Ultrasonographic Findings of Selected Liver Parameters and Their Correlation to Lipidaemia in a Nigerian Population

Introduction: This study was conducted in the University of Port Harcourt Teaching Hospital, with the sample analysis conducted in HMG Hospital private laboratory in Rivers State. Methodology: A random sampling technique was employed to select the respondents, while the Taro-Yamene formula was used to calculate the sample size and data analysed with SPSS version 20. Results: The respondents were mainly aged 30 - 39 years, 12 (40.00%), mainly females, 20 (66.67%) and obese, 16 (53.33%). They were also mainly Christians, 25 (83.33%), of Ijaw descent 20 (66.67%) and civil/public servants, 13 (43.33%). The total cholesterol was the highest, 18 (60.00%), normal for triglyceride, 24 (80.00%), low for high density lipoprotein cholesterol, 22 (73.33%) and high for low density lipoprotein cholesterol, 14 (46.67%). Maximum liver span was statistically significant to triglyceride concentration;p-value (0.001) but not for total cholesterol;p-value (0.084), high density lipoprotein cholesterol;p-value (0.477) and low density lipoprotein cholesterol;p-value (0.317). Conclusion: Liver span is a predictive tool for the probable diagnosis of dyslipidaemia.

苦参碱对油酸诱导的脂肪变性Chang Liver细胞的影响及机制

目的探讨苦参碱对油酸诱导的脂肪变性Chang Liver细胞的改善作用及可能的机制。方法将Chang Liver细胞分为空白组、模型组和苦参碱低、中、高浓度组(0.1、0.5、1.0 mmol/L)。除空白组外,其余各组细胞使用1.0 mmol/L油酸处理24 h建立脂肪变性细胞模型,苦参碱各剂量组加入相应浓度药物干预24 h。检测细胞活性,观察细胞内脂滴形态,测定细胞中的脂质含量,检测细胞中肝功能指标[丙氨酸转氨酶(ALT)、天冬氨酸转氨酶(AST)、总胆红素(TBIL)、碱性磷酸酶(ALP)]含量和法尼醇X受体(FXR)、细胞色素P4507A1(CYP7A1)、成纤维细胞生长因子19(FGF19)的mRNA及蛋白表达水平。结果油酸和苦参碱对Chang Liver细胞活性无明显影响。经油酸处理后的细胞内可见橘红色脂滴;与空白组比较,其相对脂质含量、肝功能指标水平均显著升高,FXR、CYP7A1、FGF19 mRNA及蛋白表达水平均显著降低(P<0.05)。经低、中、高浓度苦参碱干预后,上述指标均显著逆转(P<0.05)。结论苦参碱可通过调控FXR/CYP7A1/FGF19信号通路来改善油酸诱导的脂肪变性Chang Liver细胞的脂质含量和肝功能指标。

Effect of Compound 962 Capsule on Liver Lipid Peroxidation and Indexes of Thymus Gland and Spleen in Rats

Objective: To investigate the effect of compound 962 capsule (abbre. as 962) on liver lipid peroxidation and indexes of thymus and spleen in aged rats. Methods: Rats were divided into young control, aged model, Piracetam, 962 middle dose (0.9 g/kg) and high dose (1.8 g/kg) groups. All test drugs were administrated for 1 month by gastrogavage. The liver lipid peroxidation was determined by thiobarbituric (TBA) method. The thymus index and spleen index were determined by weighing method. Results: 962 (middle and high dose) attenuated liver lipid peroxidation, increased the thymus index of aged rats. There was no effect on spleen index in all drug-treated groups. Conclusion: 962 could decrease liver lipid peroxidation and increase thymus index. It suggested that 962 might be beneficial in retarding aging process.

