scholarly journals The influence of vitamin A status on the response of chickens to aflatoxin B1 and changes in liver lipid metabolism associated with aflatoxicosis

1979 ◽  
Vol 41 (3) ◽  
pp. 529-540 ◽  
Author(s):  
W. L. Bryden ◽  
R. B. Cumming ◽  
D. Balnave
Keyword(s):  
Amino Acid ◽  
Body Weight Gain ◽  
Liver Lipid ◽  
Liver Weight ◽  
Metabolizing Enzymes ◽  
Vitamin A Status ◽  
Liver Lipid Metabolism ◽  
Series Of Experiments ◽  
Liver Lipid Concentration ◽  
Aflatoxin B

1 A series of experiments were conducted to investigate the effects of dietary retinol status on chickens ingesting aflatoxin B1. The effects of dietary supplementation with biotin and α-tocopherol were also examined.2. Aflatoxin B1 levels greater than I mg/kg diet had a detrimental effect on ‘liveability’, body-weight gain, food intake and food conversion efficiency. When fed for more than 2 weeks aflatoxin increased relative liver weight and liver lipid concentration. These effects were less pronounced with avitaminotic A chickens.3. A synergistic effect on hydropericardium development was observed between aflatoxin B, and retinol. This effect was not observed when the dietary level of α-tocopherol was increased tenfold.4. The specific activities of certain hepatic lipogenic and amino acid-metabolizing enzymes were influenced by aflatoxin ingestion. A reduction in lipogenic enzyme activity was observed before a reduction in the activities of amino acid-metabolizing enzymes.5. Liver fatty acid composition was significantly influenced by aflatoxin B1. The extent of these changes was reduced by the inclusion of additional dietary biotin.

scholarly journals The influence of essential fatty acids and food restriction on the specific activities of hepatic lipogenic and glutamate-metabolizing enzymes in the laying hen

1975 ◽  
Vol 33 (3) ◽  
pp. 439-445 ◽  
Author(s):  
D. Balnave
Keyword(s):  
Essential Fatty Acids ◽  
Liver Lipid ◽  
Feeding Time ◽  
Lipid Concentration ◽  
Deficient Diet ◽  
Liver Size ◽  
Metabolizing Enzymes ◽  
Daily Food ◽  
Specific Activities ◽  
Liver Lipid Concentration

1. Extended feeding of an essential fatty acid (EFA)-deficient diet to laying hens increased liver size and liver lipid concentration.2. The specific activities of hepatic lipogenic and glutamate-metabolizing enzymes were increased by feeding the EFA-deficient diet.3. Restriction of daily food intake to 75 % of ad lib. intake did not affect the response to dietary fat concentration.4. Hepatic enzyme activities in hens fed on restricted amounts of food and killed just before, or after, the normal daily feeding time indicated no reduced capacity for lipogenesis at the earlier time.

scholarly journals Sulfur amino acid deficiency upregulates intestinal methionine cycle activity and suppresses epithelial growth in neonatal pigs

2009 ◽  
Vol 296 (6) ◽  
pp. E1239-E1250 ◽  
Author(s):  
Caroline Bauchart-Thevret ◽  
Barbara Stoll ◽  
Shaji Chacko ◽  
Douglas G. Burrin
Keyword(s):  
Amino Acid ◽  
Body Weight Gain ◽  
Liver Weight ◽  
Methionine Synthase ◽  
Whole Body ◽  
Sulfur Amino Acid ◽  
Ki 67 ◽  
Neonatal Pigs ◽  
Methionine Cycle ◽  
Epithelial Growth

