scholarly journals Population-level effects of acoustic disturbance in Atlantic cod: a size-structured analysis based on energy budgets

2020 ◽  
Vol 287 (1929) ◽  
pp. 20200490 ◽  
Author(s):  
Floor H. Soudijn ◽  
Tobias van Kooten ◽  
Hans Slabbekoorn ◽  
André M. de Roos

Anthropogenic underwater noise may negatively affect marine animals. Yet, while fishes are highly sensitive to sounds, effects of acoustic disturbances on fishes have not been extensively studied at the population level. In this study, we use a size-structured model based on energy budgets to analyse potential population-level effects of anthropogenic noise on Atlantic cod ( Gadus morhua ). Using the model framework, we assess the impact of four possible effect pathways of disturbance on the cod population growth rate. Through increased stress, changes in foraging and movement behaviour, and effects on the auditory system, anthropogenic noise can lead to (i) increased energy expenditure, (ii) reduced food intake, (iii) increased mortality, and (iv) reduced reproductive output. Our results show that population growth rates are particularly sensitive to changes in energy expenditure and food intake because they indirectly affect the age of maturation, survival and fecundity. Sub-lethal effects of sound exposure may thus affect populations of cod and fishes with similar life histories more than lethal effects of sound exposure. Moreover, anthropogenic noise may negatively affect populations when causing persistent increases of energy expenditure or decreases of food intake. Effects of specific acoustic pollutants on energy acquisition and expenditure should therefore be further investigated.

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Irene Cimino ◽  
Debra Rimmington ◽  
Y. C. Loraine Tung ◽  
Katherine Lawler ◽  
Pierre Larraufie ◽  
...  

AbstractNeuronatin (Nnat) has previously been reported to be part of a network of imprinted genes downstream of the chromatin regulator Trim28. Disruption of Trim28 or of members of this network, including neuronatin, results in an unusual phenotype of a bimodal body weight. To better characterise this variability, we examined the key contributors to energy balance in Nnat+/−p mice that carry a paternal null allele and do not express Nnat. Consistent with our previous studies, Nnat deficient mice on chow diet displayed a bimodal body weight phenotype with more than 30% of Nnat+/−p mice developing obesity. In response to both a 45% high fat diet and exposure to thermoneutrality (30 °C) Nnat deficient mice maintained the hypervariable body weight phenotype. Within a calorimetry system, food intake in Nnat+/−p mice was hypervariable, with some mice consuming more than twice the intake seen in wild type littermates. A hyperphagic response was also seen in Nnat+/−p mice in a second, non-home cage environment. An expected correlation between body weight and energy expenditure was seen, but corrections for the effects of positive energy balance and body weight greatly diminished the effect of neuronatin deficiency on energy expenditure. Male and female Nnat+/−p mice displayed subtle distinctions in the degree of variance body weight phenotype and food intake and further sexual dimorphism was reflected in different patterns of hypothalamic gene expression in Nnat+/−p mice. Loss of the imprinted gene Nnat is associated with a highly variable food intake, with the impact of this phenotype varying between genetically identical individuals.


2009 ◽  
Vol 47 (5) ◽  
pp. 129-137 ◽  
Author(s):  
Eric T. Poehlman ◽  
Edward S. Horton

Metabolites ◽  
2021 ◽  
Vol 11 (10) ◽  
pp. 709
Author(s):  
Lorraine Brennan ◽  
Frank B. Hu ◽  
Qi Sun

Traditionally, nutritional epidemiology is the study of the relationship between diet and health and disease in humans at the population level. Commonly, the exposure of interest is food intake. In recent years, nutritional epidemiology has moved from a “black box” approach to a systems approach where genomics, metabolomics and proteomics are providing novel insights into the interplay between diet and health. In this context, metabolomics is emerging as a key tool in nutritional epidemiology. The present review explores the use of metabolomics in nutritional epidemiology. In particular, it examines the role that food-intake biomarkers play in addressing the limitations of self-reported dietary intake data and the potential of using metabolite measurements in assessing the impact of diet on metabolic pathways and physiological processes. However, for full realisation of the potential of metabolomics in nutritional epidemiology, key challenges such as robust biomarker validation and novel methods for new metabolite identification need to be addressed. The synergy between traditional epidemiologic approaches and metabolomics will facilitate the translation of nutritional epidemiologic evidence to effective precision nutrition.


2018 ◽  
Vol 285 (1879) ◽  
pp. 20180489 ◽  
Author(s):  
Olivia Hicks ◽  
Sarah J. Burthe ◽  
Francis Daunt ◽  
Mark Newell ◽  
Adam Butler ◽  
...  

Parasites have profound fitness effects on their hosts, yet these are often sub-lethal, making them difficult to understand and quantify. A principal sub-lethal mechanism that reduces fitness is parasite-induced increase in energetic costs of specific behaviours, potentially resulting in changes to time and energy budgets. However, quantifying the influence of parasites on these costs has not been undertaken in free-living animals. We used accelerometers to estimate energy expenditure on flying, diving and resting, in relation to a natural gradient of endo-parasite loads in a wild population of European shags Phalacrocorax aristotelis . We found that flight costs were 10% higher in adult females with higher parasite loads and these individuals spent 44% less time flying than females with lower parasite loads. There was no evidence for an effect of parasite load on daily energy expenditure, suggesting the existence of an energy ceiling, with the increase in cost of flight compensated for by a reduction in flight duration. These behaviour specific costs of parasitism will have knock-on effects on reproductive success, if constraints on foraging behaviour detrimentally affect provisioning of young. The findings emphasize the importance of natural parasite loads in shaping the ecology and life-history of their hosts, which can have significant population level consequences.


