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Heintz, D.

Publications and source records attributed to Heintz, D..

4 recordsLinked to original sources

Decoupling glycation from mortality: glucose, but not methylglyoxal, reduces survival in zebra finches

Birds provide a unique model for ageing research, with greater longevity and slower senescence compared to mammals of similar body size, despite a higher mass-adjusted metabolic rate and blood glucose levels than other vertebrate groups. While the effects of glucose, glycation, and advanced glycation end-products (AGE) on ageing are well-documented in biomedical research, their impact on avian physiology and ageing remains poorly understood. Although birds may possess adaptations mitigating the potential detrimental effects of glucose, elevated glucose still predicts reduced lifespan, and protein glycation varies with age and can influence survival and some fitness-related traits, implying that glycation or AGE accumulation may have relevant effects on avian longevity. In this study, we experimentally investigated how one year of dietary supplementation with glucose or methylglyoxal affects survival and physiology (metabolic rate, flying performance, and beak coloration) in captive zebra finches (Taeniopygia guttata). We reveal a significant increase in mortality exclusively in glucose-supplemented birds, with also an elevated albumin glycation rate and AGE formation. However, these variables did not directly explain the increased mortality, which was also absent in methylglyoxal-treated individuals, despite similar AGE accumulation. Additionally, we observed some other effects, like an age-related constraint on seasonal metabolic adjustment, a treatment-influenced age decline in secondary sexual traits expression, and a decline in flight performance during the peak mortality period, suggesting a broader deterioration of health. Thus, although we demonstrate glucose supplementation to be more deleterious than methylglyoxal, the underlying mechanisms for the increase in mortality induced by the treatment remain unresolved.

physiology↗

Social environment and chronological age shape eusocial insect species: the case of the ant workers.

Position within the social group has consequences on individual lifespans in diverse taxa. This is especially obvious in eusocial insects, where workers differ in both the tasks they perform and their aging rates. However, in eusocial wasps, bees and ants, the performed task usually depends strongly on age. As such, untangling the effects of social role and age on worker physiology is a key step towards understanding the coevolution of sociality and aging. We performed an experimental protocol that allowed a separate analysis of these two factors using four groups of black garden ant (Lasius niger) workers: young foragers, old foragers, young nest workers, and old nest workers. We highlighted age-related differences in the proteome and metabolome of workers that were primarily related to worker subcaste and only secondarily to age. The relative abundance of proteins and metabolites suggests an improved xenobiotic detoxification, and a fuel metabolism based more on lipid use than carbohydrate use in young ants, regardless of their social role. Regardless of age, proteins related to the digestive function were more abundant in nest workers than in foragers. Old foragers were mostly characterized by weak abundances of molecules with an antibiotic activity or involved in chemical communication. Finally, our results suggest that even in tiny species, extended lifespan may require to mitigate cancer risks. This is consistent with results found in eusocial rodents and thus opens up the discussion of shared mechanisms among distant taxa and the influence of sociality on life history traits such as longevity.

physiology↗

Nitrate-regulated growth processes involve activation of gibberellin pathway

Nitrate, one of the main nitrogen (N) sources for crops, acts as a nutrient and key signaling molecule coordinating gene expression, metabolism and various growth processes throughout the plant life cycle. It is widely accepted that nitrate-triggered developmental programs cooperate with hormone synthesis and transport, to finely adapt plant architecture to N availability. Here, we report that nitrate, acting through its signaling pathway, promotes growth in Arabidopsis and wheat, in part by modulating the accumulation of gibberellin (GA)-regulated DELLA growth repressors. We show that nitrate reduces the abundance of DELLAs by increasing GA contents through activation of GA metabolism gene expression. Consistently, the growth restraint conferred by nitrate deficiency is partially rescued in global-DELLA mutant that lacks all DELLAs. At the cellular level, we show that nitrate enhances both cell proliferation and elongation in a DELLA-dependent and -independent manner, respectively. Our findings establish a connection between nitrate and GA signaling pathways that allow plants to adapt their growth to nitrate availability.

plant biology↗

Pioglitazone improves deficits of Fmr1-KO mouse model of Fragile X syndrome by interfering with excessive diacylglycerol signaling

Fragile X syndrome (FXS), the leading cause of familial intellectual disability, is an uncured disease caused by the absence or loss of function of the FMRP protein. FMRP is an RNA binding protein that controls the translation of specific proteins in neurons. A main target of FMRP in neurons is diacylglycerol kinase kappa (DGKk) and the loss of FMRP leads to a loss of DGK activity causing a diacylglycerol excess in the brain. Excessive diacylglycerol signaling could be a significant contributor to the pathomechanism of FXS. Here we tested the contribution of DAG-signaling in Fmr1-KO mouse model of FXS and we show that pioglitazone, a widely prescribed drug for type 2 diabetes, has ability to correct excessive DAG signaling in the brain and rescue behavioral alterations of the Fmr1-KO mouse. This study highlights the role of lipid signaling homeostasis in FXS and provides arguments to support the testing of pioglitazone for treatment of FXS.

neuroscience↗