scholarly journals Effect of Selenium and Lipotropic Factors on Liver Fat Accumulation in Laying Hens ,

1974 ◽  
Vol 53 (1) ◽  
pp. 296-302 ◽  
Author(s):  
L.S. Jensen ◽  
G.W. Schumaier ◽  
A.D. Funk ◽  
T.C. Smith ◽  
L. Falen
Keyword(s):  
Laying Hens ◽  
Liver Fat ◽  
Fat Accumulation

scholarly journals Effect of Distillers Dried Grain with Solubles on Reproduction and Liver Fat Accumulation in Laying Hens

1974 ◽  
Vol 53 (2) ◽  
pp. 586-592 ◽  
Author(s):  
L.S. Jensen ◽  
L. Falen ◽  
C.H. Chang
Keyword(s):  
Laying Hens ◽  
Liver Fat ◽  
Fat Accumulation

scholarly journals Iron status influences non-alcoholic fatty liver disease in obesity through the gut microbiome

Microbiome ◽  
2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Jordi Mayneris-Perxachs ◽  
Marina Cardellini ◽  
Lesley Hoyles ◽  
Jèssica Latorre ◽  
Francesca Davato ◽  
...  
Keyword(s):  
Serum Ferritin ◽  
Iron Metabolism ◽  
Gut Microbiome ◽  
Fatty Liver Disease ◽  
Iron Status ◽  
Liver Fat ◽  
Alcoholic Fatty Liver ◽  
Fat Accumulation ◽  
Glycine Transporters ◽  
Alcoholic Fatty Liver Disease

Abstract Background The gut microbiome and iron status are known to play a role in the pathophysiology of non-alcoholic fatty liver disease (NAFLD), although their complex interaction remains unclear. Results Here, we applied an integrative systems medicine approach (faecal metagenomics, plasma and urine metabolomics, hepatic transcriptomics) in 2 well-characterised human cohorts of subjects with obesity (discovery n = 49 and validation n = 628) and an independent cohort formed by both individuals with and without obesity (n = 130), combined with in vitro and animal models. Serum ferritin levels, as a markers of liver iron stores, were positively associated with liver fat accumulation in parallel with lower gut microbial gene richness, composition and functionality. Specifically, ferritin had strong negative associations with the Pasteurellaceae, Leuconostocaceae and Micrococcaea families. It also had consistent negative associations with several Veillonella, Bifidobacterium and Lactobacillus species, but positive associations with Bacteroides and Prevotella spp. Notably, the ferritin-associated bacterial families had a strong correlation with iron-related liver genes. In addition, several bacterial functions related to iron metabolism (transport, chelation, heme and siderophore biosynthesis) and NAFLD (fatty acid and glutathione biosynthesis) were also associated with the host serum ferritin levels. This iron-related microbiome signature was linked to a transcriptomic and metabolomic signature associated to the degree of liver fat accumulation through hepatic glucose metabolism. In particular, we found a consistent association among serum ferritin, Pasteurellaceae and Micrococcacea families, bacterial functions involved in histidine transport, the host circulating histidine levels and the liver expression of GYS2 and SEC24B. Serum ferritin was also related to bacterial glycine transporters, the host glycine serum levels and the liver expression of glycine transporters. The transcriptomic findings were replicated in human primary hepatocytes, where iron supplementation also led to triglycerides accumulation and induced the expression of lipid and iron metabolism genes in synergy with palmitic acid. We further explored the direct impact of the microbiome on iron metabolism and liver fact accumulation through transplantation of faecal microbiota into recipient’s mice. In line with the results in humans, transplantation from ‘high ferritin donors’ resulted in alterations in several genes related to iron metabolism and fatty acid accumulation in recipient’s mice. Conclusions Altogether, a significant interplay among the gut microbiome, iron status and liver fat accumulation is revealed, with potential significance for target therapies.

scholarly journals Empaglifozin induces changes in the liver metabolome of diabetic rats

