scholarly journals Maternal provisioning gives young-of-the-year Hammerheads a head start in early life

2020 ◽  
Vol 167 (11) ◽  
Author(s):  
Kady Lyons ◽  
Ashley S. Galloway ◽  
Douglas H. Adams ◽  
Eric A. Reyier ◽  
Amanda M. Barker ◽  
...  

AbstractFor species that do not provide parental care after birth, excess maternal provisioning during development, beyond what is required for embryogenesis, provides offspring with resources to increase their chances of survival. Maternally derived resources are expected to be important for buffering offspring against limited food resources at birth or time needed to learn how to properly feed. Young-of-the-year (YOY) cryptic Scalloped Hammerheads (Sphyrna lewini) and Carolina Hammerheads (Sphyrna gilberti) were sampled from nurseries along the US Atlantic Coast and compared for a number of biological condition metrics across three developmental stages. Large declines in liver lipid content and hepatosomatic indices were found in neonatal sharks, using umbilical scar healing as a proxy for time since birth. Feeding commenced quickly as 96% of sharks had prey remnants in their stomachs. The combination of rapid exhaustion of maternally provided resources and high occurrence of stomachs with prey contents indicate that nursery quality, with respect to prey availability, may be important for YOY hammerhead survivorship. While externally the two species are morphologically similar, longer length-at-birth in S. lewini and higher hepatic condition in neonatal S. gilberti suggest that aspects of reproductive biology, including physiology, may differ between species. While more information is needed to distinguish life history differences between these two species, data collected from YOY may serve as a useful proxy to inform management when adult samples of cryptic species are difficult to collect.

2016 ◽  
Vol 230 (1) ◽  
pp. 67-79 ◽  
Author(s):  
Giselle Adriana Abruzzese ◽  
Maria Florencia Heber ◽  
Silvana Rocio Ferreira ◽  
Leandro Martin Velez ◽  
Roxana Reynoso ◽  
...  

Prenatal hyperandrogenism is hypothesized as one of the main factors contributing to the development of polycystic ovary syndrome (PCOS). PCOS patients have high risk of developing fatty liver and steatosis. This study aimed to evaluate the role of prenatal hyperandrogenism in liver lipid metabolism and fatty liver development. Pregnant rats were hyperandrogenized with testosterone. At pubertal age, the prenatally hyperandrogenized (PH) female offspring displayed both ovulatory (PHov) and anovulatory (PHanov) phenotypes that mimic human PCOS features. We evaluated hepatic transferases, liver lipid content, the balance between lipogenesis and fatty acid oxidation pathway, oxidant/antioxidant balance and proinflammatory status. We also evaluated the general metabolic status through growth rate curve, basal glucose and insulin levels, glucose tolerance test, HOMA-IR index and serum lipid profile. Although neither PH group showed signs of liver lipid content, the lipogenesis and fatty oxidation pathways were altered. The PH groups also showed impaired oxidant/antioxidant balance, a decrease in the proinflammatory pathway (measured by prostaglandin E2 and cyclooxygenase-2 levels), decreased glucose tolerance, imbalance of circulating lipids and increased risk of metabolic syndrome. We conclude that prenatal hyperandrogenism generates both PHov and PHanov phenotypes with signs of liver alterations, imbalance in lipid metabolism and increased risk of developing metabolic syndrome. The anovulatory phenotype showed more alterations in liver lipogenesis and a more impaired balance of insulin and glucose metabolism, being more susceptible to the development of steatosis.