We recently showed that the developing gut is a significant site of methionine transmethylation to homocysteine and transsulfuration to cysteine. We hypothesized that sulfur amino acid (SAA) deficiency would preferentially reduce mucosal growth and antioxidant function in neonatal pigs. Neonatal pigs were enterally fed a control or an SAA-free diet for 7 days, and then whole body methionine and cysteine kinetics were measured using an intravenous infusion of [1-13C;methyl-2H3]methionine and [15N]cysteine. Body weight gain and plasma methionine, cysteine, homocysteine, and taurine and total erythrocyte glutathione concentrations were markedly decreased (−46% to −85%) in SAA-free compared with control pigs. Whole body methionine and cysteine fluxes were reduced, yet methionine utilization for protein synthesis and methionine remethylation were relatively preserved at the expense of methionine transsulfuration, in response to SAA deficiency. Intestinal tissue concentrations of methionine and cysteine were markedly reduced and hepatic levels were maintained in SAA-free compared with control pigs. SAA deficiency increased the activity of methionine metabolic enzymes, i.e., methionine adenosyltransferase, methionine synthase, and cystathionine β-synthase, and S-adenosylmethionine concentration in the jejunum, whereas methionine synthase activity increased and S-adenosylmethionine level decreased in the liver. Small intestine weight and protein and DNA mass were lower, whereas liver weight and DNA mass were unchanged, in SAA-free compared with control pigs. Dietary SAA deficiency induced small intestinal villus atrophy, lower goblet cell numbers, and Ki-67-positive proliferative crypt cells in association with lower tissue glutathione, especially in the jejunum. We conclude that SAA deficiency upregulates intestinal methionine cycle activity and suppresses epithelial growth in neonatal pigs.

scholarly journals Dysregulated liver lipid metabolism and innate immunity associated with hepatic steatosis in neonatal BBdp rats and NOD mice

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
D. Serrano ◽  
J. A. Crookshank ◽  
B. S. Morgan ◽  
R. W. Mueller ◽  
M.-F. Paré ◽  
...  
Keyword(s):  
Innate Immunity ◽  
Lipid Metabolism ◽  
Hepatic Steatosis ◽  
Liver Lipid ◽  
Nod Mice ◽  
Gene Signature ◽  
Enhanced Expression ◽  
Liver Lipid Metabolism ◽  
Hepatic Innate Immunity ◽  
Lipid Metabolism Genes

Abstract In a previous study we reported that prediabetic rats have a unique gene signature that was apparent even in neonates. Several of the changes we observed, including enhanced expression of pro-inflammatory genes and dysregulated UPR and metabolism genes were first observed in the liver followed by the pancreas. In the present study we investigated further early changes in hepatic innate immunity and metabolism in two models of type 1 diabetes (T1D), the BBdp rat and NOD mouse. There was a striking increase in lipid deposits in liver, particularly in neonatal BBdp rats, with a less striking but significant increase in neonatal NOD mice in association with dysregulated expression of lipid metabolism genes. This was associated with a decreased number of extramedullary hematopoietic clusters as well as CD68+ macrophages in the liver of both models. In addition, PPARɣ and phosphorylated AMPKα protein were decreased in neonatal BBdp rats. BBdp rats displayed decreased expression of antimicrobial genes in neonates and decreased M2 genes at 30 days. This suggests hepatic steatosis could be a common early feature in development of T1D that impacts metabolic homeostasis and tolerogenic phenotype in the prediabetic liver.

scholarly journals Circulating Levels of Pro-Neurotensin and Its Relationship with Nonalcoholic Steatohepatitis and Hepatic Lipid Metabolism

Metabolites ◽  
2021 ◽  
Vol 11 (6) ◽  
pp. 373
Author(s):  
Beatriz Villar ◽  
Laia Bertran ◽  
Carmen Aguilar ◽  
Jessica Binetti ◽  
Salomé Martínez ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Nonalcoholic Steatohepatitis ◽  
Liver Lipid ◽  
Normal Liver ◽  
Normal Weight ◽  
Published Data ◽  
Mrna Levels ◽  
Nonalcoholic Fatty Liver ◽  
Hepatic Expression ◽  
Liver Lipid Metabolism

Recent studies suggest a link between pro-neurotensin (pro-NT) and nonalcoholic fatty liver disease (NAFLD), but the published data are conflicting. Thus, we aimed to analyze pro-NT levels in women with morbid obesity (MO) and NAFLD to investigate if this molecule is involved in NAFLD and liver lipid metabolism. Plasma levels of pro-NT were determined in 56 subjects with MO and 18 with normal weight (NW). All patients with MO were subclassified according to their liver histology into the normal liver (NL, n = 20) and NAFLD (n = 36) groups. The NAFLD group had 17 subjects with simple steatosis (SS) and 19 with nonalcoholic steatohepatitis (NASH). We used a chemiluminescence sandwich immunoassay to quantify pro-NT in plasma and RT-qPCR to evaluate the hepatic mRNA levels of several lipid metabolism-related genes. We reported that pro-NT levels were significantly higher in MO with NAFLD than in MO without NAFLD. Additionally, pro-NT levels were higher in NASH patients than in NL. The hepatic expression of lipid metabolism-related genes was found to be altered in NAFLD, as previously reported. Additionally, although pro-NT levels correlated with LDL, there was no association with the main lipid metabolism-related genes. These findings suggest that pro-NT could be related to NAFLD progression.

