Log in

Relevant bibliographies by topics / Fatty liver syndrome of chickens / Journal articles

To see the other types of publications on this topic, follow the link: Fatty liver syndrome of chickens.

Journal articles on the topic 'Fatty liver syndrome of chickens'

Author: Grafiati

Published: 4 June 2021

Last updated: 5 February 2022

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the top 50 journal articles for your research on the topic 'Fatty liver syndrome of chickens.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.

1

Tan, Xiaodong, Ranran Liu, Siyuan Xing, Yonghong Zhang, Qinghe Li, Maiqing Zheng, Guiping Zhao, and Jie Wen. "Genome-Wide Detection of Key Genes and Epigenetic Markers for Chicken Fatty Liver." International Journal of Molecular Sciences 21, no. 5 (March 5, 2020): 1800. http://dx.doi.org/10.3390/ijms21051800.

Full text

Abstract:

Chickens are one of the most important sources of meat worldwide, and the occurrence of fatty liver syndrome (FLS) is closely related to production efficiency. However, the potential mechanism of FLS remains poorly understood. An integrated analysis of data from whole-genome bisulfite sequencing and long noncoding RNA (lncRNA) sequencing was conducted. A total of 1177 differentially expressed genes (DEGs) and 1442 differentially methylated genes (DMGs) were found. There were 72% of 83 lipid- and glucose-related genes upregulated; 81% of 150 immune-related genes were downregulated in fatty livers. Part of those genes was within differentially methylated regions (DMRs). Besides, sixty-seven lncRNAs were identified differentially expressed and divided into 13 clusters based on their expression pattern. Some lipid- and glucose-related lncRNAs (e.g., LNC_006756, LNC_012355, and LNC_005024) and immune-related lncRNAs (e.g., LNC_010111, LNC_010862, and LNC_001272) were found through a co-expression network and functional annotation. From the expression and epigenetic profiles, 23 target genes (e.g., HAO1, ABCD3, and BLMH) were found to be hub genes that were regulated by both methylation and lncRNAs. We have provided comprehensive epigenetic and transcriptomic profiles on FLS in chicken, and the identification of key genes and epigenetic markers will expand our understanding of the molecular mechanism of chicken FLS.

APA, Harvard, Vancouver, ISO, and other styles

2

Trott, K. A., F. Giannitti, G. Rimoldi, A. Hill, L. Woods, B. Barr, M. Anderson, and A. Mete. "Fatty Liver Hemorrhagic Syndrome in the Backyard Chicken." Veterinary Pathology 51, no. 4 (October 3, 2013): 787–95. http://dx.doi.org/10.1177/0300985813503569.

Full text

APA, Harvard, Vancouver, ISO, and other styles

3

Zhu, Yaling, Huirong Mao, Gang Peng, Qingjie Zeng, Qing Wei, Jiming Ruan, and Jianzhen Huang. "Effect of JAK-STAT pathway in regulation of fatty liver hemorrhagic syndrome in chickens." Animal Bioscience 34, no. 1 (January 1, 2021): 143–53. http://dx.doi.org/10.5713/ajas.19.0874.

Full text

Abstract:

Objective: To explore the molecular mechanisms of fatty liver hemorrhagic syndrome (FLHS) in laying hens, an experiment was conducted to reveal the differences in histopathological observation and gene expression between FLHS group and normal group.Methods: We compared the histopathological difference using hematoxylin and eosin staining and proceeded with RNA sequencing of adipose tissue to search differentially expressed genes and enriched biological processes and pathways. Then we validated the mRNA expression levels by real-time polymerase chain reaction and quantified protein levels in the circulation by enzyme-linked immunosorbent assay.Results: We identified 100 differentially expressed transcripts corresponding to 66 genes (DEGs) were identified between FLHS-affected group and normal group. Seven DEGs were significantly enriched in the immune response process and lipid metabolic process, including phospholipase A2 group V, WAP kunitz and netrin domain containing 2, delta 4-desaturase sphingolipid 2, perilipin 3, interleukin-6 (<i>IL-6</i>), ciliary neurotrophic factor (<i>CNTF</i>), and suppressor of cytokine signaling 3 (<i>SOCS3</i>). And these genes could be the targets of immune response and be involved in metabolic homeostasis during the process of FLHS in laying hens. Based on functional categories of the DEGs, we further proposed a model to explain the etiology and pathogenesis of FLHS. <i>IL-6</i> and <i>SOCS3</i> mediate inflammatory responses and the satiety hormone of leptin, induce dysfunction of Jak-STAT signaling pathway, leading to insulin resistance and lipid metabolic disorders. Conversely, <i>CNTF</i> may reduce tissue destruction during inflammatory attacks and confer protection from inflammation-induced insulin resistance in FLHS chickens.Conclusion: These findings highlight the therapeutic implications of targeting the JAK-STAT pathway. Inhibition of <i>IL6</i> and <i>SOCS3</i> and facilitation of <i>CNTF</i> could serve as a favorable strategy to enhance insulin action and improve glucose homoeostasis, which are of importance for treating obesity-related disorders for chickens.

APA, Harvard, Vancouver, ISO, and other styles

4

Bryden, W. L. "Tissue depletion of biotin in chickens and the development of deficiency lesions and the fatty liver and kidney syndrome." Avian Pathology 20, no. 2 (June 1991): 259–69. http://dx.doi.org/10.1080/03079459108418762.

Full text

APA, Harvard, Vancouver, ISO, and other styles

5

Karikalan, M., M. Asok Kumar, R. Raguvaran, M. Palanivelu, Umesh Dimri, and A. K. Sharma. "Fatty liver kidney syndrome (FLKS) in peafowl chicks (Pavo cristatus) and its management." Indian Journal of Veterinary Pathology 41, no. 4 (2017): 321. http://dx.doi.org/10.5958/0973-970x.2017.00077.3.