2015 ◽  
Vol 8 ◽  
Author(s):  
Azie Azri ◽  
Takaomi Arai

A total of 104 sharks were landed at fishing ports in the Malaysian South China Sea between 30 October and 24 December 2014, comprising the four families, Carcharhinidae, Hemiscylliidae, Sphyrnidae and Scyliorhinidae, and 11 of these shark species were examined. Measurements of size and weight were different and varied among species, ranging from 0.1 to 7.5 kg in body weight and from 31.1 to 105 cm in total length. Five of the 11 sharks,Carcharhinus sealei, Loxodon macrorhinus, Rhizoprionodon acutus, Hemigaleus microstomaandSphyrna lewini, were in the range of, or even less than, the lengths of those measured at birth in previous reports. The results suggest that these sharks were born just before they were landed.Sphyrna lewiniand H.microstomaare categorized as Endangered and Vulnerable species, respectively, and other sharks included in the landings are also categorized as Near Threatened. Thus, the current fishing methods could lead to critical levels of shark species in these waters, and even the future extinction of species. An improvement in the species selectiveness of fishing gear is needed to protect and conserve sharks in the area.


1973 ◽  
Vol 103 (1) ◽  
pp. 54-60 ◽  
Author(s):  
Yoritaka Aoyama ◽  
Masashi Nakanishi ◽  
Kiyoshi Ashida

2017 ◽  
Vol 2017 ◽  
pp. 1-18 ◽  
Author(s):  
Adriene A. Paiva ◽  
Helena F. Raposo ◽  
Amarylis C. B. A. Wanschel ◽  
Tarlliza R. Nardelli ◽  
Helena C. F. Oliveira

Nonalcoholic fatty liver disease (NAFLD) is the principal manifestation of liver disease in obesity and metabolic syndrome. By comparing hypertriglyceridemic transgenic mice expressing apolipoprotein (apo) CIII with control nontransgenic (NTg) littermates, we demonstrated that overexpression of apoCIII, independent of a high-fat diet (HFD), produces NAFLD-like features, including increased liver lipid content; decreased antioxidant power; increased expression of TNFα, TNFα receptor, cleaved caspase-1, and interleukin-1β; decreased expression of adiponectin receptor-2; and increased cell death. This phenotype is aggravated and additional NAFLD features are differentially induced in apoCIII mice fed a HFD. HFD induced glucose intolerance together with increased gluconeogenesis, indicating hepatic insulin resistance. Additionally, the HFD led to marked increases in plasma TNFα (8-fold) and IL-6 (60%) in apoCIII mice. Cell death signaling (Bax/Bcl2), effector (caspase-3), and apoptosis were augmented in apoCIII mice regardless of whether a HFD or a low-fat diet was provided. Fenofibrate treatment reversed several of the effects associated with diet and apoCIII expression but did not normalize inflammatory traits even when liver lipid content was fully corrected. These results indicate that apoCIII and/or hypertriglyceridemia plays a major role in liver inflammation and cell death, which in turn increases susceptibility to and the severity of diet-induced NAFLD.


2018 ◽  
Vol 85 (4) ◽  
pp. 431-438 ◽  
Author(s):  
Enrico Fiore ◽  
Laura Perillo ◽  
Massimo Morgante ◽  
Elisabetta Giudice ◽  
Barbara Contiero ◽  
...  

The aim of the present study was to evaluate the potential for diagnosis of fatty liver by means of ultrasonographic measurement of liver and perivisceral adipose tissue as an alternative to blood indicators of lipomobilization and liver biopsy in periparturient high-yielding dairy cows. Thirty cows were enrolled and divided into two groups. The evaluation of body condition score (BCS), non-esterified fatty acids (NEFA), β-hydroxybutyrate (BHB), liver and perivisceral adipose tissue ultrasonographic measurement and histological liver lipid content (GdL) was performed at 15 ± 5 d prepartum (T0), 10 ± 2 d postpartum (T1), 30 ± 2 d postpartum (T2) and 50 ± 2 d postpartum (T3). Mesenteric fat thickness (the thickness of the perivascular adipose tissue) measured on ultrasound was shown to be an independent determinant of fatty liver. The cut-off of the ultrasonographic evaluation of the liver may be useful as a first and practical approach in identifying fatty liver. In conclusion, a non-invasive and reliable diagnostic method for predicting the risk of fatty liver in high yielding dairy cows has been demonstrated.


