RESUMO
Road networks and human density are major factors contributing to habitat fragmentation and loss, isolation of wildlife populations, and reduced genetic diversity. Terrestrial mammals are particularly sensitive to road networks and encroachment by human populations. However, there are limited assessments of the impacts of road networks and human density on population-specific nuclear genetic diversity, and it remains unclear how these impacts are modulated by life-history traits. Using generalized linear mixed models and microsatellite data from 1444 North American terrestrial mammal populations, we show that taxa with large home range sizes, dense populations, and large body sizes had reduced nuclear genetic diversity with increasing road impacts and human density, but the overall influence of life-history traits was generally weak. Instead, we observed a high degree of genus-specific variation in genetic responses to road impacts and human density. Human density negatively affected allelic diversity or heterozygosity more than road networks (13 vs. 5-7 of 25 assessed genera, respectively); increased road networks and human density also positively affected allelic diversity and heterozygosity in 15 and 6-9 genera, respectively. Large-bodied, human-averse species were generally more negatively impacted than small, urban-adapted species. Genus-specific responses to habitat fragmentation by ongoing road development and human encroachment likely depend on the specific capability to (i) navigate roads as either barriers or movement corridors, and (ii) exploit resource-rich urban environments. The nonuniform genetic response to roads and human density highlights the need to implement efforts to mitigate the risk of vehicular collisions, while also facilitating gene flow between populations of particularly vulnerable taxa.
RESUMO
The human gut microbiota controls factors that relate to human metabolism with a reach far greater than originally expected. Microbial communities and human (or animal) hosts entertain reciprocal exchanges between various inputs that are largely controlled by the host via its genetic make-up, nutrition and lifestyle. The composition of these microbial communities is fundamental to supply metabolic capabilities beyond those encoded in the host genome, and contributes to hormone and cellular signalling that support the dynamic adaptation to changes in food availability, environment and organismal development. Poor functional exchange between the microbial communities and their human host is associated with dysbiosis, metabolic dysfunction and disease. This review examines the biology of the dynamic relationship between the reciprocal metabolic state of the microbiota-host entity in balance with its environment (i.e. in healthy states), the enzymatic and metabolic changes associated with its imbalance in three well-studied diseases states such as obesity, diabetes and atherosclerosis, and the effects of bariatric surgery and exercise.
Assuntos
Microbioma Gastrointestinal/fisiologia , Redes e Vias Metabólicas , Animais , Aterosclerose/metabolismo , Aterosclerose/microbiologia , Aterosclerose/terapia , Diabetes Mellitus Tipo 2/metabolismo , Diabetes Mellitus Tipo 2/microbiologia , Diabetes Mellitus Tipo 2/terapia , Disbiose/metabolismo , Disbiose/microbiologia , Disbiose/terapia , Ácidos Graxos Voláteis/metabolismo , Interações entre Hospedeiro e Microrganismos , Humanos , Obesidade/metabolismo , Obesidade/microbiologia , Obesidade/terapiaRESUMO
The priming effect of rewards is a boost in the vigor of reward seeking resulting from the previous receipt of a reward. Extensive work has been carried out on the priming effect of electrical brain stimulation, but much less research exists on the priming effect of natural rewards, such as food. While both reinforcement and motivation are linked with dopamine transmission in the brain, the priming effect of rewards does not appear to be dopamine-dependent. In the present study, an operant method was developed to measure the priming effect of food and then applied to investigate whether it is affected by dopamine receptor antagonism. Long-Evans rats were administered saline or one of the three doses (0.01, 0.05, 0.075 mg/kg) of the dopamine D1 receptor family antagonist, SCH23390, or the dopamine D2 receptor family antagonist, eticlopride. Although dopamine receptor antagonism affected pursuit of food, it did not eliminate the priming effect. These data suggest that despite the involvement of dopamine transmission in reinforcement and motivation, the priming effect of food does not depend on dopamine transmission.
Assuntos
Benzazepinas/farmacologia , Alimentos , Priming de Repetição/efeitos dos fármacos , Salicilamidas/farmacologia , Animais , Condicionamento Operante/efeitos dos fármacos , Antagonistas de Dopamina/farmacologia , Masculino , RatosRESUMO
Population genetic data from nuclear DNA has yet to be synthesized to allow broad scale comparisons of intraspecific diversity versus species diversity. The MacroPopGen database collates and geo-references vertebrate population genetic data across the Americas from 1,308 nuclear microsatellite DNA studies, 897 species, and 9,090 genetically distinct populations where genetic differentiation (FST) was measured. Caribbean populations were particularly distinguished from North, Central, and South American populations, in having higher differentiation (FST = 0.12 vs. 0.07-0.09) and lower mean numbers of alleles (MNA = 4.11 vs. 4.84-5.54). While mammalian populations had lower MNA (4.86) than anadromous fish, reptiles, amphibians, freshwater fish, and birds (5.34-7.81), mean heterozygosity was largely similar across groups (0.57-0.63). Mean FST was consistently lowest in anadromous fishes (0.06) and birds (0.05) relative to all other groups (0.09-0.11). Significant differences in Family/Genera variance among continental regions or taxonomic groups were also observed. MacroPopGen can be used in many future applications including latitudinal analyses, spatial analyses (e.g. central-margin), taxonomic comparisons, regional assessments of anthropogenic impacts on biodiversity, and conservation of wild populations.