Endocrinology ◽  
2021 ◽  
Author(s):  
Manita Shakya ◽  
Surbhi Gahlot ◽  
Anne White ◽  
C Bruce Verchere ◽  
Malcolm J Low ◽  
...  

Abstract Pro-opiomelanocortin (POMC) neurons form an integral part of the central melanocortin system regulating food intake and energy expenditure. Genetic and pharmacological studies have revealed that defects in POMC synthesis, processing, and receptor signaling lead to obesity. It is well established that POMC is extensively processed by a series of enzymes, including prohormone convertases PC1/3 and PC2, and that genetic insufficiency of both PC1/3 and POMC is strongly associated with obesity risk. However, whether PC1/3-mediated POMC processing is absolutely tied to body weight regulation is not known. To investigate this question, we generated a Pomc-CreER  T2; Pcsk1  lox/lox mouse model in which Pcsk1 is specifically and temporally knocked out in POMC-expressing cells of adult mice by injecting tamoxifen at eight weeks of age. We then measured the impact of Pcsk1 deletion on POMC cleavage to ACTH and α-MSH, and on body weight. In whole pituitary, POMC cleavage was significantly impacted by the loss of Pcsk1, while hypothalamic POMC-derived peptide levels remained similar in all genotypes. However, intact POMC levels were greatly elevated in Pomc-CreER  T2; Pcsk1  lox/lox mice. Males expressed two-fold greater levels of pituitary PC1/3 protein than females, consistent with their increased POMC cleavage. Past studies show that mice with germline removal of PC1/3 do not develop obesity, while mice expressing mutant PC1/3 forms do develop obesity. We conclude that obesity pathways are not disrupted by PC1/3 loss solely in POMC-expressing cells, further disfavoring the idea that alterations in POMC processing underlie obesity in PCSK1 deficiency.


Endocrinology ◽  
2012 ◽  
Vol 153 (9) ◽  
pp. 4136-4143 ◽  
Author(s):  
Pierre Cardinal ◽  
Luigi Bellocchio ◽  
Samantha Clark ◽  
Astrid Cannich ◽  
Matthias Klugmann ◽  
...  

Cannabinoid type 1 (CB1) receptor activation is generally considered a powerful orexigenic signal and inhibition of the endocannabinoid system is beneficial for the treatment of obesity and related metabolic diseases. The hypothalamus plays a critical role in regulating energy balance by modulating both food intake and energy expenditure. Although CB1 receptor signaling has been implicated in the modulation of both these mechanisms, a complete understanding of its role in the hypothalamus is still lacking. Here we combined a genetic approach with the use of adeno-associated viral vectors to delete the CB1 receptor gene in the adult mouse hypothalamus and assessed the impact of such manipulation on the regulation of energy balance. Viral-mediated deletion of the CB1 receptor gene in the hypothalamus led to the generation of Hyp-CB1-KO mice, which displayed an approximately 60% decrease in hypothalamic CB1 receptor mRNA levels. Hyp-CB1-KO mice maintained on a normocaloric, standard diet showed decreased body weight gain over time, which was associated with increased energy expenditure and elevated β3-adrenergic receptor and uncoupling protein-1 mRNA levels in the brown adipose tissue but, surprisingly, not to changes in food intake. Additionally, Hyp-CB1-KO mice were insensitive to the anorectic action of the hormone leptin (5 mg/kg) and displayed a time-dependent hypophagic response to the CB1 inverse agonist rimonabant (3 mg/kg). Altogether these findings suggest that hypothalamic CB1 receptor signaling is a key determinant of energy expenditure under basal conditions and reveal its specific role in conveying the effects of leptin and pharmacological CB1 receptor antagonism on food intake.


2021 ◽  
Author(s):  
Ella Valleroy ◽  
Aaron Reed ◽  
Joseph S. Lightner

Abstract BackgroundSexually transmitted infection rates continue to increase across the US, further developing health disparities and economic burdens of disease, especially as migration occurs. In this study, we assessed the relationships among STI rates and migration at the county-level in Missouri from 2008–2017.MethodsTwo data sources were used: STI rates of chlamydia, gonorrhea, syphilis, HIV reported to Missouri DHSS and ACS 1-year county population estimates. Linear regression models and ANOVA tests were conducted in SPSS for each STI from year-to-year and 2008–2017. Covariates included in the analyzes were county-level income, employment rate, race, ethnicity, age, and percent poverty. Further, Akaike Information Criterion tests were performed to indicate the best predictor models and averaged standardized beta values.ResultsSignificant relationships among STI rates and population growth were identified. Chlamydia, syphilis, and HIV were positively associated with population growth from 2008–2017 (β = 0.15; β = 0.01; β = 0.05, respectively). Gonorrhea was negative associated with population growth (β= -0.02) but positively associated with unemployment rates (β = 0.01) highlighting the need to address population growth, as well as other variables in a population.ConclusionsThere seems to be a positive relationship among population change and rates of STIs. As populations change, rates of STIs change. Moving forward, quantitative work should be conducted in various states and the nation to understand this relationship in different contexts. Qualitative studies should assess individual county health departments, identifying strengths and weaknesses, implementation of community health improvement plans. Lastly, public policy should be implemented to buffer the impact of migration on health outcomes.


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