significance as a regulatory mechanism in HIV-1 infection. Author SummaryN6-methyladenosine (m6A) is a common chemical modification on mRNA that helps control RNA stability, localization, and gene expression. m6A modification of viral and cellular RNA is important for HIV-1 infection. In this study, we found that HIV-1 infection of CD4+ T cells enhanced the interaction between two proteins, METTL3 and METTL14, which are responsible for adding m6A modifications to RNA. Using m6A-specific RNA sequencing, we identified several mRNAs with altered m6A modifications during HIV-1 infection, including one called PLIN3. Interestingly, HIV-1 infection stabilized and increased PLIN3 mRNA levels, but reduced PLIN3 protein expression in primary CD4+ T cells. When we knocked down PLIN3 in primary CD4+ T cells, it decreased HIV-1 production but made the HIV-1 particles more infectious. In contrast, in the Jurkat CD4+ T cell line, HIV-1 infection did not affect PLIN3 expression and knockout of PLIN3 did not alter HIV-1 production or infectivity, suggesting that the effect is specific to primary CD4+ T cells. Our findings show the importance of m6A RNA modification in HIV-1 infection by regulating host genes like PLIN3 and suggest a unique regulatory mechanism in HIV-1 infected primary CD4+ T cells.

microbiology↗

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↗