Full text

APA, Harvard, Vancouver, ISO, and other styles

6

Bannister, D. W., D. I. Sales, and Alison Lee. "Biotin deficiency and susceptibility to fatty liver and kidney syndrome in broiler chicks: reduced 6-phosphofructokinase (EC 2.7.1.11) activity but normal fructose 2,6-bisphosphate content in birds with hepatomegaly." British Journal of Nutrition 54, no. 2 (September 1985): 535–43. http://dx.doi.org/10.1079/bjn19850138.

Full text

Abstract:

1. In two separate experiments, using different strains, broiler chicks were reared on either a commercial-type chick mash (control) or a fatty liver and kidney syndrome (FLKS)-inducing diet.2. In Expt a, chicks were killed on day 29 and in Expt b, on day 32. Body-weights and liver weights were measured, and values from those given the control ration used to construct a hepatomegaly index by employing a variant of linear discriminant analysis.3. Application of the index to FLKS birds revealed a statistically significant bimodal distribution of liver size.4. The birds with enlarged livers (high index) also possessed metabolic abnormalities in that 6- phosphofructokinase (EC 2. 7. 1. 11; PFK-1) activity (measured at low substrate concentration) was depressed despite the presence of normal, or even slightly elevated fructose 2,6-bisphosphate concentration.5. This indicates the presence of an uncharacterized regulatory mechanism for PFK- 1 in FLKS-susceptible birds.

APA, Harvard, Vancouver, ISO, and other styles

7

PROUDFOOT, F. G., and H. W. HULAN. "THE PERFORMANCE OF ONE NORMAL AND TWO DWARF MEAT MATERNAL GENOTYPES AND THEIR PROGENY AS AFFECTED BY REARING AND ADULT DIETARY TREATMENTS." Canadian Journal of Animal Science 66, no. 1 (March 1, 1986): 245–56. http://dx.doi.org/10.4141/cjas86-025.

Full text

Abstract:

The performances of one normal and two dwarf meat maternal genotypes were compared in a factorial experiment designed to estimate the combined effects of feeding two juvenile diets (low protein (LP) high energy (HE) versus high protein (HP) low energy (LE)) from 106 to 140 days and four adult dietary treatments (LPHE, HPHE, HPLE and an HPLE excluding canola meal) fed from 141 to 420 days. The performance of the three genotypes differed significantly (P < 0.05) for egg production, egg fertility at 322 days, feed efficiency, live body weights and monetary returns less the cost of chicks and feed. One of the dwarf gentoypes exhibited the highest monetary returns. Juvenile dietary treatments had no significant (P > 0.05) effect on the traits measured except age at sexual maturity and female body weights at 154 d. Several traits were affected by the adult dietary treatments including mortality, incidence of fatty liver syndrome, hen-day egg production, feed efficiency up to 322 and 420 days and live body weights. Mortality due to fatty liver syndrome was significantly (P < 0.01) lower among hens fed the high protein, low energy diet without canola meal compared with hens fed the other three adult diets, all of which included canola meal as a feed ingredient. Key words: Dwarf, meat breeders, hens, broilers, diets, fatty liver syndrome, genotypes

APA, Harvard, Vancouver, ISO, and other styles

8

Mirderikvandi, Maryam, Heshmatollah Khosravinia, and Bahman Parizadian Kavan. "Independent and combined effects of Satureja khuzistanica essential oils and acetic acid on prevalence and intensity of fatty liver syndrome in broiler chickens." Journal of Animal Physiology and Animal Nutrition 104, no. 1 (October 17, 2019): 166–77. http://dx.doi.org/10.1111/jpn.13220.

Full text

APA, Harvard, Vancouver, ISO, and other styles

9

Liu, Xueqin, Shailendra Kumar Mishra, Tao Wang, Zhongxian Xu, Xiaoling Zhao, Yan Wang, Huadong Yin, et al. "AFB1 Induced Transcriptional Regulation Related to Apoptosis and Lipid Metabolism in Liver of Chicken." Toxins 12, no. 5 (May 4, 2020): 290. http://dx.doi.org/10.3390/toxins12050290.

Full text

Abstract:

Aflatoxin B1 (AFB1) leads to a major risk to poultry and its residues in meat products can also pose serious threat to human health. In this study, after feeding 165-day-old Roman laying hens for 35 days, the toxic effects of aflatoxin B1 at different concentrations were evaluated. The purpose of this study was to explore the mechanism of liver toxicosis responses to AFB1. We found that highly toxic group exposure resulted in liver fat deposition, increased interstitial space, and hepatocyte apoptosis in laying hens. Furthermore, a total of 164 differentially expressed lnRNAs and 186 differentially expressed genes were found to be highly correlated (Pearson Correlation Coefficient > 0.80, p-value < 0.05) by sequencing the transcriptome of control (CB) and highly toxic group (TB3) chickens. We also identify 29 differentially expressed genes and 19 miRNAs that have targeted regulatory relationships. Based on the liver cell apoptosis and fatty liver syndrome that this research focused on, we found that the highly toxic AFB1 led to dysregulation of the expression of PPARG and BCL6. They are cis-regulated by TU10057 and TU45776, respectively. PPARG was the target gene of gga-miR-301a-3p, gga-miR-301b-3p, and BCL6 was the target gene of gga-miR-190a-3p. In summary, highly toxic AFB1 affects the expression levels of protein-coding genes and miRNAs in the liver of Roman layer hens, as well as the expression level of long non-coding RNA in the liver, which upregulates the expression of PPARG and downregulates the expression of Bcl-6. Our study provides information on possible genetic regulatory networks in AFB1-induced hepatic fat deposition and hepatocyte apoptosis.

