scholarly journals Adaptations of energy metabolism in cetaceans have consequences for their response to foraging disruption

2019 ◽  
Author(s):  
Davina Derous ◽  
Jagajjit Sahu ◽  
Alex Douglas ◽  
David Lusseau ◽  
Marius Wenzel

AbstractCetaceans have varied their anatomical structure, physiology and metabolism to adapt to the challenges of aquatic life. Key to this change is the deposition of blubber. This adipose tissue plays a significant regulatory and signaling role in mammalian metabolism. As foraging disruption by human activities is emerging as a key conservation threat for cetaceans, we need to understand how selection for aquatic life might have altered key nutrient sensing pathways associated with adipose signaling. We compared selection pressure on those energy metabolism biological pathways by contrasting the rate of substitution observed in genes associated with them in cetacean and artiodactyl genomes. We then estimated the likely consequence of these selection pressures for pathway functions. Here we show that genes involved in the insulin, mTOR, SIRT and NF-κB pathways were under significant positive selection in cetaceans compared to their terrestrial sister taxon. Our results suggest these genes may have been positively selected to adapt to a glucose-poor diet and it is unlikely that fat depots signaling function in the same manner as in terrestrial mammals. Secondary adaptation to life in water significantly affected functions in nutrient sensing pathways in cetaceans. Insulin is not likely to play the same role in energy balance as it does in terrestrial mammals and adiposity is not likely to have the deleterious health consequences it has in terrestrial mammals. The physiological ecology of cetacean fat deposition, and therefore its value as a condition index, needs to be interpreted in this evolutionary context.

Glycobiology ◽  
2021 ◽  
Author(s):  
Hannah M Stephen ◽  
Trevor M Adams ◽  
Lance Wells

Abstract Thousands of nuclear and cytosolic proteins are modified with a single β-N-acetylglucosamine on serine and threonine residues in mammals, a modification termed O-GlcNAc. This modification is essential for normal development and plays important roles in virtually all intracellular processes. Additionally, O-GlcNAc is involved in many disease states, including cancer, diabetes, and X-linked intellectual disability. Given the myriad of functions of the O-GlcNAc modification, it is therefore somewhat surprising that O-GlcNAc cycling is mediated by only two enzymes: the O-GlcNAc transferase (OGT), which adds O-GlcNAc, and the O-GlcNAcase (OGA), which removes it. A significant outstanding question in the O-GlcNAc field is how do only two enzymes mediate such an abundant and dynamic modification. In this review, we explore the current understanding of mechanisms for substrate selection for the O-GlcNAc cycling enzymes. These mechanisms include direct substrate interaction with specific domains of OGT or OGA, selection of interactors via partner proteins, posttranslational modification of OGT or OGA, nutrient sensing, and localization alteration. Altogether, current research paints a picture of an exquisitely regulated and complex system by which OGT and OGA select substrates. We also make recommendations for future work, toward the goal of identifying interaction mechanisms for specific substrates that may be able to be exploited for various research and medical treatment goals.


2021 ◽  
Vol 22 (15) ◽  
pp. 7899
Author(s):  
Yu-Chin Lien ◽  
Zhe Zhang ◽  
Yi Cheng ◽  
Erzsebet Polyak ◽  
Laura Sillers ◽  
...  

A well-functioning placenta is crucial for normal gestation and regulates the nutrient, gas, and waste exchanges between the maternal and fetal circulations and is an important endocrine organ producing hormones that regulate both the maternal and fetal physiologies during pregnancy. Placental insufficiency is implicated in spontaneous preterm birth (SPTB). We proposed that deficits in the capacity of the placenta to maintain bioenergetic and metabolic stability during pregnancy may ultimately result in SPTB. To explore our hypothesis, we performed a RNA-seq study in male and female placentas from women with SPTB (<36 weeks gestation) compared to normal pregnancies (≥38 weeks gestation) to assess the alterations in the gene expression profiles. We focused exclusively on Black women (cases and controls), who are at the highest risk of SPTB. Six hundred and seventy differentially expressed genes were identified in male SPTB placentas. Among them, 313 and 357 transcripts were increased and decreased, respectively. In contrast, only 61 differentially expressed genes were identified in female SPTB placenta. The ingenuity pathway analysis showed alterations in the genes and canonical pathways critical for regulating inflammation, oxidative stress, detoxification, mitochondrial function, energy metabolism, and the extracellular matrix. Many upstream regulators and master regulators important for nutrient-sensing and metabolism were also altered in SPTB placentas, including the PI3K complex, TGFB1/SMADs, SMARCA4, TP63, CDKN2A, BRCA1, and NFAT. The transcriptome was integrated with published human placental metabolome to assess the interactions of altered genes and metabolites. Collectively, significant and biologically relevant alterations in the transcriptome were identified in SPTB placentas with fetal sex disparities. Altered energy metabolism, mitochondrial function, inflammation, and detoxification may underly the mechanisms of placental dysfunction in SPTB.


