scholarly journals Protein-synthesizing, bile-forming, urea-forming and carbohydrate functions in cows with fatty degeneration of the liver

2021 ◽  
Vol 23 (104) ◽  
pp. 60-65
Author(s):  
V. V. Vlizlo ◽  
O. I. Prystupa ◽  
L. G. Slivinska ◽  
Shan Hu ◽  
R. V. Voloshyn ◽  
...  

In dairy farms of Ukraine, where highly productive dairy cows are kept, liver lesions are often diagnosed in the postpartum period. Postmortem studies of the liver of cows that were forcibly slaughtered showed that in mostly animals were diagnosed with fatty degeneration of the liver. The main causes of fatty hepatosis were violations of the structure of rations, imbalance of feeding on essential nutrients and biologically active substances, low content of easily digestible carbohydrates and high protein content. The study was performed on cows aged 4–5 years with productivity for the previous lactation of 5.600–7.500 L of milk, in a winter-stall period of keeping, 2–3 weeks after calving. According to clinical and biochemical blood tests, two groups of cows were formed – 50 clinically healthy and 50 cows with fatty liver disease. In cows diagnosed with fatty liver degeneration, the disease was manifested by decreased productivity and fatness, loss of appetite, oppression, hypotony of the rumen, reticulum and omasum. In some cows, there was pain at the liver area, increasing boundaries of hepatic dullness, jaundice of the visible mucous membranes and sclera. The blood serum of all cows with fatty liver disease established a decrease in albumin content, indicating impaired protein synthesis function of the liver. In some cows, the content of total protein in the serum increased due to globulin fractions, mainly gamma globulins. The ratio between the content of albumins and globulins decreased, which indicates the development in the blood of sick animals dysproteinemia. The development of fatty infiltration of the liver caused an increase in the concentration of bile acids in the serum of all sick cows. This is due to reduced conjugation and excretion of cholates by affected hepatocytes from the bile capillaries. The formation, absorption, conjugation, and excretion of bilirubin in the bile is disturbed, which causes the accumulation of total and conjugated bilirubin in the serum of sick animals. The cholesterol content in the blood of cows decreased, caused a violation of the esterification of its esters by hepatocytes. The established changes in the content of bile acids, total and conjugated bilirubin, and cholesterol in the blood of sick cows indicate a violation of bile secretion, bile production, and cholestasis development. In some cows with fatty liver degeneration, urea formation function and carbohydrate function are impaired, leading to a decrease in blood urea content and glucose.

Author(s):  
Оксана Константиновна Мустафина ◽  
Элеонора Николаевна Трушина ◽  
Николай Александрович Ригер ◽  
Илья Владимирович Аксенов

В исследовании установлено, что использование высококалорийного холинодефицитного рациона (ВКХДР) у крыс привело к снижению уровня гемоглобина и эритроцитарных показателей, лейкоцитозу. Не выявлено достоверного влияния ВКХДР на общее количество тромбоцитов и эритроцитов. Добавление в рационы крыс карнозина и альфа-липоевой кислоты не оказало протективного влияния на изменения гематологического статуса в условиях развития НАЖБП. Studies on the effect of minor biologically active substances on the hematological parameters of rats against the background of induced fatty liver dystrophy. The addition of carnosine and alpha-lipoic acid to rat diets did not have a significant protective effect on changes in the hematological status in conditions of non-alcoholic fatty liver disease.