APA, Harvard, Vancouver, ISO, and other styles

10

Tramunt, Blandine, Alexandra Montagner, Nguan Soon Tan, Pierre Gourdy, Hervé Rémignon, and Walter Wahli. "Roles of Estrogens in the Healthy and Diseased Oviparous Vertebrate Liver." Metabolites 11, no. 8 (July 30, 2021): 502. http://dx.doi.org/10.3390/metabo11080502.

Full text

Abstract:

The liver is a vital organ that sustains multiple functions beneficial for the whole organism. It is sexually dimorphic, presenting sex-biased gene expression with implications for the phenotypic differences between males and females. Estrogens are involved in this sex dimorphism and their actions in the liver of several reptiles, fishes, amphibians, and birds are discussed. The liver participates in reproduction by producing vitellogenins (yolk proteins) and eggshell proteins under the control of estrogens that act via two types of receptors active either mainly in the cell nucleus (ESR) or the cell membrane (GPER1). Estrogens also control hepatic lipid and lipoprotein metabolisms, with a triglyceride carrier role for VLDL from the liver to the ovaries during oogenesis. Moreover, the activation of the vitellogenin genes is used as a robust biomarker for exposure to xenoestrogens. In the context of liver diseases, high plasma estrogen levels are observed in fatty liver hemorrhagic syndrome (FLHS) in chicken implicating estrogens in the disease progression. Fishes are also used to investigate liver diseases, including models generated by mutation and transgenesis. In conclusion, studies on the roles of estrogens in the non-mammalian oviparous vertebrate liver have contributed enormously to unveil hormone-dependent physiological and physiopathological processes.

APA, Harvard, Vancouver, ISO, and other styles

11

Liu, Zhen, Qinghe Li, Ranran Liu, Guiping Zhao, Yonghong Zhang, Maiqing Zheng, Huanxian Cui, et al. "Expression and methylation of microsomal triglyceride transfer protein and acetyl-CoA carboxylase are associated with fatty liver syndrome in chicken." Poultry Science 95, no. 6 (June 2016): 1387–95. http://dx.doi.org/10.3382/ps/pew040.

Full text

APA, Harvard, Vancouver, ISO, and other styles

12

Choi, Y. I., H. J. Ahn, B. K. Lee, S. T. Oh, B. K. An, and C. W. Kang. "Nutritional and Hormonal Induction of Fatty Liver Syndrome and Effects of Dietary Lipotropic Factors in Egg-type Male Chicks." Asian-Australasian Journal of Animal Sciences 25, no. 8 (June 21, 2012): 1145–52. http://dx.doi.org/10.5713/ajas.2011.11418.

Full text

APA, Harvard, Vancouver, ISO, and other styles

13

PROUDFOOT, F. G., H. W. HULAN, and K. B. McRAE. "EFFECTS OF AGE AT PHOTOPERIOD CHANGE AND DIETARY PROTEIN ON PERFORMANCES OF FOUR DWARF MATERNAL MEAT PARENT GENOTYPES AND THEIR BROILER CHICKEN PROGENY." Canadian Journal of Animal Science 65, no. 1 (March 1, 1985): 113–24. http://dx.doi.org/10.4141/cjas85-012.

Full text

Abstract:

A factorial experiment was conducted with 3030 chickens of four maternal dwarf genotypes mated with normal males to estimate the effects of age at a photoperiod change from 8 to 12 h (daily) at 140 or 154 days, and two levels of dietary protein (15 or 17%) on general performance, incidence of Fatty Liver Syndrome and monetary returns. Three of the four maternal genotypes performed similarly for most traits measured but one genotype exhibited better feed efficency of egg production, produced more eggs and, although the eggs were smaller resulted in the highest monetary returns. Delaying the increase in photoperiod change retarded sexual maturity and reduced egg weight at 203 days and egg specific gravity at 406 days. The 17% protein diet improved egg production (including hatching eggs), feed efficiency of egg production, egg weights; and female body weights at 154 and 446 days of age were also heavier. Dietary protein levels had no effect on mortality (P > 0.05). Mean monetary returns from the sale of table eggs, hatching eggs and salvage meat in excess of the costs of day-old breeder stock and feed, averaged $1.07 more per bird fed the 17% diet. The progeny test revealed significant differences among genotypes for male mortality, male and female body weights, and feed conversion; however, monetary returns over feed and chick cost were similar. The time of change in photoperiod and dietary treatments had no significant effect on the overall performance of broiler progeny but there was a genotype × parental diet interaction for 43 day female body weights. Key words: Dwarfs, meat breeders, hens, broilers, photoperiods, diets

APA, Harvard, Vancouver, ISO, and other styles

14

Cempaka, Anggun Rindang, Sung-Hui Tseng, Kuo-Ching Yuan, Chyi-Huey Bai, Alexey A. Tinkov, Anatoly V. Skalny, and Jung-Su Chang. "Dysregulated Iron Metabolism-Associated Dietary Pattern Predicts an Altered Body Composition and Metabolic Syndrome." Nutrients 11, no. 11 (November 11, 2019): 2733. http://dx.doi.org/10.3390/nu11112733.

