scholarly journals Effect of Dietary Marula Nut Meal on Liver Lipid Content and Surrogate Markers of Liver and Kidney Function of Broiler and Layer Japanese Quail

2022 ◽  
Author(s):  
Bulelani Elvis Mazizi ◽  
Kennedy Honey Erlwanger ◽  
Eliton Chivandi
Keyword(s):  
Kidney Function ◽  
Japanese Quail ◽  
Lipid Content ◽  
General Health ◽  
Egg Production ◽  
Liver Lipid ◽  
Surrogate Markers ◽  
Liver Lipid Content ◽  
Old Japanese ◽  
Liver And Kidney

Abstract Marula nut meal (MNM) can substitute soyabean meal (SBM) as a dietary protein source in Japanese quail diets without compromising growth performance and egg production. However, MNM has a high residual oil content which may impact metabolic health. The effects of MNM on hepatic lipid content and general, liver and kidney health have not been determined in both broilers and layers. Accordingly, two studies were run. In the broiler study two hundred 9-days old Japanese quail were randomly allocated to five diets wherein MNM replaced SBM on a crude protein (CP) basis at 0%, 25%, 50%, 75% and 100%, respectively, in both grower and finisher diets. In the layer study, sixty 5-weeks old Japanese maiden hens, individually housed, were randomly allocated to five-layer diets where MNM replaced SBM on a graded CP basis as for the broilers and fed for 8 weeks. At study termination the birds were slaughtered, blood collected and plasma harvested. Livers were excised, weighed and liver lipid content determined. Plasma surrogate markers of general health, liver and kidney function were determined. Dietary MNM had no effect (P > 0.05) on liver lipid content as well plasma surrogate markers of general health, liver and kidney function of the broiler quail. Dietary MNM at 75% of SBM CP significantly increased plasma phosphorus concentration of quail hens compared to that of counterparts fed control. Dietary MNM can be used in broiler and layer Japanese quail diets without risking development of fatty livers and compromising liver and kidney function.

scholarly journals Prenatal hyperandrogenism induces alterations that affect liver lipid metabolism

2016 ◽  
Vol 230 (1) ◽  
pp. 67-79 ◽  
Author(s):  
Giselle Adriana Abruzzese ◽  
Maria Florencia Heber ◽  
Silvana Rocio Ferreira ◽  
Leandro Martin Velez ◽  
Roxana Reynoso ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Lipid Metabolism ◽  
Glucose Tolerance ◽  
Fatty Liver ◽  
Lipid Content ◽  
Liver Lipid ◽  
Acid Oxidation ◽  
Liver Lipid Content ◽  
Increased Risk ◽  
Liver Lipid Metabolism

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.

Effect of Methionine on Liver Lipid Content and Lipid Metabolism of Rats Fed a Protein-free Diet

1973 ◽  
Vol 103 (1) ◽  
pp. 54-60 ◽  
Author(s):  
Yoritaka Aoyama ◽  
Masashi Nakanishi ◽  
Kiyoshi Ashida
Keyword(s):  
Lipid Metabolism ◽  
Lipid Content ◽  
Liver Lipid ◽  
Liver Lipid Content ◽  
Protein Free Diet

scholarly journals Apolipoprotein CIII Overexpression-Induced Hypertriglyceridemia Increases Nonalcoholic Fatty Liver Disease in Association with Inflammation and Cell Death

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
Keyword(s):  
Cell Death ◽  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Lipid Content ◽  
Fatty Liver Disease ◽  
Liver Lipid ◽  
Hepatic Insulin Resistance ◽  
Nonalcoholic Fatty Liver ◽  
Liver Lipid Content

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.