scholarly journals 146 Prematurity Blunts the Protein Synthetic Response of Skeletal Muscle to Insulin and Amino Acids

2020 ◽  
Vol 98 (Supplement_4) ◽  
pp. 118-119
Author(s):  
Teresa A Davis ◽  
Marko Rudar ◽  
Jane Naberhuis ◽  
Agus Suryawan ◽  
Marta Fiorotto
Keyword(s):  
Skeletal Muscle ◽  
Amino Acids ◽  
Protein Synthesis ◽  
Amino Acid ◽  
Body Weight Gain ◽  
Human Infant ◽  
Long Term Effects ◽  
Plasma Insulin Concentration ◽  
Akt Phosphorylation ◽  
Relative Body Weight

Abstract Livestock animals are important dual-purpose models that benefit both agricultural and biomedical research. The neonatal pig is an appropriate model for the human infant to assess long-term effects of early life nutrition on growth and metabolic outcomes. Previously we have demonstrated that prematurity blunts the feeding-induced stimulation of translation initiation and protein synthesis in skeletal muscle of neonatal pigs. The objective of this study was to determine whether reduced sensitivity to insulin and/or amino acids drives this blunted response. Pigs were delivered by caesarean section at preterm (PT, 103 d gestation) or at term (T, 112 d gestation) and fed parenterally for 4 d. On day 4, pigs were subject to euinsulinemic-euaminoacidemic-euglycemic (FAST), hyperinsulinemic-euaminoacidemic-euglycemic (INS), or euinsulinemic-hyperaminoacidemic-euglycemic (AA) clamps for 120 min, yielding six treatments: PT-FAST (n = 7), PT-INS (n = 9), PT-AA (n = 9), T-FAST (n = 8), T-INS (n = 9), and T-AA (n = 9). A flooding dose of L-[4-3H]Phe was injected into pigs 30 min before euthanasia. Birth weight and relative body weight gain were lower in PT than T pigs (P < 0.001). Plasma insulin concentration was increased from ~3 to ~100 µU/mL in INS compared to FAST and AA pigs (P < 0.001); plasma BCAA concentration was increased from ~250 to ~1,000 µmol/L in AA compared to FAST and INS pigs (P < 0.001). Despite achieving similar insulin and amino acid levels, longissimus dorsi AKT phosphorylation, mechanistic target of rapamycin (mTOR)·Rheb abundance, mTOR activation, and protein synthesis were lower in PT-INS than T-INS pigs (Table 1). Although amino-acid induced dissociation of Sestrin2 from GATOR2 was not affected by prematurity, mTOR·RagA abundance, mTOR·RagC abundance, mTOR activation, and protein synthesis were lower in PT-AA than T-AA pigs. The impaired capacity of premature skeletal muscle to respond to insulin or amino acids and promote protein synthesis likely contributes to reduced lean mass accretion. Research was supported by NIH and USDA.

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.

scholarly journals Saturated fat-rich diet increases fetal lipids and modulates LPL and leptin receptor expression in rat placentas

2013 ◽  
Vol 217 (3) ◽  
pp. 303-315 ◽  
Author(s):  
M B Mazzucco ◽  
R Higa ◽  
E Capobianco ◽  
M Kurtz ◽  
A Jawerbaum ◽  
...  
Keyword(s):  
Leptin Receptor ◽  
Fetal Liver ◽  
Liver Lipid ◽  
Saturated Fat ◽  
Receptor Expression ◽  
Lipid Concentration ◽  
Old Rats ◽  
Liver Lipid Concentration ◽  
Leptin Expression ◽  
Layer Chromatography