Full text

Abstract:

Diet plays an important role in the development of obesity and may contribute to dysregulated iron metabolism (DIM). A cross-sectional survey of 208 adults was conducted in Taipei Medical University Hospital (Taipei, Taiwan). A reduced-rank regression from 31 food groups was used for a dietary pattern analysis. DIM was defined as at least four of the following criteria: serum hepcidin (men >200 ng/mL and women >140 ng/mL), hyperferritinemia (serum ferritin of >300 ng/mL in men and >200 ng/mL in women), central obesity, non-alcoholic fatty liver disease, and two or more abnormal metabolic profiles. Compared to non-DIM patients, DIM patients were associated with an altered body composition and had a 4.52-fold (95% confidence interval (CI): (1.95–10.49); p < 0.001) greater risk of metabolic syndrome (MetS) after adjusting for covariates. A DIM-associated dietary pattern (high intake of deep-fried food, processed meats, chicken, pork, eating out, coffee, and animal fat/skin but low intake of steamed/boiled/raw foods and dairy products) independently predicted central obesity (odds ratio (OR): 1.57; 95% CI: 1.05–2.34; p < 0.05) and MetS (OR: 1.89; 95% CI: 1.07–3.35; p < 0.05). Individuals with the highest DIM pattern scores (tertile 3) had a higher visceral fat mass (%) (β = 0.232; 95% CI: 0.011–0.453; p < 0.05) but lower skeletal muscle mass (%) (β = −1.208; 95% CI: −2.177–−0.239; p < 0.05) compared to those with the lowest DIM pattern scores (tertile 1). In conclusion, a high score for the identified DIM-associated dietary pattern was associated with an unhealthier body composition and a higher risk of MetS.

APA, Harvard, Vancouver, ISO, and other styles

15

Shevchuk, M. O., V. G. Stoyanovskyy, and I. A. Kolomiiets. "Technological stress in poultry." Scientific Messenger of LNU of Veterinary Medicine and Biotechnologies 20, no. 88 (November 13, 2018): 63–68. http://dx.doi.org/10.32718/nvlvet8811.

Full text

Abstract:

The article presents the data of domestic and foreign literature on the changes that occur in the bird of industrial cultivation for the development of technological stress. Stress factors are outlined, among which the most significant for the bird organism is the high density of content, the microclimate of the production premises, the conditions of content and composition of the diet, vaccination, transportation. Investigators include high excitability, fear, aggressiveness, anxiety, fatigue, loss of appetite, and disturbance of behavioral reactions of young chickens, quail, ducks, and industrial growth to inadequate changes in external and internal environmental factors. Common signs of stress in the mature chickens, quails, ducks during the development of technological stress set premature mass maturation, decrease and complete cessation of oviposition, reproductive function, weakening of muscle tone. In stress, the activity of all systems of an organism, directed on self-defense and adaptation to new conditions of existence, strains. A prerequisite for the development of stress-reaction is to strengthen the function of the glands of the inner secretion and especially the hypothalamus system – the anterior part of the pituitary gland – the adrenal cortex. It has been established that in the process of adaptation of the organism to the action of adverse factors the concentration of blood sugar increases due to the cleavage of the glycogen in the liver, the mobilization of lipids from the fat depots increases, the intensity of metabolic processes in the adipose tissue increases, and this ensures an increase in the concentration of fatty acids in the blood. The negative influence of stress factors on resistance, immunological reactivity, microbiocenosis state, functioning of the digestive system, preservation and productivity of the bird population are shown. These states are directly related to the activity of the hormonal and autonomic nervous systems and are determined by nonspecific protective factors of the organism. Different ways of correction of disturbed homeostasis are shown. The effectiveness of the use of probiotics, symbiotics, humic substances in the poultry diet is given to prevent the development of negative stress phenomena in their body. It is proved that the management of the processes of development of adaptive ability of the bird organism is one of the key aspects of the development of the corresponding complex of technological measures of their growing and feeding that is conducive to the increase of economic efficiency. The search for methods for the prevention of stress in poultry farming is aimed at eliminating the etiological factors of stress, the removal of birds resistant to stress, the use in feeding substances that reduce the response to the action of adverse stimuli or increase resistance to the organism. Affecting the formation of adaptive reactions of the bird organism long before the stress, as well as in the development of the adaptive syndrome, it is possible to implement its prophylaxis, that is, to ensure the consistent functioning of all physiological systems and the activation of protective forces through the use of biologically active harmless feed additives in diets.

APA, Harvard, Vancouver, ISO, and other styles

16

Schwehr, Megan, and Mayumi Endo. "Pleurihormonal Pituitary Adenomas Presenting as Acromegaly." Journal of the Endocrine Society 5, Supplement_1 (May 1, 2021): A602. http://dx.doi.org/10.1210/jendso/bvab048.1227.

Full text

Abstract:

Abstract Background: Pleurihormonal pituitary adenomas represent 10-15% of all functioning pituitary adenomas1. One of the rarest combinations is ACTH-GH co-secretion with concomitant acromegaly and Cushing’s disease. Clinical Case: 30-year-old female with type 2 diabetes (A1c 11.4%) developed rapidly progressive peripheral neuropathy. Labs revealed a transaminitis. Hepatic ultrasound revealed fatty infiltration of the liver consistent with steatosis. Patient endorsed life-long “chicken legs”, buffalo hump, and easy bruising. She continued to have worsening paresthesias and stated her teeth were “more translucent”. At an endocrinology visit peripheral muscle wasting, atraumatic bruising at the ankles and toes,and striae on the abdomen, shoulders, breasts, and armpits were noted. She had also noted teeth separation and thinning over time and worsening diffuse joint aches. Lab results showed elevated cortisol value of 8.4 mcg/dl after 1 mg dexamethasone suppression test. 24-hour urine cortisol was elevated (87 ug/24 hrs, nl < 45 ug/24 hrs), confirming the diagnosis of Cushing’s syndrome. ACTH was inappropriately normal (56 pg/mL, nl 7.2 – 63 pg/mL), suggesting ACTH dependency. IGF-1 was elevated twice (328 ng/dL and 391 ng/dL, nl <303 ng/dL), and a GH suppression test was abnormal (GH 1.14 ng/mL at 90 minutes) confirming the diagnosis of acromegaly. Brain MRI revealed a cystic pituitary microadenoma (0.5 x 0.5 x 0.6 cm), and the patient underwent surgical resection via transnasal transsphenoidal pituitary surgery with total tumor removal. Immunostaining was positive for only synaptophysin and ACTH. Postoperative diagnosis of Cushing’s disease was made, with formal diagnosis of acromegaly pending improvement in follow-up IGF-1 levels. Literature reviews have revealed very few cases of pleurihormonal pituitary adenomas presenting with concomitant Cushing’s Syndrome and acromegaly. Roca et. al examined 17 studies which described 20 patients with this condition; only 4 presented with symptoms of both acromegaly and Cushing’s disease. In many cases previously reported, the clinical presentation of Cushing’s syndrome was subtle, often with subclinical Cushing’s syndrome, while patients had florid symptoms of acromegaly.1. Conclusion: This Cushing’s predominant case of a GH-ACTH co-secreting tumor is an incredibly rare presentation for this pleurihormonal pituitary adenoma, which is already a rare diagnosis. References: 1.Roca E, Mattogno PP, Porcelli T, Poliani L, Belotti F, Schreiber A, Maffezzoni F, Fontanella MM, Doglietto F. Plurihormonal ACTH-GH Pituitary Adenoma: Case Report and Systematic Literature Review. World Neurosurg. 2018 Jun;114:e158-e164. PMID: 29501516.

APA, Harvard, Vancouver, ISO, and other styles

17

Soujanya, S., M. Lakshman, and D. Madhuri. "Fatty Liver Haemorrhagic Syndrome in Layers." International Journal of Current Microbiology and Applied Sciences 9, no. 10 (October 10, 2020): 3080–85. http://dx.doi.org/10.20546/ijcmas.2020.910.370.

Full text

APA, Harvard, Vancouver, ISO, and other styles

18

Neuschwander-Tetri, Brent A. "Fatty liver and the metabolic syndrome." Current Opinion in Gastroenterology 23, no. 2 (March 2007): 193–98. http://dx.doi.org/10.1097/mog.0b013e32801421a9.

Full text

APA, Harvard, Vancouver, ISO, and other styles

19

Shimizu, Masanori, Makoto Okumura, Kouichi Yuh, Jiro Oita, and Hiroshi Shimizu. "Ultrasonically Undetectable Fatty Liver in Acute Fatty Liver of Pregnancy and Reye's Syndrome." Journal of Clinical Ultrasound 13, no. 9 (November 1985): 679–82. http://dx.doi.org/10.1002/j.1097-0096.1985.tb00015.x.

Full text

APA, Harvard, Vancouver, ISO, and other styles

20

SOBACK, S., G. ZIV, E. BOGIN, Z. COHEN, and Y. EARON. "Pharmacokinetic changes of several antibiotics in chickens during induced fatty liver." Research in Veterinary Science 43, no. 1 (July 1987): 49–54. http://dx.doi.org/10.1016/s0034-5288(18)30740-9.

Full text

APA, Harvard, Vancouver, ISO, and other styles

21

Oyewale, A. O., and E. B. Sonaiya. "Evaluation of polyunsaturated to saturated fatty acid ratio in the fat of different chicken types Ke." Nigerian Journal of Animal Production 44, no. 5 (December 31, 2020): 104–8. http://dx.doi.org/10.51791/njap.v44i5.1536.

Full text

Abstract:

Samples were taken from the liver and the abdominal fat of the carcasses of male and female broilers (meat type), layers (egg type) and locals (dual purpose type). Lipids were extracted and subjected to volumetric analysis, iodine number determination, thin layer chromatography (TLC)with iodine staining and high performance liquid chromatography – mass spectrometry (HPLC-MS) to determine the polyunsaturated to saturated fatty acid (P/S) ratio. The result showed that female chickens, meat type chickens and abdominal fat samples had higher (P<0.05) lipid quantities than male chickens, layer and dual purpose chickens and liver samples, respectively. The P/S ratio of lipids extracted fromthe abdominal fat and fromthe liver did not differ (P<0.05) fromeach other.

APA, Harvard, Vancouver, ISO, and other styles

22

Gavril, Oana Irina, Lidia Iuliana Arhire, Ovidiu Mitu, Radu Sebastian Gavril, Alexandra Mastaleru, Madalina Ioana Zota, Maria-Magdalena Leon-Constantin, Teodor Vasilcu, Laura Mihalache, and Florin Mitu. "Metabolic Syndrome and Nonalcoholic Fatty Liver Disease." Internal Medicine 16, no. 1 (January 1, 2019): 51–58. http://dx.doi.org/10.2478/inmed-2019-0052.

Full text

Abstract:

AbstractIntroduction. Non-alcoholic fatty liver disease (NAFLD) is regarded as the hepatic expression of the metabolic syndrome, both conditions presenting similar clinical features.Aim. The aim of this study was to evaluate, among diabetic subjects, the relationship between fatty liver load and the presence of metabolic syndrome criteria.Methods. An observational study was conducted on 92 subjects with type 2 diabetes. We followed anthropometric measurments, lipid profile, blood pressure and the degree of hepatic steatosis using ultrasonography.Results. The average age of the study group was 60,38 ± 10,37 years, with an approximately equal distribution by gender (48% male and 52% female). More than half of the subjects presented hypercholesterolemia, hypertriglyceridemia, and low HDL cholesterol level. Most of the patients included in the study had varying degrees of liver fat load (only 9,89% of cases of apparently normal liver on ultrasound), and met the criteria for metabolic syndrome (81,31%). It was found that the frequency of the cases with fatty liver impairment was significantly higher in subjects with metabolic syndrome (32,43% compared to 5,88% for those without metabolic syndrome, p = 0,01) and the frequency of the cases with normal liver were significantly higher in subjects without metabolic syndrome (23,53% to 6,76%, p=0,02).Conclusion. We can say that NAFLD is a risk factor for the presence of metabolic syndrome and it can be considered the hepatic expression of this syndrome.