Recovery of fertility from adult ovarian tissue transplanted into week-old Japanese quail chicks

2015 ◽  
Vol 27 (2) ◽  
pp. 281 ◽  
Author(s):  
Jianan Liu ◽  
Kimberly M. Cheng ◽  
Frederick G. Silversides
Keyword(s):  
Japanese Quail ◽  
Sexual Maturity ◽  
Egg Production ◽  
In Vitro Maturation ◽  
Ovarian Tissue ◽  
Reproductive Potential ◽  
Special Importance ◽  
Old Japanese ◽  
Cryopreserved Ovarian Tissue

Fertility of cryopreserved ovarian tissue from immature chickens and Japanese quail has been recovered by transplantation. This is of special importance for non-mammalian vertebrates in which cryopreservation and in vitro maturation of oocytes are challenging because their oogenesis is characterised by vitellogenesis. This study tested whether fertility of adult quail ovarian tissue could be recovered by transplantation. Ovaries were isolated from mature Japanese quail hens, trimmed, cut into 3- to 4-mm2 pieces and transplanted into ovariectomised, week-old chicks. Recipients were administered an immunosuppressant for two weeks. Ten of 12 recipients survived until sexual maturity and seven laid eggs, but all stopped laying by 17 weeks of age. The age at first egg of recipients laying eggs (75.7 ± 4.2 days) was greater than that of untreated hens (51.8 ± 1.7 days) and egg production of recipients during the laying period (21.7 ± 5.7) was less than that of untreated hens (60.8 ± 3.5). Recipients were paired with males from the WB line for test mating. Only two hens laid eggs during the test period but both produced 100% donor-derived offspring. This research demonstrated that the reproductive potential of ovarian tissue from adult quail hens can be restored by transplantation.

Effects of ovariectomy and resistance training on lipid content in skeletal muscle, liver, and heart; fat depots; and lipid profile

2009 ◽  
Vol 34 (6) ◽  
pp. 1079-1086 ◽  
Author(s):  
Richard Diego Leite ◽  
Jonato Prestes ◽  
Celene Fernandes Bernardes ◽  
Gilberto Eiji Shiguemoto ◽  
Guilherme Borges Pereira ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Resistance Training ◽  
Lipid Profile ◽  
Lipid Content ◽  
Liver Lipid ◽  
Atherogenic Index ◽  
Ovariectomized Rats ◽  
Muscle Lipid ◽  
Liver Lipid Content ◽  
Fat Depots

The aim of the present study was to investigate the effects of resistance training on skeletal muscle lipid content, liver lipid content, heart lipid content, fat depots, and lipid profile in ovariectomized rats. Wistar adult female rats were divided into 4 groups (n = 10 per group): sedentary (Sed-Intact), sedentary ovariectomized (Sed-Ovx), strength trained (ChronicEx-intact), and strength trained ovariectomized (ChronicEx-Ovx). A 12-week strength-training period was used, during which the animals climbed a 1.1-m vertical ladder with weights attached to their tails. The sessions were performed once every 3 days, with 4–9 climbs and 8–12 dynamic movements per climb. Ovariectomy increased liver lipid content and fat depots, and heart and muscle lipid content. There was an increase in the atherogenic index and a negative change in lipid profile because of the ovariectomy. Resistance training decreased lipid content in the liver, soleus, and tibialis anterior, decreased fat depots (mesenteric and retroperitoneal), and changed the lipid profile, independently of ovarian hormone status. These results indicate the potential benefits of resistance training as an alternative strategy to control the effects of ovariectomy on fat depot, lipid profile, and tissue lipid content.

scholarly journals Adipocyte JAK2 Regulates Hepatic Insulin Sensitivity Independently of Body Composition, Liver Lipid Content, and Hepatic Insulin Signaling

Diabetes ◽  
2017 ◽  
Vol 67 (2) ◽  
pp. 208-221 ◽  
Author(s):  
Kevin C. Corbit ◽  
João Paulo G. Camporez ◽  
Lia R. Edmunds ◽  
Jennifer L. Tran ◽  
Nicholas B. Vera ◽  
...  
Keyword(s):  
Body Composition ◽  
Insulin Sensitivity ◽  
Lipid Content ◽  
Insulin Signaling ◽  
Liver Lipid ◽  
Hepatic Insulin Sensitivity ◽  
Liver Lipid Content ◽  
Hepatic Insulin Signaling
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