A silybin-phospholipids complex counteracts rat fatty liver degeneration and mitochondrial oxidative changes

AIM:To investigate the effectiveness of antioxidant compounds in modulating mitochondrial oxidative alterations and lipids accumulation in fatty hepatocytes.METHODS:Silybin-phospholipid complex containing vitamin E(Realsil) was daily administered by gavage(one pouch diluted in 3 mL of water and containing 15 mg vitamin E and 47 mg silybin complexed with phospholipids) to rats fed a choline-deprived(CD) or a high fat diet [20% fat,containing 71% total calories as fat,11% as carbohydrate,and 18% as protein,high fat diet(HFD)] for 30 d and 60 d,respectively.The control group was fed a normal semi-purified diet containing adequate levels of choline(35% total calories as fat,47% as carbohydrate,and 18% as protein).Circulating and hepatic redox active and nitrogen regulating molecules(thioredoxin,glutathione,glutathione peroxidase),NO metabolites(nitrosothiols,nitrotyrosine),lipid peroxides [malondialdehyde-thiobarbituric(MDA-TBA)],and pro-inflammatory keratins(K-18) were measured on days 0,7,14,30,and 60.Mitochondrial respiratory chain proteins and the extent of hepatic fatty infiltration were evaluated.RESULTS:Both diet regimens produced liver steatosis(50% and 25% of liver slices with CD and HFD,respectively) with no signs of necro-inflammation:fat infiltration ranged from large droplets at day 14 to disseminated and confluent vacuoles resulting in microvesicular steatosis at day 30(CD) and day 60(HFD).In plasma,thioredoxin and nitrosothiols were not significantly changed,while MDA-TBA,nitrotyrosine(from 6 ± 1 nmol/L to 14 ± 3 nmol/L day 30 CD,P < 0.001,and 12 ± 2 nmol/L day 60 HFD,P < 0.001),and K-18(from 198 ± 20 to 289 ± 21 U/L day 30 CD,P < 0.001,and 242 ± 23 U/L day 60 HFD,P < 0.001) levels increased significantly with ongoing steatosis.In the liver,glutathione was decreased(from 34.0 ± 1.3 to 25.3 ± 1.2 nmol/mg prot day 30 CD,P < 0.001,and 22.4 ± 2.4 nmol/mg prot day 60 HFD,P < 0.001),while thioredoxin and glutathione peroxidase were initially increased and then decreased.Nitrosothiols were constantly increased.MDA-TBA levels were five-fold increased from 9.1 ± 1.2 nmol/g to 75.6 ± 5.4 nmol/g on day 30,P < 0.001(CD) and doubled with HFD on day 60.Realsil administration significantly lowered the extent of fat infiltration,maintained liver glutathione levels during the first half period,and halved its decrease during the second half.Also,Realsil modulated thioredoxin changes and the production of NO derivatives and significantly lowered MDA-TBA levels both in liver(from 73.6 ± 5.4 to 57.2 ± 6.3 nmol/g day 30 CD,P < 0.01 and from 27.3 ± 2.1 nmol/g to 20.5 ± 2.2 nmol/g day 60 HFD,P < 0.01) and in plasma.Changes in mitochondrial respiratory complexes were also attenuated by Realsil in HFD rats with a major protective effect on Complex Ⅱ subunit CII-30.CONCLUSION:Realsil administration effectively contrasts hepatocyte fat deposition,NO derivatives formation,and mitochondrial alterations,allowing the liver to maintain a better glutathione and thioredoxin antioxidant activity.

Anti-lipid peroxidation and protection of liver mitochondria against injuries by picroside Ⅱ