2021 ◽  
pp. 2719-2730
Author(s):  
Phillip B. Hylemon ◽  
Lianyong Su ◽  
Po‐Cheng Zheng ◽  
Jasmohan S. Bajaj ◽  
Huiping Zhou

Author(s):  
Elisabeth Miller ◽  
Julian Schmidberger ◽  
Wolfgang Kratzer

Abstract Background As part of a prospective clinical study, the degree of hepatic fatty degeneration was quantified in a patient population with nonalcoholic fatty liver disease and sonographically diagnosed with hepatic steatosis using attenuation imaging. Methods A total of 113 patients with hepatic steatosis were examined, of whom 35 showed focal fatty sparing. Patients with the condition after right nephrectomy, other known liver diseases, and relevant alcohol consumption were excluded from the evaluation. B-scan sonography and sonographic quantification of steatosis content using attenuation imaging (Aplio i800 Canon Medical Systems) were performed. Attenuation imaging is a new ultrasound-based measurement technique that allows objective detection and quantification of hepatic steatosis. Results The prevalence of focal fatty sparing was 31.0% in the patient population examined. Patients with focal fatty sparing showed a statistically significantly higher attenuation coefficient in contrast to patients without focal fatty sparing (0.79 ± 0.10 vs. 0.66 ± 0.09 dB/cm/MHz, p < 0.0001). Conclusion Detection of focal fatty sparing is associated with an increased attenuation coefficient and is thus an expression of higher-grade hepatic fatty degeneration. Patients with focal fatty sparing are more often male and have a higher BMI and a larger liver than patients with nonalcoholic fatty liver disease without focal fatty sparing.


Author(s):  
Jiake Yu ◽  
Hu Zhang ◽  
Liya Chen ◽  
Yufei Ruan ◽  
Yiping Chen ◽  
...  

Children with nonalcoholic fatty liver disease (NAFLD) display an altered gut microbiota compared with healthy children. However, little is known about the fecal bile acid profiles and their association with gut microbiota dysbiosis in pediatric NAFLD. A total of 68 children were enrolled in this study, including 32 NAFLD patients and 36 healthy children. Fecal samples were collected and analyzed by metagenomic sequencing to determine the changes in the gut microbiota of children with NAFLD, and an ultra-performance liquid chromatography coupled to tandem mass spectrometry (UPLC-MS/MS) system was used to quantify the concentrations of primary and secondary bile acids. The associations between the gut microbiota and concentrations of primary and secondary bile acids in the fecal samples were then analyzed. We found that children with NAFLD exhibited reduced levels of secondary bile acids and alterations in bile acid biotransforming-related bacteria in the feces. Notably, the decrease in Eubacterium and Ruminococcaceae bacteria, which express bile salt hydrolase and 7α-dehydroxylase, was significantly positively correlated with the level of fecal lithocholic acid (LCA). However, the level of fecal LCA was negatively associated with the abundance of the potential pathogen Escherichia coli that was enriched in children with NAFLD. Pediatric NAFLD is characterized by an altered profile of gut microbiota and fecal bile acids. This study demonstrates that the disease-associated gut microbiota is linked with decreased concentrations of secondary bile acids in the feces. The disease-associated gut microbiota likely inhibits the conversion of primary to secondary bile acids.


2021 ◽  
Vol 12 ◽  
Author(s):  
Hongguo Guan ◽  
Yiyan Wang ◽  
Huitao Li ◽  
Qiqi Zhu ◽  
Xiaoheng Li ◽  
...  

Background: 11β-Hydroxysteroid dehydrogenase one is responsible for activating inert glucocorticoid cortisone into biologically active cortisol in humans and may be a novel target for the treatment of nonalcoholic fatty liver disease.Methods: A series of benzylidene cyclopentanone derivatives were synthesized, and the selective inhibitory effects on rat, mouse and human 11β-hydroxysteroid dehydrogenase one and two were screened. The most potent compound [5-bis-(2,6-difluoro-benzylidene)-cyclopentanone] (WZS08), was used to treat nonalcoholic fatty liver disease in mice fed a high-fat-diet for 100 days.Results: WZS08 was the most potent inhibitor of rat, mouse, and human 11β-hydroxysteroid dehydrogenase 1, with half maximum inhibitory concentrations of 378.0, 244.1, and 621.1 nM, respectively, and it did not affect 11β-hydroxysteroid dehydrogenase two at 100 μM. When mice were fed WZS08 (1, 2, and 4 mg/kg) for 100 days, WZS08 significantly lowered the serum insulin levels and insulin index at 4 mg/kg. WZS08 significantly reduced the levels of serum triglycerides, cholesterol, low-density lipoprotein, and hepatic fat ratio at low concentration of 1 mg/kg. It down-regulated Plin2 expression and up-regulated Fabp4 expression at low concentration of 1 mg/kg. It significantly improved the morphology of the non-alcoholic fatty liver.Conclusion: WZS08 selectively inhibits rat, mouse, and human 11β-hydroxysteroid dehydrogenase 1, and can treat non-alcoholic fatty liver disease in a mouse model.


