RESUMO
Silver nanoparticles (AgNPs) are known to affect the physiology and morphology of plants in various ways, but the exact mechanism by which they interact with plant cells remains to be elucidated. An unresolved question of silver nanotoxicology is whether the interaction is triggered by the physical features of the particles, or by silver ions leached from their surface. In this study, we germinated and grew Arabidopsis thaliana seedlings in synthetic medium supplemented with sub-morbid concentrations (4 µg/mL) of AgNPs and silver nitrate (AgNO3). This treatment led to in planta accumulation of 106 µg/g and 97 µg/g of silver in the AgNO3- and AgNP-exposed seedlings, respectively. Despite the statistically indistinguishable silver accumulation, RNA sequencing data demonstrated distinct changes in the transcriptome of the AgNP-exposed, but not in the AgNO3-exposed plants. AgNP exposure induced changes in the expression of genes involved in immune response, cell wall organization, photosynthesis and cellular defense against reactive oxygen species. AgNO3 exposure, on the other hand, caused the differential expression of only two genes, neither of which belonged to any AgNP-enriched gene ontology categories. Moreover, AgNP exposure led to a 39% reduction (p < 0.001) in total chlorophyll concentration relative to untreated plants which was associated with a 56.9% and 56.2% drop (p < 0.05) in carbon assimilation rate at ambient and saturating light, respectively. Stomatal conductance was not significantly affected by AgNP exposure, and limitations to carbon assimilation, as determined through analysis of light and carbon dioxide (A/Ci) curves, were attributed to rates of electron transport, maximum carboxylation rates and triose phosphate use. AgNO3-exposure, on the other hand, did not lead to significant reduction either in chlorophyll concentration or in carbon assimilation rate. Given these data, we propose that the impact of AgNPs cannot be simply attributed to the presence of the metal in plants, but is innate to the particulate nature of nanosilver.
RESUMO
CONTEXT: The role of glucagon-like peptide-1 (GLP-1) in type 2 diabetes (T2D) and obesity is not fully understood. OBJECTIVE: We investigate the association of cardiometabolic, diet, and lifestyle parameters on fasting and postprandial GLP-1 in people at risk of, or living with, T2D. METHODS: We analyzed cross-sectional data from the two Innovative Medicines Initiative (IMI) Diabetes Research on Patient Stratification (DIRECT) cohorts, cohort 1 (n = 2127) individuals at risk of diabetes; cohort 2 (n = 789) individuals with new-onset T2D. RESULTS: Our multiple regression analysis reveals that fasting total GLP-1 is associated with an insulin-resistant phenotype and observe a strong independent relationship with male sex, increased adiposity, and liver fat, particularly in the prediabetes population. In contrast, we showed that incremental GLP-1 decreases with worsening glycemia, higher adiposity, liver fat, male sex, and reduced insulin sensitivity in the prediabetes cohort. Higher fasting total GLP-1 was associated with a low intake of wholegrain, fruit, and vegetables in people with prediabetes, and with a high intake of red meat and alcohol in people with diabetes. CONCLUSION: These studies provide novel insights into the association between fasting and incremental GLP-1, metabolic traits of diabetes and obesity, and dietary intake, and raise intriguing questions regarding the relevance of fasting GLP-1 in the pathophysiology T2D.