Endocrinology ◽  
2015 ◽  
Vol 157 (2) ◽  
pp. 570-585 ◽  
Author(s):  
Camella G. Wilson ◽  
Jennifer L. Tran ◽  
Derek M. Erion ◽  
Nicholas B. Vera ◽  
Maria Febbraio ◽  
...  

Abstract CD36/FAT (fatty acid translocase) is associated with human and murine nonalcoholic fatty liver disease, but it has been unclear whether it is simply a marker or whether it directly contributes to disease pathogenesis. Mice with hepatocyte-specific deletion of Janus kinase 2 (JAK2L mice) have increased circulating free fatty acids (FAs), dramatically increased hepatic CD36 expression and profound fatty liver. To investigate the role of elevated CD36 in the development of fatty liver, we studied two models of hepatic steatosis, a genetic model (JAK2L mice) and a high-fat diet (HFD)-induced steatosis model. We deleted Cd36 specifically in hepatocytes of JAK2L mice to generate double knockouts and from wild-type mice to generate CD36L single-knockout mice. Hepatic Cd36 disruption in JAK2L livers significantly improved steatosis by lowering triglyceride, diacylglycerol, and cholesterol ester content. The largest differences in liver triglycerides were in species comprised of oleic acid (C18:1). Reduction in liver lipids correlated with an improvement in the inflammatory markers that were elevated in JAK2L mice, namely aspartate aminotransferase and alanine transaminase. Cd36 deletion in mice on HFD (CD36L-HFD) reduced liver lipid content and decreased hepatic 4,4-difluoro-4-bora-3a,4a-diaza-s-indacene-FA uptake as compared with CON-HFD. Additionally, CD36L-HFD mice had improved whole-body insulin sensitivity and reduced liver and serum inflammatory markers. Therefore, CD36 directly contributes to development of fatty liver under conditions of elevated free FAs by modulating the rate of FA uptake by hepatocytes. In HFD-fed animals, disruption of hepatic Cd36 protects against associated systemic inflammation and insulin resistance.


2007 ◽  
Vol 97 (2) ◽  
pp. 289-297 ◽  
Author(s):  
L. M. P. Valente ◽  
N. M. Bandarra ◽  
A. C. Figueiredo-Silva ◽  
P. Rema ◽  
P. Vaz-Pires ◽  
...  

The effects of graded levels (0 %, 0·5 %, 0·75 and 1 %) of dietary conjugated linoleic acid (CLA) were assessed on 97 g rainbow trout. Fish were fed to satiation twice a day for 12 weeks. At the end of the experiment, all groups of fish weighed more than 250 g and no significant differences were detected in growth performance, feed conversion, nutrient or energy utilisation or body composition between treatments. A decrease in liver lipid content resulted from including CLA and was accompanied by a reduction in malic enzyme activity. The muscle saturated acid and PUFA content did not vary between dietary treatments, despite the increasing concentration of stearic acid and CLA. In the liver, however, both fractions increased significantly with dietary CLA. Moreover, the MUFA decreased significantly in both muscle and liver. CLA was incorporated into tissue lipids, with levels in flesh (2·1–4·2 %) being 2-fold higher than in liver (0·8–1·9 %). In muscle, the percentage of cis-9, trans-11 isomer ranged from 39·5 % to 41·8 % and that of trans-10, cis-12 isomer from 31·4 % to 33·4 % of total CLA. The incorporation of CLA isomers in the liver varied with dietary treatment, and the cis-9, trans-11 isomer seemed to be more efficiently incorporated than trans-10, cis-12. Sensory data indicated slight-to-moderate differences between the trout fed with and without CLA. The present results suggest that 250 g rainbow trout can incorporate CLA in both muscle and liver, contributing to the production of a functional food.


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