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
A Aragon Herrera ◽  
S Feijoo-Bandin ◽  
M Otero Santiago ◽  
S Moranha Fernandez ◽  
L Anido Varela ◽  
...  
Keyword(s):  
Amino Acids ◽  
Liver Fibrosis ◽  
Diabetic Rats ◽  
Liver Fat ◽  
Favorable Effect ◽  
Funding Source ◽  
Metabolomics Data ◽  
Fat Accumulation ◽  
Glucose Levels ◽  
The Impact

Abstract Background Empagliflozin is a potent, highly selective sodium glucose cotransporter-2 (SGLT2) inhibitor used as an effective and well-tolerated antihyperglycaemic agent. Beyond lowering glucose, empagliflozin exerts a favorable effect on a number of nonglycaemic outcomes, including modest reductions in bodyweight and blood pressure, and it has cardioprotective and renoprotective properties in patients with T2D and established cardiovascular disease (EMPA-REG OUTCOME). Purpose Since liver fat content represents a risk factor for cardiovascular diseases, and empagliflozin has been recently suggested to be able to contribute to the early treatment of nonalcoholic fatty liver disease in T2D, we aimed to study the effect of the empagliflozin treatment in the liver metabolome of type 2 diabetic rats. Methods Male ZDF-Leprfa/fa rats were treated with 30 mg/kg/d of empagliflozin p.o for six weeks. Metabolic profiling of the hepatic tissue was analyzed using UHPLC-MS based platforms. We performed a hematoxylin/eosin staining to determine the tissue integrity and liver fat accumulation, and a Masson's trichrome staining to analyze liver fibrosis. All animals were maintained and euthanized following protocols approved by the Animal Care Committee of the University of Santiago de Compostela in accordance with European Union Directive 2010/63. Results Empaglifozin treatment reduced blood glucose levels to normal (128.2±6.51 mg/dL), while untreated control rats showed high glucose levels (404.3±17.49 mg/dL). Hepatic histological analysis did not show differences regarding neither fat accumulation nor fibrosis between empagliflozin treated and control rats. Circulating levels of cholesterol, HDL, LDL, GTP, GGT triglycerides remained unaltered after empaglifozin treatment vs. control. 384 metabolites were analyzed in the liver tissue samples, observing significantly increased levels of 10 types of glycerolipids, 24 phosphatidylcholines, 8 amino acids, 1 polyunsaturated fatty acid, 4 lysophosphatidylethanolamines, 7 lysophosphatidylinositols, 1 carboxylic acid and 1 nucleoside in the empagliflozin treated rats with respect to the control group. In addition, treatment with empagliflozin produced a significant decrease of 1 glycerolipid, 1 phosphatidylcholine, 1 bile acid, 1 nucleoside and the NAD oxidoreduction coenzyme. Conclusions We demonstrated that empagliflozin significantly modify the liver content of the different lipid species, with the most relevant altered metabolic classes belonging to glycerophospholipids, especially monoacyl-species, and aromatic amino acids. Considering the suggested potential beneficial effect of the treatment with empagliflozin in the prevention of liver fibrosis, our metabolomics data can help to evaluate the impact and the mechanism of action of SGLT2 inhibitors at hepatic level. Funding Acknowledgement Type of funding source: Private company. Main funding source(s): Boehringer Ingelheim

scholarly journals Effect of Dietary Cereal Grain, Citrus Penctin, and Guar Gum on Liver Fat in Laying Hens and Young Chicks

1981 ◽  
Vol 60 (3) ◽  
pp. 631-636 ◽  
Author(s):  
M.B. PATEL ◽  
J. MCGINNIS ◽  
M.H. PUBOLS
Keyword(s):  
Guar Gum ◽  
Laying Hens ◽  
Liver Fat ◽  
Cereal Grain ◽  
Young Chicks

scholarly journals Effects of Exercise Training on Molecular Markers of Lipogenesis and Lipid Partitioning in Fructose-Induced Liver Fat Accumulation