Doctor Ru ◽  
2020 ◽  
Vol 19 (7) ◽  
pp. 21-30
Author(s):  
N.B. Gubergritz ◽  
◽  
N.V. Belyaeva ◽  
T.L. Mozhina ◽  
N.E. Monogarova ◽  
...  

Objective of the Review: to analyse changes in bile acids (BA) metabolism due to nonalcoholic fatty liver disease (NAFL), nonalcoholic fatty pancreas disease (NAFP); to assess the efficiency of ursodeoxycholic acid (UDCA) for their correction. Key Points. NAFL and NAFP have much in common, including BA synthesis imbalance and reduced farnesoid X receptor (FXR) expression. One possible therapy of NAFL and NAFP is BA synthesis correction and increase in FXR expression using FXR agonists. The article discusses clinical and experimental trials of the efficiency of selective FXR agonist — UDCA — in NAFL and NAFP. Conclusion. The multifactorial UDCA mechanism of action including anti-inflammatory, antioxidant, cytoprotective and antiapoptotic actions, can normalise carbohydrate, lipid metabolism and activate FXR; it can justify medicine inclusion into NAFL and NAFP therapeutic regimens. Keywords: nonalcoholic fatty liver disease, nonalcoholic fatty pancreas disease, ursodeoxycholic acid.


2019 ◽  
Vol 2019 ◽  
pp. 1-13 ◽  
Author(s):  
Caihua Wang ◽  
Chunpeng Zhu ◽  
Liming Shao ◽  
Jun Ye ◽  
Yimin Shen ◽  
...  

Nonalcoholic fatty liver disease (NAFLD) is a major health threat around the world and is characterized by dysbiosis. Primary bile acids are synthesized in the liver and converted into secondary bile acids by gut microbiota. Recent studies support the role of bile acids in modulating dysbiosis and NAFLD, while the mechanisms are not well elucidated. Dysbiosis may alter the size and the composition of the bile acid pool, resulting in reduced signaling of bile acid receptors such as farnesoid X receptor (FXR) and Takeda G protein-coupled receptor 5 (TGR5). These receptors are essential in lipid and glucose metabolism, and impaired bile acid signaling may cause NAFLD. Bile acids also reciprocally regulate the gut microbiota directly via antibacterial activity and indirectly via FXR. Therefore, bile acid signaling is closely linked to dysbiosis and NAFLD. During the past decade, stimulation of bile acid receptors with their agonists has been extensively explored for the treatment of NAFLD in both animal models and clinical trials. Early evidence has suggested the potential of bile acid receptor agonists in NAFLD management, but their long-term safety and effectiveness need further clarification.


PLoS ONE ◽  
2016 ◽  
Vol 11 (5) ◽  
pp. e0151829 ◽  
Author(s):  
Marialena Mouzaki ◽  
Alice Y. Wang ◽  
Robert Bandsma ◽  
Elena M. Comelli ◽  
Bianca M. Arendt ◽  
...  

Hepatology ◽  
2015 ◽  
Vol 63 (5) ◽  
pp. 1739-1740 ◽  
Author(s):  
Lucia Carulli ◽  
Chiara Gabbi ◽  
Marco Bertolotti

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