AIM: To investigate the anti-lipid peroxidation and protection of liver mitochondria against injuries in mice with liverdamage by picroside Ⅱ.METHODS: Three animal models of liver damageinduced by carbon tetrachloride (CCl4:0.1 mL/10 g, ip),D-galactosamine (D-GalN: 500 mg/kg,ip) and acetaminophen (AP: 0.15 g/kg, ip) were respectively treated with various concentrations of picroside Ⅱ (5, 10, 20 mg/kg, ig). Then we chose the continuously monitoring method (recommended by International Clinical Chemistry League) to analyze serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) values, Marland method to detect the activity of manganese-superoxide dismutase (SOD) in liver mitochondria, TBA colorimetry to determine the content of malonicdialdehyde (MDA) in liver tissue, DTNB method to evaluate the activity of glutathioneperoxidase (GSH-Px) and Lowry method to detect protein level in liver tissue. Meanwhile, effects of picroside Ⅱ on the activity of ATPase and swelling extent of mitochondria in hepatocytes damaged by AP were also evaluated.RESULTS: Picroside Ⅱ could significantly prevent liver toxicity in the three models of liver damage. It decreased the high levels of ALT and AST in serum induced by theadministration of CCl4, D-GalN and AP, reduced the cellular damage of liver markedly, and appeared to be even more potent than the positive control drug of biphenyl dimethyl dicarboxylate pilules (DDB). In groups treated with different doses of picroside Ⅱ, compared to the model group, the content of MDA in serum decreased evidently, whereas the content of SOD and GSH-Px increased in a dosedependent manner, and the difference was statistically significant. Further, in the study of AP model, picroside Ⅱinhibited AP-induced liver toxicity in mice, enhanced the activity of ATPase, improved the swelling extent of mitochondria and helped to maintain a normal balance of energy metabolism.CONCLUSION: Picroside Ⅱ can evidently relieve hepatocyteinjuries induced by CCl4, D-GalN and AP, help scavenge free radicals, protect normal constructions of mitochondria membrane and enhance the activity of ATPase in mitochondria,thereby modulating the balance of liver energy metabolism, which might be part of the mechanisms of hepatoprotectiveeffects of picroside Ⅱ.

Liver-protecting effects of omega-3 fish oil lipid emulsion in liver transplantation

AIM:To investigate the liver-protecting effect of parenteral nutrition(PN) support with omega-3 fatty acids in a randomized controlled clinical trial.METHODS:Sixty-six patients with the diagnosis of end-stage liver disease or hepatic cellular carcinoma were admitted to the Affiliated Drum Tower Hospital,Nanjing University,China for orthotopic liver transplantation.The patients were randomly divided into two groups:PN group(n = 33) and polyunsaturated fatty acid(PUFA) group(n = 33).All patients received isocaloric and isonitrogenous PN for seven days after surgery,and in PUFA group omega-3 fish oil lipid emulsion replaced part of the standard lipid emulsion.Liver function was tested on days 2 and 9 after surgery.Pathological examination was performed after reperfusion of the donor liver and on day 9.Clinical outcome was assessed based on the post-transplant investigations,including:(1) post-transplant mechanical ventilation;(2) total hospital stay;(3) infectious morbidities;(4) acute and chronic rejection;and(5) mortality(intensive care unit mortality,hospital mortality,28-d mortality,and survival at a one-year post-transplant surveillance period).RESULTS:On days 2 and 9 after operation,a significant decrease of alanine aminotransferase(299.16 U/L ± 189.17 U/L vs 246.16 U/L ± 175.21 U/L,P = 0.024) and prothrombin time(5.64 s ± 2.06 svs 2.54 s ± 1.15 s,P = 0.035) was seen in PUFA group compared with PN group.The pathological results showed that omega-3 fatty acid supplement improved the injury of hepatic cells.Compared with PN group,there was a significant decrease of post-transplant hospital stay in PUFA group(18.7 d ± 4.0 d vs 20.6 d ± 4.6 d,P = 0.041).Complications of infection occurred in 6 cases of PN group(2 cases of pneumonia,3 cases of intra-abdominal abscess and 1 case of urinary tract infection),and in 3 cases of PUFA group(2 cases of pneumonia and 1 case of intra-abdominal abscess).No acute or chronic rejection and hospital mortality were found in both groups.The one-year mortality in PN group was 9.1%(3/33),one died of pulmonary infection,one died of severe intra-hepatic cholangitis and hepatic dysfunction and the other died of hepatic cell carcinoma recurrence.Only one patient in PUFA group(1/33,3.1%) died of biliary complication and hepatic dysfunction during follow-up.CONCLUSION:Post-transplant parenteral nutritional support combined with omega-3 fatty acids can significantly improve the liver injury,reduce the infectious morbidities,and shorten the post-transplant hospital stay.

