scholarly journals Study on the Effect of Different Types of Sugar on Lipid Deposition in Goose Fatty Liver

2022 ◽  
pp. 101729
Author(s):  
Rongxue Wei ◽  
Donghang Deng ◽  
Yongqiang Teng ◽  
Cangcang Lu ◽  
Zhaoyun Luo ◽  
...  
2018 ◽  
Vol 17 (5) ◽  
pp. 0-10
Author(s):  
Hong-Shan Li ◽  
Hao Ying ◽  
Zhe-Yun He

Introduction and aim. Salidroside and curcumin (SC) formula could alleviate lipid deposition in high fat diet-induced nonalcoholic fatty liver disease (NAFLD). However, the mechanisms are still unknown, and the magnitude of potential therapeutic benefit remains understudied. Material and methods. The rats were treated with high fat diet for 14 weeks to induce NAFLD. The experiment was divided into control, model (NAFLD), SC formula and rosiglitazone groups (n = 7 in each group). Hematoxylin-eosin (H&E) staining was applied to detect liver morphological changes. Biochemical, metabolic indices and inflammation factors in liver tissue and serum were detected. Additionally, the activities of related enzymes were detected by enzyme-linked immunosorbent assay. Results. In the established rat model, typical lipid deposition and liver steatosis were observed. Liver triglyceride, free fatty acids, sera alanine aminotransferase, aspartate aminotransferase, gamma-glutamyl transferase, fasting insulin, fasting blood glucose and homeostasis model assessment of insulin resistance were elevated in model group. Liver malondialdehyde was significantly elevated, while superoxide dismutase was significantly decreased in model group, compared with control. Moreover, tumor necrosis factor-α and Interleukin-1 were significantly produced in model group, compared with control. As a mechanism, high fat diet decreased tissue AMP-activated protein kinase (AMPK), phosphorylated AMPK, carnitine palmitoyltransferase 1 and increased inacetyl-CoA carboxylase (ACCase), phosphorylated ACCase. Importantly, these abnormal changes caused by high fat diet were reduced by SC formula administration. Conclusion. SC formula could ameliorate the injury caused by high fat diet. The effect was likely mediated via its influence on insulin resistance, lipid peroxidation injury and AMPK signaling pathway.


Gut ◽  
2020 ◽  
pp. gutjnl-2020-321774
Author(s):  
Nannan Sun ◽  
Chuangpeng Shen ◽  
Lei Zhang ◽  
Xiaojie Wu ◽  
Yuanyuan Yu ◽  
...  

ObjectiveImpaired hepatic fatty acids oxidation results in lipid accumulation and redox imbalance, promoting the development of fatty liver diseases and insulin resistance. However, the underlying pathogenic mechanism is poorly understood. Krüppel-like factor 16 (KLF16) is a transcription factor that abounds in liver. We explored whether and by what mechanisms KLF16 affects hepatic lipid catabolism to improve hepatosteatosis and insulin resistance.DesignKLF16 expression was determined in patients with non-alcoholic fatty liver disease (NAFLD) and mice models. The role of KLF16 in the regulation of lipid metabolism was investigated using hepatocyte-specific KLF16-deficient mice fed a high-fat diet (HFD) or using an adenovirus/adeno-associated virus to alter KLF16 expression in mouse primary hepatocytes (MPHs) and in vivo livers. RNA-seq, luciferase reporter gene assay and ChIP analysis served to explore the molecular mechanisms involved.ResultsKLF16 expression was decreased in patients with NAFLD, mice models and oleic acid and palmitic acid (OA and PA) cochallenged hepatocytes. Hepatic KLF16 knockout impaired fatty acid oxidation, aggravated mitochondrial stress, ROS burden, advancing hepatic steatosis and insulin resistance. Conversely, KLF16 overexpression reduced lipid deposition and improved insulin resistance via directly binding the promoter of peroxisome proliferator-activated receptor α (PPARα) to accelerate fatty acids oxidation and attenuate mitochondrial stress, oxidative stress in db/db and HFD mice. PPARα deficiency diminished the KLF16-evoked protective effects against lipid deposition in MPHs. Hepatic-specific PPARα overexpression effectively rescued KLF16 deficiency-induced hepatic steatosis, altered redox balance and insulin resistance.ConclusionsThese findings prove that a direct KLF16–PPARα pathway closely links hepatic lipid homeostasis and redox balance, whose dysfunction promotes insulin resistance and hepatic steatosis.


2020 ◽  
Vol 6 (2) ◽  
pp. 294-298
Author(s):  
Shafaat Mahjabun ◽  
Humayun Kabir ◽  
Meftah Islam ◽  
Abdur Rahim Azad ◽  
Sumon Kumar Sarker ◽  
...  