APA, Harvard, Vancouver, ISO, and other styles

23

Fodor, Miklós. "Role of fatty liver in metabolic syndrome." Orvosi Hetilap 151, no. 35 (August 1, 2010): 1430–33. http://dx.doi.org/10.1556/oh.2010.28897.

Full text

Abstract:

Humán epidemiológiai vizsgálatok, az állatkísérleti modellek azt mutatják, hogy összefüggés van a zsigeri elhízás, a cardiovascularis rizikófaktorok, a dyslipidaemia, inzulinrezisztencia és a 2-es típusú diabetes mellitus között. Az utóbbi időben a figyelem arra irányult, hogy a trigliceridek (TG) túlzott felhalmozódása a májban része a metabolikus szindrómának. Több bizonyíték azt mutatja, hogy a TG felhalmozódása a májban oki tényezőként részt vesz a máj-inzulinrezisztencia kialakulásában normális testsúlyú és mérsékelten túlsúlyos egyéneken.

APA, Harvard, Vancouver, ISO, and other styles

24

Diehl, A. M. "Fatty liver, hypertension, and the metabolic syndrome." Gut 53, no. 7 (July 1, 2004): 923–24. http://dx.doi.org/10.1136/gut.2003.037309.

Full text

APA, Harvard, Vancouver, ISO, and other styles

25

Goyal, Anita, Hobinder Arora, and Sumit Arora. "Prevalence of fatty liver in metabolic syndrome." Journal of Family Medicine and Primary Care 9, no. 7 (2020): 3246. http://dx.doi.org/10.4103/jfmpc.jfmpc_1108_19.

Full text

APA, Harvard, Vancouver, ISO, and other styles

26

Lerchbaum, Elisabeth, Hans-Jürgen Gruber, Verena Schwetz, Albrecht Giuliani, Reinhard Möller, Thomas R. Pieber, and Barbara Obermayer-Pietsch. "Fatty liver index in polycystic ovary syndrome." European Journal of Endocrinology 165, no. 6 (December 2011): 935–43. http://dx.doi.org/10.1530/eje-11-0614.

Full text

Abstract:

IntroductionWomen with polycystic ovary syndrome (PCOS) frequently suffer from metabolic disturbances and might be affected by hepatic steatosis. The fatty liver index (FLI) was developed as a simple and accurate predictor of hepatic steatosis. We aimed to analyze the association of FLI with endocrine and metabolic parameters in a cohort of PCOS and control women.MethodsFLI was calculated using body mass index (BMI), waist circumference, triglycerides, and gamma-glutamyl transferase in 611 PCOS and 139 BMI-matched control women within the same age range. Elevated FLI was defined as >60. Metabolic, endocrine, and anthropometric measurements and oral glucose tolerance tests were performed.ResultsPCOS women had significantly higher FLI levels than control women in age-adjusted analyses (11.4 (4.3–48.8) and 8.8 (3.9–35.0), respectively,P=0.001), whereas fibrosis indices were similar (aspartate amino transferase-to-platelet ratio index) or lower (FIB-4) respectively. In binary logistic regression analysis adjusted for age, odds ratio (OR) for elevated FLI was 2.52 (1.31–4.85),P=0.006, for PCOS women when compared with controls. PCOS women with high FLI levels had an adverse anthropometric, metabolic, and endocrine risk profile. The prevalence of elevated FLI was 88.7% in PCOS women with metabolic syndrome (MS) and 11.3% in PCOS women without MS (P<0.001). In control women, elevated FLI was present in 66.7% of women with MS and 30.8% of women without MS.ConclusionHigh FLI levels are a common finding in obese PCOS women and are closely linked to MS. FLI calculation might be a useful tool for identifying PCOS patients at high risk for metabolic and hepatic disturbances.

APA, Harvard, Vancouver, ISO, and other styles

27

Kim, Donghee, Alexis Touros, and W. Ray Kim. "Nonalcoholic Fatty Liver Disease and Metabolic Syndrome." Clinics in Liver Disease 22, no. 1 (February 2018): 133–40. http://dx.doi.org/10.1016/j.cld.2017.08.010.

Full text

APA, Harvard, Vancouver, ISO, and other styles

28

., Rahim Aydin. "Type of Fatty Acids, Lipoprotein Secretion from Liver and Fatty Liver Syndrome in Laying Hens." International Journal of Poultry Science 4, no. 11 (October 15, 2005): 917–19. http://dx.doi.org/10.3923/ijps.2005.917.919.

Full text

APA, Harvard, Vancouver, ISO, and other styles

29

Cheng, Yuan-Lung, Yuan-Jen Wang, Keng-Hsin Lan, Teh-Ia Huo, Yi-Hsiang Huang, Chien-Wei Su, Wei-Yao Hsieh, et al. "Fatty Liver Index and Lipid Accumulation Product Can Predict Metabolic Syndrome in Subjects without Fatty Liver Disease." Gastroenterology Research and Practice 2017 (2017): 1–12. http://dx.doi.org/10.1155/2017/9279836.