Review:Lipids changes in liver cancer

Liver is one of the most important organs in energy metabolism. Most plasma apolipoproteins and endogenous lipids and lipoproteins are synthesized in the liver. It depends on the integrity of liver cellular function, which ensures homeostasis of lipid and lipoprotein metabolism. When liver cancer occurs, these processes are impaired and the plasma lipid and lipoprotein patterns may be changed. Liver cancer is the fifth common malignant tumor worldwide, and is closely related to the infections of hepatitis B virus (HBV) and hepatitis C virus (HCV). HBV and HCV infections are quite common in China and other Southeast Asian countries. In addition, liver cancer is often followed by a procession of chronic hepatitis or cirrhosis, so that hepatic function is damaged obviously on these bases, which may significantly influence lipid and lipoprotein metabolism in vivo. In this review we summarize the clinical significance of lipid and lipoprotein metabolism under liver cancer.

Lipid lowering effects of iodothyronines:In vivo and in vitro studies on rat liver

Non-alcoholic fatty liver disease(NAFLD) is emerging as one of the most common liver diseases,leading to the increasing interest for new therapeutic approaches for its treatment.NAFLD primarily depends on a hypercaloric and/or unbalanced diet leading to overweight and obesity.The liver,in fact,plays a central role in lipid metabolism by importing free fatty acids from the blood and synthesizing,storing,oxidizing and exporting lipids.Furthermore,the liver is the target for the thyroid hormones,thyroxine(T4) and 3,3',5-triiodo-L-thyronine(T3),that stimulate the basal metabolic rate and lead to body weight loss.In the last decade,other iodothyronines have been shown to possess biological relevance and play some thyromimetic activities; in particular,3,5-diiodo-L-thyronine(T2) gained large interest.The global effect of iodothyronines on liver lipid metabolism results from the balance between direct and indirect actions on the hepatocyte,leading to stimulation of lipid synthesis,oxidation and autophagy.In this review,the results so far obtained on both in vivo and in vitro models of hepatosteatosis are summarized in order to obtain an updated picture of the lipid-lowering effects of iodothyronines on mammalian liver.

Lipids in liver transplant recipients

Hyperlipidemia is very common after liver transplantation and can be observed in up to 71% of patients. The etiology of lipid disorders in these patients is multifactorial, with different lipid profiles observed depending on the immunosuppressive agents administered and the presence of additional risk factors, such as obesity, diabetes mellitus and nutrition. Due to recent improvements in survival of liver transplant recipients, the prevention of cardiovascular events has become more important, especially as approximately 64% of liver transplant recipients present with an increased risk of cardiovascular events. Management of dyslipidemia and of other modifiable cardiovascular risk factors, such as hypertension, diabetes and smoking, has therefore become essential in these patients. Treatment of hyperlipidemia after liver transplantation consists of life style modification, modifying the dose or type of immunosuppressive agents and use of lipid lowering agents. At the start of administration of lipid lowering medications, it is important to monitor drugdrug interactions, especially between lipid lowering agents and immunosuppressive drugs. Furthermore, as combinations of various lipid lowering drugs can lead to severe side effects, such as myopathies and rhabdomyolysis, these combinations should therefore be avoided. To our knowledge, there are no current guidelines targeting the management of lipid metabolism disorders in liver transplant recipients. This paper therefore recommends an approach of managing lipid abnormalities occurring after liver transplantation.