Ultrasonography is an easy, noninvasive, rapid investigation advised by doctors worldwide. Hence we diagnosed different types of cases through ultrasonography at outdoor patients admitted to Department of Rangpur Medical College Hospital, Rangpur Bangladesh over a period of four months. Our objective was to investigate the prevalence of different types of cases diagnosed and evaluated by ultrasonography in a variety of physical conditions with multiple clinical scenarios. Ultrasonography were performed using GE Logiq V5 Expert ultrasound machine with linear and curved linear phased array transducers. A total 300 cases were diagnosed, where female and male cases were 204 (68%), 96 (32%) respectively. Most ultrasound examinations were abdominal, with the remainder being obstetric, pelvic, breast, and genitourinary examinations. In this study, abdominal ultrasonography represented 118 case (39.33%), Pelvic 54 (18%), KUB 57 (19%), Breast 7 (2.33%) and Obstetrics 64 (21.33%). We found general clinical prevalence of abdominal cases were Cholelithiasis 17 (5.67%), Cholecystitis 3 (1%), Fatty liver 24 (8%), Hepatic Mass 2 (0.67%), Hepatic cyst 1 (0.33%), Acute hepatitis 2 (0.67%), Acute appendicitis 6 (2%), Ascites 2 (0.67%), Hernia 3(1%), Acute pancreatitis 2 (0.67%), Choledocholithiasis 2 (0.67%), Splenomegaly 1 (0.33 %), Abscess 1 (0.33%) and normal cases were 54 (18%). In genitourinary, Stone 20 (6.67%), Cyst 7 (2.33%), RPD 11 (3.67), Cystitis 4 (1.33), Ectopic kidney 1 (0.33%), Enlarged prostate 6 (2%), Hydronephrosis 1 (0.33%), Mass lesion 2 (0.67%) and normal cases were 7 (2.33%). In Pelvic, RPC 11 (3.67%), Ovarian and adnexal cyst 11 (3.67%), Uterine Anomaly 14 (4.67%), Mass lesion 2 (0.67%), Collection 7 (2.33) and normal cases were 5 (1.67%). In Obstetrics, normal pregnancy with no or minor complications, pregnancy with severe complications and abnormal pregnancy were 31(10.33%), 30(10%) and 3(1.0%) respectively. In Breast, dilated duct 1 (0.33%), Abscess 2 (0.67%), Fibroadenoma 2 (0.67%) and normal cases were 2 (0.67%). Here, we found that Fatty liver, stone in genitourinary tract and gall stone were highly prevalent. So, health care providers need to concern and raise awareness to reduce the number of cases. Asian J. Med. Biol. Res. June 2020, 6(2): 294-298


2021 ◽  
Author(s):  
Xiao Lin ◽  
Ya Xing ◽  
Yihui Zhang ◽  
Biao Dong ◽  
Minmeng zhao ◽  
...  

Abstract Background Previous studies indicate that microRNA33 (miR-33) and its target gene, CROT, are implicated in hepatic lipid metabolism, but it is unclear whether miR-33 participates in the development of goose fatty liver via CROT. Methods The expression of miR-33 in goose fatty liver, muscle and fat tissues, as well as the mRNA and protein expression of CROT in goose fatty liver was determined by q-PCR or Western-blot. The targeting regulatory relationship between miR-33 and CROT in goose liver cells was validated by miR-33 overexpression and interference assays. The effects of miR-33 mimic and CROT overexpression on lipid deposition and the expression of downstream genes were determined in goose primary hepatocytes. The treatment of high concentrations of glucose and insulin was performed to determine their regulation on the expression of miR-33 and CROT in goose primary hepatocytes. Results Here, data showed that miR-33 expression was significantly increased in the liver, muscle and fat tissues of overfed geese. Consistently, miR-33 mimic promoted lipid deposition in goose primary hepatocytes. Moreover, the regulatory targeting relationship between miR-33 and CROT was validated in goose primary hepatocytes. Consistently, the mRNA and protein expression of CROT were significantly reduced in goose fatty liver. Interestingly, CROT overexpression could induce the expression of fatty acid oxidation associated genes including CRAT, PEX5, EHHADH, CAT and ACOT8 in goose primary hepatocytes, but only the expression of PEX5 was significantly inhibited in goose fatty liver. However, it seemed conflicting that CROT overexpression increased lipid deposition and reduced lipid peroxidation in goose primary hepatocytes. Additionally, high glucose inhibited miR-33 expression and induced CROT expression in goose primary hepatocytes. Conclusions These findings suggest that miR-33 potentially participates in the development of goose fatty liver via CROT, and that miR-33/CROT may partially mediate the effect of glucose in goose liver cells.


