scholarly journals Influence of Orotic Acid on Performance, Liver Lipid Content, and Egg Cholesterol Level of Laying Hens

1991 ◽  
Vol 70 (11) ◽  
pp. 2322-2328 ◽  
Author(s):  
R. SCOTT BEYER ◽  
LEO S. JENSEN
1982 ◽  
Vol 112 (2) ◽  
pp. 299-308 ◽  
Author(s):  
Yukio Akiba ◽  
L. S. Jensen ◽  
C. R. Barb ◽  
R. R. Kraeling

1975 ◽  
Vol 54 (3) ◽  
pp. 806-813 ◽  
Author(s):  
J.D. Garlich ◽  
J.D. Olson ◽  
W.E. Huff ◽  
P.B. Hamilton

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.


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.


2009 ◽  
Vol 34 (6) ◽  
pp. 1079-1086 ◽  
Author(s):  
Richard Diego Leite ◽  
Jonato Prestes ◽  
Celene Fernandes Bernardes ◽  
Gilberto Eiji Shiguemoto ◽  
Guilherme Borges Pereira ◽  
...  

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.


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 ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document