Evaluation of Lipid Peroxidation and Some Antioxidant Activities in Patients with Primary and Metastatic Liver Cancer

Abstract: HCC is the 6th most common cancer in the world. The main risk factors associated with HCC are hepatitis B (HBV) and hepatitis C viral infections and other factors that play a role in HCC development, include aflatoxin B1 (AFB1) cigarette smoking, and chronic inflammation. The aim of this study is to investigate lipid peroxidation and some antioxidant enzyme activities in patients with primary and metastatic liver cancer. For this purpose, 25 primary and metastatic liver cancer patients and 15 healthy controls were included in the study. In blood samples taken from the patient and control groups, the main product of lipid peroxidation MDA and SOD, GSH, GPx activity levels were examined. In result of study serum MDA level is higher and erythrocyte SOD, GSH, and GPx activities were found to be significantly lower in the patient group compared with the control group (p 0.05). As a result, liver cancer is associated with oxidative stress and antioxidant system weakens, which is an important indicator of oxidative stress, lipid peroxidation levels increased and promotes the tissue damage.

Comparison of lipid profile in different grades of non-alcoholic fatty liver disease diagnosed on ultrasound

Objective:To detect and compare serum lipid abnormalities in patients diagnosed with different grades of non-alcoholic fatly liver on ultrasonography.Methods:A total of 70 cases which included 30 males and 40 females,diagnosed as nonalcoholic fatty liver disease(NAFLD)on ultrasound were investigated with serum lipid profile.Then a comparison of lipid abnormalities between different grades of fatty liver diagnosed on ultrasound was done.P value was calculated by using analysis of variance lest(ANOVA)and P value<0.05 was considered as statistically significant.Results:Out of 70 cases which were diagnosed as NAFLD on ultrasonography,gradeⅠNAFLD cases were 47.15%,gradeⅡwere 42.85%and gradeⅢwere 10%.The mean age of the patients was49.14 years.Male to female ratio was 3:4.Serum triglycerides,total cholesterol,LDL and VLDL levels were raised in 67.14%,45.71%34.28%,25.71%of cases respectively.Low serum HDL levels were seen in 62.85%of patients.On statistical analysis we found increasing grades of NAFLD were significantly associated with increasing values of total cholesterol(P value-0.001),LDL(P value-0.000)and VLDL(P value-0.003)and decreasing HDL(P value-0.000).Conclusion:Most of the patients of NAFLD in India is asymptomatic,non-diabetic and non-hypertensive.Though liver biopsy is the gold standard melhod for diagnosis of NAFLD,Ultrasonography which is non-invasive,simple tool,can be used for the early detection of NAFLD in asymptomatic patients.

Micro RNA-185 regulates expression of lipid metabolism genes and improves insulin sensitivity in mice with non-alcoholic fatty liver disease

AIM:To assess the regulatory effect of micro RNA-185(mi R-185)on lipid metabolism and the insulin signalling pathway in human Hep G2 hepatocytes and a high-fat diet mouse model.METHODS:Quantitative reverse transcription-polymerase chain reaction was used to assess the m RNA levels of lipogenic genes after loss or gain of mi R-185.In addition,the amounts of insulin signalling intermediates were determined after transfection of Hep G2 cells with pre-mi R-185.RESULTS:Mi R-185 levels decreased in a time-and dose-dependent manner in response to palmitic acid in human Hep G2 hepatocytes.Transfection of Hep G2 cells with mi R-185 significantly decreased the m RNA levels of fatty acid synthase,3-hydroxy-3-methylglutaryl-Co A reductase,sterol-regulatory element binding protein-2,and sterol-regulatory element binding protein-1c,whereas inhibition of mi R-185 using an anti-mi R-185oligonucleotide produced the opposite effect in Hep G2cells.In a high-fat diet mouse model,the accumulation of lipids was significantly improved after treatment with mi R-185,compared with control animals.Induction of mi R-185 enhanced the insulin signalling pathway by upregulating the insulin-receptor substrate-2.CONCLUSION:These findings suggest that mi R-185plays an important role in regulating fatty-acid metabolism and cholesterol homeostasis in hepatocytes,as well as in improving insulin sensitivity,both in vitro and in vivo.