Metabolic alterations in obese and overweight mothers impact the placenta and the fetus, leading to anomalies in fetal growth and lipid accretion. The primary aim of the study was to examine the effect of a saturated fat-rich diet (FD) on growth, lipid accretion, and lipases, leptin and leptin receptor (ObR) expression in the placenta and fetal liver. We also aimed to find a role for fetal leptin in the modulation of placental and fetal liver lipase and ObR expression. Six-week-old rats were fed with a standard rat chow (control) or a 25% FD for 7 weeks until mating and during pregnancy. Also, in a group of control rats, fetuses were injected with leptin on days 19, 20, and 21 of pregnancy. On day 21, we assessed lipidemia, insulinemia, and leptinemia in mothers and fetuses. In the placenta and fetal liver, lipid concentration was assessed by thin layer chromatography (TLC) and the gene expression of lipoprotein lipase (LPL), endothelial lipase, insulin receptor (Insr), leptin, and ObR by RT-PCR. The FD induced hypertriglyceridemia and hyperleptinemia (P<0.01) in mothers and fetuses, an increase in maternal (P<0.05) and fetal weight (P<0.01), overaccumulation of lipids in fetal liver (P<0.01), and enhanced leptin expression in the placenta and fetal liver (P<0.05). Placental expression of IR and LPL was increased (P<0.05), and ObR decreased (P<0.05) in the FD group. Fetal administration of leptin induced the placental and fetal liver downregulation of ObR (P<0.05) and upregulation of LPL expression (P<0.05). The FD led to increased fetal lipid levels, which may result from high maternal lipid availability and fetal leptin effects.

Abstract 037: Role of Pro-opiomelanocortin (POMC) Specific PTP1B in Differential Regulation of Blood Pressure, Liver Lipid Accumulation and Glucose Tolerance in Response to a High Fat Diet

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Nicola Aberdein ◽  
Jussara M do Carmo ◽  
Zhen Wang ◽  
Taolin Fang ◽  
Cecilia P de Lara ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Glucose Tolerance ◽  
Fat Mass ◽  
Lipid Accumulation ◽  
High Fat Diet ◽  
Acute Stress ◽  
Liver Lipid ◽  
Liver Weight ◽  
Metabolic Effects ◽  
High Fat

Obese subjects are often resistant to leptin’s metabolic effects although blood pressure (BP) and sympathetic nervous system responses appear to be preserved. Protein tyrosine phosphatase 1B (PTP1B), a negative regulator of leptin signaling, may play a role in promoting this selective leptin resistance and causing metabolic dysfunction in obesity. Our previous studies suggest that the chronic BP responses to leptin are mediated via activation of pro-opiomelanocortin (POMC) neurons. The goal of this study was to determine if PTP1B in POMC neurons differentially controls metabolic functions and BP in mice fed a high fat diet (HFD). Male mice with POMC specific PTP1B deletion (POMC/PTP1B -/- ) and littermate controls (PTP1B flox/flox ) were fed a HFD from 6 to 22 wks of age. Baseline BP after 16 weeks of a HFD (95±2 vs. 95±3 mmHg) and BP responses to acute stress (Δ32±0 vs. Δ32±6 mmHg), measured by telemetry, were not different in POMC/PTP1B -/- compared to control mice, respectively. Heart rate (HR) was not different in POMC/PTP1B -/- and control mice during acute stress (699±4 vs. 697±15 bpm, respectively). Total body weight (TBW) and fat mass were reduced at 20 weeks of age in POMC/PTP1B -/- compared to controls (36.7±0.1 vs. 42.0±1 g TBW and 12.7±0.4 vs. 16.1±1.0 g fat mass, respectively). Liver weight of POMC/PTP1B -/- mice was less than in controls, and this was evident even when liver weight was normalized as % of TBW (4.5±0.2 vs. 5.0±0.2 %). POMC/PTP1B -/- males had reduced liver lipid accumulation compared to controls as measured by EchoMRI (0.08±0.03 vs. 0.15±0.03 g/g liver weight). Glucose tolerance was also improved by 46% in POMC/PTP1B -/- compared to controls as measured by AUC, 25856±1683 vs. 47267±5616 mg/dLx120min, respectively. These findings indicate that PTP1B signaling in POMC neurons plays a crucial role in regulating liver lipid accumulation and glucose tolerance but does not appear to mediate changes in BP or BP responses to acute stress in mice fed a high HFD (supported by NHLBI-PO1HL51971 and NIGMS P20GM104357)

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