Full text

Abstract:

Background. Fatty liver index (FLI) and lipid accumulation product (LAP) are indexes originally designed to assess the risk of fatty liver and cardiovascular disease, respectively. Both indexes have been proven to be reliable markers of subsequent metabolic syndrome; however, their ability to predict metabolic syndrome in subjects without fatty liver disease has not been clarified.Methods. We enrolled consecutive subjects who received health check-up services at Taipei Veterans General Hospital from 2002 to 2009. Fatty liver disease was diagnosed by abdominal ultrasonography. The ability of the FLI and LAP to predict metabolic syndrome was assessed by analyzing the area under the receiver operating characteristic (AUROC) curve.Results. Male sex was strongly associated with metabolic syndrome, and the LAP and FLI were better than other variables to predict metabolic syndrome among the 29,797 subjects. Both indexes were also better than other variables to detect metabolic syndrome in subjects without fatty liver disease (AUROC: 0.871 and 0.879, resp.), and the predictive power was greater among women.Conclusion. Metabolic syndrome increases the cardiovascular disease risk. The FLI and LAP could be used to recognize the syndrome in both subjects with and without fatty liver disease who require lifestyle modifications and counseling.

APA, Harvard, Vancouver, ISO, and other styles

30

Paster, Michael B., and Alan M. Fudge. "Fatty Liver Syndrome or Normal Chemistry of Egglayers?" Journal of the Association of Avian Veterinarians 6, no. 3 (1992): 139. http://dx.doi.org/10.2307/30136687.

Full text

APA, Harvard, Vancouver, ISO, and other styles

31

OZKAYA, Halit, Abdullah Baris AKCAN, Gokhan AYDEMIR, and Mustafa KUL. "An unusual presentation of Seckel syndrome: Fatty liver." Turkish Journal of Gastroenterology 23, no. 5 (October 1, 2012): 621–23. http://dx.doi.org/10.4318/tjg.2012.0401.

Full text

APA, Harvard, Vancouver, ISO, and other styles

32

Vassilatou, Evangeline. "Nonalcoholic fatty liver disease and polycystic ovary syndrome." World Journal of Gastroenterology 20, no. 26 (2014): 8351. http://dx.doi.org/10.3748/wjg.v20.i26.8351.

Full text

APA, Harvard, Vancouver, ISO, and other styles

33

Polyzos, Stergios A., Dimitrios G. Goulis, and Jannis Kountouras. "Nonalcoholic fatty liver disease and polycystic ovary syndrome." Annals of Hepatology 14, no. 6 (November 2015): 941–43. http://dx.doi.org/10.5604/16652681.1171803.

Full text

APA, Harvard, Vancouver, ISO, and other styles

34

Almeda-Valdés, Paloma, Daniel Cuevas-Ramos, and Carlos Alberto Aguilar-Salinas. "Metabolic syndrome and non-alcoholic fatty liver disease." Annals of Hepatology 8 (2009): S18—S24. http://dx.doi.org/10.1016/s1665-2681(19)31822-8.

Full text

APA, Harvard, Vancouver, ISO, and other styles

35

Diehl, MD, Anna Mae, Jeanne Clarke, MD, and Frederick Brancati, MD. "INSULIN RESISTANCE SYNDROME AND NONALCOHOLIC FATTY LIVER DISEASE." Endocrine Practice 9, Supplement 2 (October 2003): 93–96. http://dx.doi.org/10.4158/ep.9.s2.93.

Full text

APA, Harvard, Vancouver, ISO, and other styles

36

Fehér, János. "1st Congress of Fatty Liver and Metabolic Syndrome." Clinical and Experimental Medical Journal 3, no. 4 (December 2009): 525–642. http://dx.doi.org/10.1556/cemed.3.2009.4.1.

Full text

APA, Harvard, Vancouver, ISO, and other styles

37

Page ACNP-BC, Jeni. "Nonalcoholic fatty liver disease: The hepatic metabolic syndrome." Journal of the American Academy of Nurse Practitioners 24, no. 6 (April 20, 2012): 345–51. http://dx.doi.org/10.1111/j.1745-7599.2012.00716.x.

Full text

APA, Harvard, Vancouver, ISO, and other styles

38

Marchesini, G. "Nonalcoholic fatty liver, steatohepatitis, and the metabolic syndrome." Hepatology 37, no. 4 (April 2003): 917–23. http://dx.doi.org/10.1053/jhep.2003.50161.

Full text

APA, Harvard, Vancouver, ISO, and other styles

39

Rahimi, Robert S., and Carmen Landaverde. "Nonalcoholic Fatty Liver Disease and the Metabolic Syndrome." Nutrition in Clinical Practice 28, no. 1 (January 3, 2013): 40–51. http://dx.doi.org/10.1177/0884533612470464.

Full text

APA, Harvard, Vancouver, ISO, and other styles

40

Marchesini, Giulio, Rebecca Marzocchi, Federica Agostini, and Elisabetta Bugianesi. "Nonalcoholic fatty liver disease and the metabolic syndrome." Current Opinion in Lipidology 16, no. 4 (August 2005): 421–27. http://dx.doi.org/10.1097/01.mol.0000174153.53683.f2.

Full text

APA, Harvard, Vancouver, ISO, and other styles

41

Squires, E. J., and S. Leeson. "Aetiology of fatty liver syndrome in laying hens." British Veterinary Journal 144, no. 6 (November 1988): 602–9. http://dx.doi.org/10.1016/0007-1935(88)90031-0.