Effect of dietary supplementation with olive and sunflower oils on lipid profile and liver histology in rats fed high cholesterol diet

Objective: To compare the effects of high-monounsaturated(MUFA) and polyunsaturated fatty acids(PUFA) against the metabolic disorders elicited by a high-cholesterol diet(HC) in rats. Methods: Using in vivo dietary manipulation, rats were fed with different diets containing 4% soybean oil(cholesterol free diet) and 1% HC containing 12% olive oil(HC+OO) enriched with MUFA and 12% sunflower oil(HC+SO) enriched with PUFA for 60 d. Serum lipid levels and hepatic steatosis were evaluated after the treatment period. Results: Comparatively, rats treated with HC+OO diet experienced a decrease in the serum LDL-C, VLDL-C and CT levels compared to those fed with HC+SO diet(P<0.05). Otherwise, HC+OO provoked significant microvesicular steatosis situated in the hepatic acinar zone 1. Conclusions: HC+OO diet has high absorption velocity in the acinar zone 1 of liver compared to the HC+SO diet. Based on this, the reduction of the LDL-C, VLDL-C and CT serum levels in the animals treated with HC+OO diet can be caused by the delay in the FA release to the blood.

Incidence of Parenteral Nutrition-Associated Liver Disease in Infants on Prolonged Parenteral Nutrition with a Soybean-Based Lipid Emulsion: A 7-Year Experience

Parenteral nutrition associated liver disease (PNALD) is a significant complication in infants receiving long-term parenteral nutrition (PN). Chronic administration of PN has been associated with its development. Our purpose is to characterize our incidence of PNALD over an extended period and identify risk factors for its development, including administration of soybean-based injectable lipid emulsions (ILEs) as we transit to novel ILEs in our practice. Infants receiving 30 days or more of PN were included. PNALD was defined as a direct bilirubin ≥ 2 mg/dL. Data collected included: patient demographics, clinical and enteral feeding characteristics. Macronutrient intake was recorded using these cut-offs: glucose infusion rate (GIR) of ≤14 mg/kg/min or above, protein doses of ≤3 g/kg/day or above and lipid doses of ≤2 g/kg/day or above. A total of 349 infants were included, with an annual incidence of PNALD ranging between 34% - 54%. Infants with PNALD were younger by gestation (27 vs. 29.5 weeks) and smaller by birthweight (900 vs. 1248 grams). Sepsis, GI disease including necrotizing enterocolitis and bowel resection were significantly associated with an increased risk for development of PNALD. PNALD infants received lower protein doses (3.0 vs 3.3 g/kg/day, p = 0.014) while receiving higher GIR (11.4 vs 10.7 mg/kg/min, p = 0.012) compared to non-PNALD infants. Low birth weight, sepsis and bowel resection remain strong indicators of risk for PNALD. No single macronutrient increased our infants’ risk for PNALD. The use of newer ILEs when available should be evaluated for their impact on PNALD development.

Flavonoids Reduce Lipid Peroxides and Increase Glutathione Levels in Pooled Human Liver Microsomes (HLMs)

The effects of each of the flavonoids;genistein (G), quercetin (Q) and kaempferol (K) at several doses on lipid peroxides (LP) and reduced glutathione (GSH) in pooled human liver microsomes (HLMs) were investigated following the oxidative damage for 4, 6, 18 and 24 hr. HLMs (1 mg/ml) were exposed to each of the above flavonoids at 0, 5, 10, 15, 20 or 25 μM and incubated for the respective times as previously stated. Our hypothesis was that HLMs exposed to the flavonoids for the respective exposure times can decrease LP and increase GSH in HLMs to better cope with the oxidative stress. The results of our studies indicate that each of the flavonoids significantly (p < 0.01) decreased LP compared to their respective controls. The highest decrease in LP was observed for K followed by Q and G. Significant increases (p < 0.01) in GSH were observed for the flavonoid doses tested with the highest levels observed for Q for the 24-hr. incubation. The findings suggest that the flavonoids modulate oxidative stress in HLMs by decreasing LP and such decreases in LPs may be due to the increasing and or the replenished levels of GSH in the said cells to better cope with the oxidative stress.

mi R-192-5p regulates lipid synthesis in non-alcoholic fatty liver disease through SCD-1