2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Siham Yasari ◽  
Denis Prud'homme ◽  
Frédérique Tesson ◽  
Marek Jankowski ◽  
Jolanta Gutkowska ◽  
...  
Keyword(s):  
Gene Expression ◽  
Exercise Training ◽  
Unsaturated Fatty Acids ◽  
Regulatory Element ◽  
Female Rats ◽  
Liver Fat ◽  
Standard Diet ◽  
Fat Accumulation ◽  
High Fructose ◽  
The Impact

The present study was designed to investigate the impact of exercise training on lipogenic gene expression in liver and lipid partitioning following the ingestion of a high fructose load. Female rats were exercise-trained for 8 wk or kept sedentary before being submitted to a fasting/refeeding protocol. Rats were further subdivided as follow: rats were fasted for 24 h, refed a standard diet for 24 h, starved for another 24 h, and refed with a standard or a high-fructose diet 24 h before sacrifice. Fructose refeeding was associated with an increase in hepatic lipid content, endocannabinoid receptor 1, sterol regulatory element-binding protein1c, and stearoyl-CoA desaturase1 gene expression in both Sed and TR rats. However, desaturation indexes measured in liver (C16 : 1/C16 : 0 and C18 : 1/C18 : 0) and plasma (C18 : 1/C18 : 0) were higher (P<0.01) in TR than in Sed rats following fructose refeeding. It is concluded that exercise training does not significantly affect fat accumulation and the molecular expression of genes involved in lipogenesis after fasting and fructose refeeding but does modify the partitioning of lipids so as to provide more unsaturated fatty acids in liver without affecting liver fat content.

Effect of dietary lutein and flax on performance, egg composition and liver status of laying hens

2007 ◽  
Vol 87 (3) ◽  
pp. 365-372 ◽  
Author(s):  
S. Leeson ◽  
L. Caston ◽  
H. Namkung
Keyword(s):  
Laying Hens ◽  
Age Related Macular Degeneration ◽  
Liver Fat ◽  
Age Related ◽  
Long Term Effect ◽  
Early Production ◽  
Egg Composition ◽  
Lutein Content ◽  
Feeding Diets

Lutein is considered a protective nutrient against age-related macular degeneration in humans. An experiment was designed to study the long-term effect of feeding lutein in combination with flaxseed on layer performance, egg parameters, and lutein deposition in eggs and tissues. Laying hens were fed diets with 0 or 10% flax supplemented with 0, 125 or 250 ppm lutein for 11 consecutive 28-d periods beginning at 18 wk of age. Early production was reduced (P < 0.01) by feeding diets with 10% flax and when supplemented with 250 ppm lutein. Diet treatments had no effect on feed intake, egg weight or eggshell deformation. Addition of lutein to the diets significantly (P < 0.01) increased yolk color, and lutein content in the egg, liver, and the preen gland. Egg lutein content increased (P < 0.01) from a basal level of 0.10 mg to 1.60 mg 60g-1 egg by addition of lutein to the diet. Liver fat was lower (P < 0.05) in hens fed 10% flaxseed. Liver hemorrhage score was dramatically reduced (P < 0.01) in birds fed lutein. Key words: egg composition, flaxseed, lutein, layers

Liver fat accumulation is associated with circulating PCSK9

2016 ◽  
Vol 48 (5) ◽  
pp. 384-391 ◽  
Author(s):  
Massimiliano Ruscica ◽  
Nicola Ferri ◽  
Chiara Macchi ◽  
Marica Meroni ◽  
Claudia Lanti ◽  
...  
Keyword(s):  
Liver Fat ◽  
Fat Accumulation

scholarly journals Pregnancy facilitates maternal liver regeneration after partial hepatectomy

2020 ◽  
Vol 318 (4) ◽  
pp. G772-G780
Author(s):  
Joonyong Lee ◽  
Veronica Garcia ◽  
Shashank Manohar Nambiar ◽  
Huaizhou Jiang ◽  
Guoli Dai
Keyword(s):  
Cell Cycle ◽  
Growth Factor ◽  
Liver Resection ◽  
Liver Regeneration ◽  
Partial Hepatectomy ◽  
Liver Fat ◽  
Fat Accumulation ◽  
Positive Effects ◽  
Maternal Liver ◽  
Hepatic Fat

