scholarly journals Female variation in allocation of steroid hormones, antioxidants and fatty acids: a multilevel analysis in a wild passerine bird

2019 ◽  
Vol 50 (1) ◽  
Author(s):  
Lucia Mentesana ◽  
Caroline Isaksson ◽  
Wolfgang Goymann ◽  
Martin N. Andersson ◽  
Monika Trappschuh ◽  
...  
2018 ◽  
Author(s):  
Lucia Mentesana ◽  
Caroline Isaksson ◽  
Wolfgang Goymann ◽  
Martin N. Andersson ◽  
Monika Trappschuh ◽  
...  

AbstractThe environment where an embryo develops can be influenced by components of maternal origin, which can shape offspring phenotypes and therefore maternal fitness. In birds that produce more than one egg per clutch, females differ in the concentration of components they allocate into the yolk along the laying sequence. However, identification of processes that shape female yolk allocation and thus offspring phenotype still remains a major challenge within evolutionary ecology. A way to increase our understanding is by acknowledging that allocation patterns can differ depending on the level of analysis, such as the populationversusthe among-female (within-population) level. We employed mixed models to analyze at both levels the variation in allocation along the laying sequence of four steroid hormones, three antioxidants, and four groups of fatty acids present in the egg yolks of wild great tits (Parus major). We also quantified repeatabilities for each component to study female consistency. At a population level, the concentrations/proportions of five yolk components varied along the laying sequence, implying that the developmental environment is different for offspring developing in firstversuslast eggs. Females varied substantially in the mean allocation of components and in their plasticity along the laying sequence. For most components, these two parameters were negatively correlated. Females were also remarkably repeatable in their allocation. Overall, our data emphasize the need to account for female variation in yolk allocation along the laying sequence at multiple levels, as variation at a population level is underpinned by different individual patterns. Our findings also highlight the importance of considering both levels of analysis in future studies investigating the causes and fitness consequences of yolk compounds. Finally, our results on female repeatability confirm that analyzing one egg per nest is a suitable way to address the consequences of yolk resource deposition for the offspring.


Endocrinology ◽  
2008 ◽  
Vol 149 (6) ◽  
pp. 3158-3166 ◽  
Author(s):  
Annelie Brolinson ◽  
Stéphane Fourcade ◽  
Andreas Jakobsson ◽  
Aurora Pujol ◽  
Anders Jacobsson

The Elovl3 gene belongs to the Elovl gene family, which encodes for enzymes involved in the elongation of very long chain fatty acids. The recognized role for the enzyme is to control the elongation of saturated and monounsaturated fatty acids up to 24 carbons in length. Elovl3 was originally identified as a highly expressed gene in brown adipose tissue on cold exposure. Here we show that hepatic Elovl3 mRNA expression follows a distinct diurnal rhythm exclusively in mature male mice, with a sharp increase early in the morning Zeitgeber time (ZT) 20, peaks around ZT2, and is back to basal level at the end of the light period at ZT10. In female mice and sexually immature male mice, the Elovl3 expression was constantly low. Fasting and refeeding mice with chow or high-fat diet did not alter the Elovl3 mRNA levels. However, animals that were exclusively fed during the day for 9 d displayed an inverted expression profile. In addition, we show that Elovl3 expression is transcriptionally controlled and significantly induced by the exposure of the synthetic glucocorticoid dexamethasone. Taken together, these data suggest that Elovl3 expression in mouse liver is under strict diurnal control by circulating steroid hormones such as glucocorticoids and androgens. Finally, Elovl3 expression was found to be elevated in peroxisomal transporter ATP-binding cassette, subfamily D(ALD), member 2 ablated mice and suppressed in ATP-binding cassette subfamily D(ALD) member 2 overexpressing mice, implying a tight cross talk between very long chain fatty acid synthesis and peroxisomal fatty acid oxidation.


1968 ◽  
Vol 51 (11) ◽  
pp. 1862-1866
Author(s):  
L.W. Aurand ◽  
J.A. Singleton ◽  
L.C. Ulberg ◽  
J. Britt

2021 ◽  
Author(s):  
Siqi Xia ◽  
Jiahao Shao ◽  
Mauricio A. Elzo ◽  
Tao Tang ◽  
Yanhong Li ◽  
...  

Abstract Backgroud:High-fat diet (HFD) has been widely recognized as a significant modifiable risk for insulin resistance, inflammation, type 2-diabetes (T2D), atherosclerosis and other metabolic diseases. The biological mechanisms responsible for disturbances in perirenal adipose tissue (PAT) and other tissues in rodents fed a HFD are well understood. However, the biological mechanism responsible for key metabolic disorders in PAT of rabbits subject to HFD remains unclear. Methods: Here, untargeted metabolomics (LC-MS/MS) combined with liquid chromatography (LC) and high resolution mass spectrometry (MS) were used to evaluate PAT metabolic changes. Histological observations showed that the adipocytes cells and density of PAT was significantly increased in HFD rabbits. Principal component analysis (PCA) and partial least squares-discriminant analysis (PLS-DA) showed noticeable changes in PAT metabolites between the HFD and standard normal diet (SND) rabbit groups. Results: Our study revealed 206 differential metabolites (21 up-regulated and 185 down-regulated), and then the 47 differential metabolites (13 up-regulated and 34 down-regulated), mainly phospholipids, fatty acids, steroid hormones and amino acids, chosen as potential biomarkers to help explain metabolic disorders caused by HFD. These metabolites were mainly associated with biosynthesis of unsaturated fatty acids, the arachidonic acid metabolic pathway, the ovarian steroidogenesis pathway, and the platelet activation pathway. Our study revealed that a HFD caused significant metabolic disorders in rabbit PAT. Conclusion: High levels of phospholipids, fatty acids, steroid hormones and l-methionine may inhibit oxygen respiration by increasing the adipocytes cells and density cause mitochondrial and endoplasmic reticulum dysfunction, produce inflammation, and finally lead to insulin resistance, thus increasing the risk of T2D , atherosclerosis, and other metabolic syndromes.


2018 ◽  
Vol 63 (2) ◽  
pp. 77-87
Author(s):  
Yudha Trinoegraha Adiputra ◽  
Muhammad Zairin jr ◽  
Muhammad Agus Suprayudi ◽  
Wasmen Manalu ◽  
Widanarni

Lipids ◽  
1990 ◽  
Vol 25 (10) ◽  
pp. 633-638 ◽  
Author(s):  
Sadao Watanabe ◽  
Takayuki Tani ◽  
Shigenobu Watanabe ◽  
Manabu Senō

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