2018 ◽  
Author(s):  
Justin L. Buchanan ◽  
Colin D. Meiklejohn ◽  
Kristi L. Montooth

AbstractPhysiological responses to short-term environmental stress, such as infection, can have long-term consequences for fitness, particularly if the responses are inappropriate or nutrient resources are limited. Genetic variation affecting energy acquisition, storage, and usage can limit cellular energy availability and may influence resource-allocation tradeoffs even when environmental nutrients are plentiful. Here, we utilize well-characterized Drosophila mitochondrial-nuclear genotypes to test whether disrupted energy metabolism interferes with nutrient-sensing pathways, and whether this disruption has consequences for tradeoffs between immunity and fecundity. We find that this energetically compromised genotype is resistant to rapamycin – a drug that stimulates nutrient-sensing pathways that are activated when resources are limited. Resource limitation also compromises survival in energetically-compromised genotypes, suggesting that this genotype may have little excess energetic capacity and fewer cellular nutrients, even when environmental nutrients are not limiting. Accordingly, we find that immune function is compromised in this genotype, but only in females, and that these females experience immunity-fecundity tradeoffs that are not evident in genotypic controls with normal energy metabolism. Thus, genetic variation in energy metabolism may act to limit the resources available for allocation to life-history traits in ways that generate tradeoffs even when environmental resources are not limiting.


Meat Science ◽  
2013 ◽  
Vol 93 (1) ◽  
pp. 37-45 ◽  
Author(s):  
J. Faure ◽  
L. Lefaucheur ◽  
N. Bonhomme ◽  
P. Ecolan ◽  
K. Meteau ◽  
...  

2019 ◽  
Vol 47 (2019) ◽  
pp. 21-34
Author(s):  
Barry C. Poulton ◽  
Jing Tao

Abstract During 2012-2014, we evaluated macroinvertebrate communities in streams draining the non-connected stormwater management region (Municipal Separate Storm Sewer System, or MS4) within the Kansas City metropolitan area utilizing the Missouri bioassessment protocols. Trends in aquatic life impairment status based on Missouri's Macroinvertebrate Stream Condition Index (MSCI), as well as richness and abundance of EPT indicator metrics (Ephemeroptera, Plecoptera, Trichoptera), were compared between rural control sites and both transitional and urban stream sites representing varying stages of land use conversion. As compared to non-urban control sites, EPT taxa richness was significantly lower at MS4 urban sites during all three years (p = 0.007 – 0.013) and MS4 transitional sites during one of three years (p=0.48). EPT abundance (%) was significantly lower at MS4 urban sites during all years (p = 0.008 – 0.013) and MS4 transitional sites during one of three years (p=0.34). Mean EPT abundances ranged between 0.6% - 10.3% at urban MS4 sites, and always exceeded 18% at control sites. Both EPT richness and abundance were lower at the MS4 control site but means for EPT and other core metrics at this site were most often similar to non-urban control sites based on analysis of variance (ANOVA). MS4 transitional sites with active development in their watersheds were partially-supporting in their impairment status, and EPT metrics had lower means and generally more variability than control sites. Temporal trends indicate non-urban control and MS4 control sites consistently meet fully-supporting impairment status based on overall MSCI scores, but no study sites currently meet regional expectations (as defined by state reference streams) for either of the EPT metrics. Results indicate that Missouri and Kansas biocriteria for both EPT metrics are not consistently being met at any stream sites in the Kansas City metro area, including fully-supporting control sites and MS4 streams that receive stormwater runoff in watersheds with urban development that is well-established or currently transitioning to urban or suburban land uses.