Liver resection induces robust liver regrowth or regeneration to compensate for the lost tissue mass. In a clinical setting, pregnant women may need liver resection without terminating pregnancy in some cases. However, how pregnancy affects maternal liver regeneration remains elusive. We performed 70% partial hepatectomy (PH) in nonpregnant mice and gestation day 14 mice, and histologically and molecularly compared their liver regrowth during the next 4 days. We found that compared with the nonpregnant state, pregnancy altered the molecular programs driving hepatocyte replication, indicated by enhanced activities of epidermal growth factor receptor and STAT5A, reduced activities of cMet and p70S6K, decreased production of IL-6, TNFα, and hepatocyte growth factor, suppressed cyclin D1 expression, increased cyclin A1 expression, and early activated cyclin A2 expression. As a result, pregnancy allowed the remnant hepatocytes to enter the cell cycle at least 12 h earlier, increased hepatic fat accumulation, and enhanced hepatocyte mitosis. Consequently, pregnancy ameliorated maternal liver regeneration following PH. In addition, a report showed that maternal liver regrowth after PH is driven mainly by hepatocyte hypertrophy rather than hyperplasia during the second half of gestation in young adult mice. In contrast, we demonstrate that maternal liver relies mainly on hepatocyte hyperplasia instead of hypertrophy to restore the lost mass after PH. Overall, we demonstrate that pregnancy facilitates maternal liver regeneration likely via triggering an early onset of hepatocyte replication, accumulating excessive liver fat, and promoting hepatocyte mitosis. The results from our current studies enable us to gain more insights into how maternal liver regeneration progresses during gestation. NEW & NOTEWORTHY We demonstrate that pregnancy may generate positive effects on maternal liver regeneration following partial hepatectomy, which are manifested by early entry of the cell cycle of remnant hepatocytes, increased hepatic fat accumulation, enhanced hepatocyte mitosis, and overall accelerated liver regrowth.

scholarly journals Sphingosine 1-Phosphate Receptor Blockade Affects Pro-Inflammatory Bone Marrow-Derived Macrophages and Relieves Mouse Fatty Liver Injury

2019 ◽  
Vol 20 (19) ◽  
pp. 4695 ◽  
Author(s):  
Jingjing Yang ◽  
Na Chang ◽  
Le Yang ◽  
Xiaofang Ji ◽  
Xuan Zhou ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Liver Injury ◽  
Fatty Liver ◽  
Pathological Process ◽  
Liver Fat ◽  
Inflammatory Factor ◽  
Gene Expressions ◽  
Fat Accumulation ◽  
Sphingosine 1 Phosphate

Fatty liver injury is characterized by liver fat accumulation and results in serious health problems worldwide. There is no effective treatment that reverses fatty liver injury besides etiological therapy. Inflammation is an important macrophage-involving pathological process of liver injury. Here, we investigated the role of sphingosine 1-phosphate receptors (S1PRs) in fatty liver injury and explored whether S1PR2/3 blockade could cure fatty liver injury. A methionine-choline-deficient and a high-fat (MCDHF) diet was used to induce fatty liver injury, and the number of macrophages was evaluated by flow cytometry. Gene expressions were detected using RT-qPCR and cytometric bead array. In MCDHF-diet-fed mice, pro-inflammatory factor expressions were upregulated by fatty liver injury. The S1P level and S1PR2/3 expressions were significantly elevated. Moreover, increased S1P level and S1PR2/3 mRNA expressions were positively correlated with pro-inflammatory factor expressions in the liver. Furthermore, the number of pro-inflammatory macrophages (iMφ) increased in injured liver, and they were mainly bone-marrow-derived macrophages. In vivo, S1PR2/3 blockade decreased the amount of iMφ and inflammation and attenuated liver injury and fibrosis, although liver fat accumulation was unchanged. These data strongly suggest that anti-inflammatory treatment by blocking the S1P/S1PR2/3 axis attenuates fatty liver injury, which might serve as a potential target for fatty liver injury.

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