Nutrients ◽  
2021 ◽  
Vol 14 (1) ◽  
pp. 76
Author(s):  
Jinwang Li ◽  
Siyu Xie ◽  
Wendi Teng

Nonalcoholic fatty liver disease (NAFLD) is characterized by lipotoxicity and ectopic lipid deposition within hepatocytes. Sulforaphane (SFA), an active compound used for inhibiting tumors, was found to have the potency to improve lipid metabolism. However, its molecular mechanisms on ameliorating NAFLD are still incompletely understood. This research evaluated if SFA could inhibit hepatic steatosis and apoptosis. The effects of SFA on cell viability, lipid accumulation, triglyceride (TG) contents, apoptosis, ceramide contents, and reactive oxygen species (ROS) levels were analyzed in palmitic acid (PA)-treated HepG2 cells and high-fat diet (HFD)-fed mice. The related molecular mechanisms were further explored in hepatocytes. The results showed SFA alleviated lipid accumulation and regulated AMPK/SREBP1c/FAS signaling pathway in PA-stressed HepG2 cells. In addition, SFA alleviated PA-mediated apoptosis, downregulated the expressions of cleaved caspase 3, as well as reduced ceramide contents and ROS levels. Moreover, SFA treatment reduced HFD-induced body weight gain, alleviated insulin resistance, decreased serum TG, total cholesterol (TC), and alanine aminotransferase (ALT) levels, and prevented lipid deposition and apoptosis in the liver. This study showed SFA suppressed lipid deposition and apoptosis both in vitro and in vivo, indicating that SFA may be a potential candidate for preventing and treating NAFLD.


Biochemistry ◽  
2019 ◽  
Vol 58 (37) ◽  
pp. 3911-3917
Author(s):  
Jon R. Beck ◽  
Fatima Cabral ◽  
Karuna Rasineni ◽  
Carol A. Casey ◽  
Edward N. Harris ◽  
...  

2021 ◽  
Author(s):  
Rongxue Wei ◽  
Donghang Deng ◽  
Yongqiang Teng ◽  
Cangcang Lu ◽  
Zhaoyun Luo ◽  
...  

Abstract Backgroud: Early research in our lab is indicated that the effect of glucose, fructose and sucrose on the levels of triacylglycerol and inflammatory factor was significantly different, and it is speculated that the regulatory mechanism of lipid deposition by different type of sugar in the liver is different. Methods: In order to explore lipid deposition difference mediated by different type of sugar (glucos, fructose and sucrose) in goose fatty liver formation, this experiment was performed from cell culture, overfeeding experiment and transcriptome analysis three level. Results: Cell culture experiment results indicated that the levels of intracellular triglyceride (TG), total cholesterol (T-CHO) and lipid content of fructose treatment and sucrose treatment were significantly higher than those of glucose treatment (P < 0.05). In slaughter performance, the liver weight, the ratio of liver weight to body weight, feed conversion ratio (liver weight / feed consumption ) were better in sucrose overfeeding group (P < 0.05). In addition, the liver of the sucrose overfeeding group contained a lot of unsaturated fatty acids, especially (n-3) polyunsaturated fatty acids (n-3 PUFA ) (P < 0.05). Transcriptome analysis shown that the PPAR signaling pathway is highly enriched in the fructose and sucrose overfeeding groups; cell cycle and DNA replication pathways were highly enriched in the glucose overfeeding group. Conclusions: Due to lipids outward transportation decrease and anti-imflammation of unsaturated fatty acids (UFA), thereby, fructose and sucrose hve better ability to induce steatosis in foie gras formation.


Nutrients ◽  
2021 ◽  
Vol 14 (1) ◽  
pp. 91
Author(s):  
Gracjan Różański ◽  
Derek Pheby ◽  
Julia L. Newton ◽  
Modra Murovska ◽  
Paweł Zalewski ◽  
...  

Metabolic-associated fatty liver disease (MAFLD), previously called non-alcoholic fatty liver disease (NAFLD), is the most common chronic liver disease worldwide. It is characterised by excessive fat accumulation in hepatocytes. Currently, no pharmacological therapy is effective for this disease, so non-pharmacological alternatives such as diet, supplementation or physical activity are being sought. For this reason, we reviewed the available databases to analyse the studies conducted to date using different modifications of intermittent fasting among patients with MAFLD. Eight studies using this dietary strategy were included in this review. The results obtained in the different trials are varied and do not allow a clear determination of the effect of the different types of intermittent fasting on anthropometric and biochemical parameters among patients with MAFLD. However, this type of diet seems to show some therapeutic potential, but further studies are needed.


Sign in / Sign up

Export Citation Format

Share Document