Cells ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 736
Author(s):  
Christina Walz ◽  
Julia Brenmoehl ◽  
Nares Trakooljul ◽  
Antonia Noce ◽  
Caroline Caffier ◽  
...  

It is assumed that crosstalk of central and peripheral tissues plays a role in the adaptive response to physical activity and exercise. Here, we wanted to study the effects of training and genetic predisposition in a marathon mouse model on mRNA expression in the pituitary gland. Therefore, we used a mouse model developed by phenotype selection for superior running performance (DUhTP) and non-inbred control mice (DUC). Both mouse lines underwent treadmill training for three weeks or were kept in a sedentary condition. In all groups, total RNA was isolated from the pituitary gland and sequenced. Molecular pathway analysis was performed by ingenuity pathway analysis (IPA). Training induced differential expression of 637 genes (DEGs) in DUC but only 50 DEGs in DUhTP mice. Genetic selection for enhanced running performance strongly affected gene expression in the pituitary gland and identified 1732 DEGs in sedentary DUC versus DUhTP mice. Training appeared to have an even stronger effect on gene expression in both lines and comparatively revealed 3828 DEGs in the pituitary gland. From the list of DEGs in all experimental groups, candidate genes were extracted by comparison with published genomic regions with significant effects on training responses in mice. Bioinformatic modeling revealed induction and coordinated expression of the pathways for ribosome synthesis and oxidative phosphorylation in DUC mice. By contrast, DUhTP mice were resistant to the positive effects of three-week training on protein and energy metabolism in the pituitary gland.


2000 ◽  
Vol 79 (4) ◽  
pp. 519-524 ◽  
Author(s):  
M.M. Mashaly ◽  
M.J. Heetkamp ◽  
H.K. Parmentier ◽  
J.W. Schrama

2020 ◽  
Vol 21 (18) ◽  
pp. 6606 ◽  
Author(s):  
Simona Damiano ◽  
Concetta Sozio ◽  
Giuliana La Rosa ◽  
Bruna Guida ◽  
Raffaella Faraonio ◽  
...  

Energy metabolism and redox state are strictly linked; energy metabolism is a source of reactive oxygen species (ROS) that, in turn, regulate the flux of metabolic pathways. Moreover, to assure redox homeostasis, metabolic pathways and antioxidant systems are often coordinately regulated. Several findings show that superoxide dismutase 1 (SOD1) enzyme has effects that go beyond its superoxide dismutase activity and that its functions are not limited to the intracellular compartment. Indeed, SOD1 is secreted through unconventional secretory pathways, carries out paracrine functions and circulates in the blood bound to lipoproteins. Striking experimental evidence links SOD1 to the redox regulation of metabolism. Important clues are provided by the systemic effects on energy metabolism observed in mutant SOD1-mediated amyotrophic lateral sclerosis (ALS). The purpose of this review is to analyze in detail the involvement of SOD1 in redox regulation of metabolism, nutrient sensing, cholesterol metabolism and regulation of mitochondrial respiration. The scientific literature on the relationship between ALS, mutated SOD1 and metabolism will also be explored, in order to highlight the metabolic functions of SOD1 whose biological role still presents numerous unexplored aspects that deserve further investigation.


1980 ◽  
Vol 31 (1) ◽  
pp. 1-11 ◽  
Author(s):  
P. Allen ◽  
J. C. McCarthy

ABSTRACTThe growth of adipose tissue was investigated in lines of mice selected for high and low body weight at 5 and 10 weeks of age, by dissecting and weighing individual fat depots from mice aged 5, 7·5, 10 and 15 weeks. At fixed ages most depots were heavier in the High lines and lighter in the Low lines. Depots grew at different rates and the rate of total fat deposition relative to gain in body weight was greater in High than in Low lines. At about 20g live weight High and Low lines had similar proportions of total fat; at lower weights the High lines were relatively leaner. These correlated effects of selection were more pronounced in the faster growing depots of the kidneys and gonads. In consequence, the High an d Low lines had different fat distributions at fixed ages, at fixed body weights and at fixed weights of fat.


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