Full text

APA, Harvard, Vancouver, ISO, and other styles

42

Gitto, Stefano, and Erica Villa. "Non-Alcoholic Fatty Liver Disease and Metabolic Syndrome after Liver Transplant." International Journal of Molecular Sciences 17, no. 4 (April 2, 2016): 490. http://dx.doi.org/10.3390/ijms17040490.

Full text

APA, Harvard, Vancouver, ISO, and other styles

43

Rompala, R. E., and M. J. Darre. "Effect of albuterol on oxygen uptake and Na+–K+ ATPase activity of jejunal epithelia and liver in chickens." Canadian Journal of Physiology and Pharmacology 67, no. 5 (May 1, 1989): 431–34. http://dx.doi.org/10.1139/y89-069.

Full text

Abstract:

Changes in metabolic characteristics of the liver and jejunal epithelia as a result of feeding the β-agonist albuterol to chickens for 3 and 6 weeks were studied. Feeding albuterol resulted in a change in weights of the liver and small intestines. Chickens fed albuterol for 6 weeks had greater levels of plasma nonesterified fatty acids than those fed the control diet. Oxygen uptake by liver and jejunal epithelial tissues were 25 and 26% greater for chickens fed the diet with albuterol than for those fed the control diet, respectively. No changes in Na+–K+ ATPase activity of both liver and jejunal epithelia were detected as a result of feeding albuterol. These findings indicate that certain β-agonists may elevate thermogenesis in chickens as a result of increasing metabolic rates of splanchnic tissues. However, the changes resulting in altering oxygen uptake in liver and jejunal epithelia due to feeding albuterol were not associated with Na+–K+ ATPase activity.Key words: albuterol, oxygen uptake, Na+–K+ ATPase, chickens.

APA, Harvard, Vancouver, ISO, and other styles

44

Zhang, Lijun, Chunyan Li, Fang Wang, Shenghua Zhou, Mingjun Shangguan, Lina Xue, Bianying Zhang, et al. "Treatment with PPARαAgonist Clofibrate Inhibits the Transcription and Activation of SREBPs and Reduces Triglyceride and Cholesterol Levels in Liver of Broiler Chickens." PPAR Research 2015 (2015): 1–10. http://dx.doi.org/10.1155/2015/347245.

Full text

Abstract:

PPARαagonist clofibrate reduces cholesterol and fatty acid concentrations in rodent liver by an inhibition of SREBP-dependent gene expression. In present study we investigated the regulation mechanisms of the triglyceride- and cholesterol-lowering effect of the PPARαagonist clofibrate in broiler chickens. We observed that PPARαagonist clofibrate decreases the mRNA and protein levels of LXRαand the mRNA and both precursor and nuclear protein levels of SREBP1 and SREBP2 as well as the mRNA levels of the SREBP1 (FASNandGPAM) and SREBP2 (HMGCRandLDLR) target genes in the liver of treated broiler chickens compared to control group, whereas the mRNA level ofINSIG2, which inhibits SREBP activation, was increased in the liver of treated broiler chickens compared to control group. Taken together, the effects of PPARαagonist clofibrate on lipid metabolism in liver of broiler chickens involve inhibiting transcription and activation of SREBPs and SREBP-dependent lipogenic and cholesterologenic gene expression, thereby resulting in a reduction of the triglyceride and cholesterol levels in liver of broiler chickens.

APA, Harvard, Vancouver, ISO, and other styles

45

Shafeghati, Y. "HELLP Syndrome, Acute Fatty Liver of Pregnancy, and Fatty Acids Oxidation Defects." Sarem Journal of Reproductive Medicine 1, no. 4 (October 1, 2016): 187–90. http://dx.doi.org/10.29252/sjrm.1.4.187.

Full text

APA, Harvard, Vancouver, ISO, and other styles

46

Chen, Y. L. "PO212 LIVER FUNCTION TESTS AND METABOLIC SYNDROME IN NON-FATTY LIVER ELDERLY." Diabetes Research and Clinical Practice 106 (November 2014): S156—S157. http://dx.doi.org/10.1016/s0168-8227(14)70506-6.

Full text

APA, Harvard, Vancouver, ISO, and other styles

47

Hammoud, Ghassan M., and Jamal A. Ibdah. "Preeclampsia‐induced Liver Dysfunction, HELLP syndrome, and acute fatty liver of pregnancy." Clinical Liver Disease 4, no. 3 (September 2014): 69–73. http://dx.doi.org/10.1002/cld.409.

Full text

APA, Harvard, Vancouver, ISO, and other styles

48

Machado, Mariana Verdelho, and Helena Cortez-Pinto. "Management of fatty liver disease with the metabolic syndrome." Expert Review of Gastroenterology & Hepatology 8, no. 5 (March 26, 2014): 487–500. http://dx.doi.org/10.1586/17474124.2014.903798.

Full text

APA, Harvard, Vancouver, ISO, and other styles

49

Narayanan, Santhosh, Divya Prakash, Gomathy Subramaniam, and Lakshminarayanan Lakshminarayanan. "ACUTE FATTY LIVER OF PREGNANCY MASQUERADING AS HELLP SYNDROME." Journal of Evidence Based Medicine and Healthcare 5, no. 20 (May 14, 2018): 1592–95. http://dx.doi.org/10.18410/jebmh/2018/335.

Full text

APA, Harvard, Vancouver, ISO, and other styles

50

Martins, Clarice, Andreia Pizarro, Luísa Aires, Gustavo Silva, Francisco Silva, Jorge Mota, and Maria Paula Santos. "Fitness and metabolic syndrome in obese fatty liver children." Annals of Human Biology 40, no. 1 (October 4, 2012): 99–101. http://dx.doi.org/10.3109/03014460.2012.727470.

Full text

APA, Harvard, Vancouver, ISO, and other styles

We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!