AIM To evaluate the levels of mi R-192-5 p in non-alcoholic fatty liver disease(NAFLD) models and demonstrate the role of mi R-192-5 p in lipid accumulation. METHODS Thirty Sprague Dawley rats were randomly divided into three groups, which were given a standard diet, a high-fat diet(HFD), and an HFD with injection of liraglutide. At the end of 16 weeks, hepatic mi R-192-5 p and stearoyl-Co A desaturase 1(SCD-1) levels were measured. Mi R-192-5 p mimic and inhibitor and SCD-1 si RNA were transfected into Huh7 cells exposed to palmitic acid(PA). Lipid accumulation was evaluated by oil red O staining and triglyceride assays. Direct interaction was validated by dual-luciferase reporter gene assays.RESULTS The HFD rats showed a 0.46-fold decrease and a 3.5-fold increase in hepatic mi R-192-5 p and SCD-1 protein levels compared with controls, respectively, which could be reversed after disease remission by liraglutide injection(P < 0.01). The Huh7 cells exposed to PA also showed down-regulation and up-regulation of mi R-192-5 p and SCD-1 protein levels, respectively(P < 0.01). Transfection with mi R-192-5 p mimic and inhibitor in Huh7 cells induced dramatic repression and promotion of SCD-1 protein levels, respectively(P < 0.01). Luciferase activity was suppressed and enhanced by mi R-192-5 p mimic and inhibitor, respectively, in wild-type SCD-1(P < 0.01) but not in mutant SCD-1. Mi R-192-5 p overexpression reduced lipid accumulation significantly in PA-treated Huh7 cells, and SCD-1 si RNA transfection abrogated the lipid deposition aggravated by mi R-192-5 p inhibitor(P < 0.01).CONCLUSION This study demonstrates that mi R-192-5 p has a negative regulatory role in lipid synthesis, which is mediated through its direct regulation of SCD-1.

Non Alcoholic Fatty Liver Disease: Assessment of Lipid Profile Estimation in Different Grades of Fatty Liver on Ultrasound

Background: Non Alcoholic Fatty Liver Disease (NAFLD) is common hepatic disorder which is recognized as a great health problem causing different diseases worldwide. To determine non-alcoholic fatty liver and assess the relation of fasting total lipids with different grades of fatty liver (NAFLD) subjects diagnosed through ultrasound. By identifying the risk factors of Lipid Profile and NAFLD, the health care provider can properly manage it, even awareness specific for patients and community as general being launched to diminish the morbidity and mortality by this study. Methods: This cross-sectional research carried out at Medicine Department of PMCH, Shaheed Benazirabad. This study comprises 300 subjects of NAFLD. Patients who attended the medicine department with abdominal complains after examination consultant advised ultrasound. The ultrasound performed in Radiology department, patients with findings of fatty liver selected, and history taken from all the patients with special regard to alcoholism. Fasting lipid profile done in all patients included in present study. The blood samples collected from a vein and immediately sent to the laboratory. Results: This present study enlisted total 300 patients out of them 203 (67.7%) belonged to male gender and 97 (32.3%) were females. A ratio of 2.1:1 observed in male and female subjects. There were 176 (58.7%) patients in grade I, while 82 (27.3%) patients in grade II and 42 (14%) patients in grade III. The cholesterol value was abnormal in 186 (62%), while normal in remaining 114 (38%) patients. Triglycerides were abnormal in 152 (50.7%) while in 148 (49.3%) patients were normal. HDL in 155 (51.7%) patients was abnormal while 145 (48.3%) patients had normal values. Low density lipoprotein value in 117 (39%) patient was abnormal and 183 (61%) patient normal. Very low-density lipoprotein in 117 (39%) patients was abnormal and 183 (61%) patient normal. The mean age and SD of patients in present study was 46.83 ± 8.82, with minimum 30 years and maximum age 65 years respectively (p value 0.000). The mean and SD of total cholesterol value was 154.66 ± 58.88 mg/dl (p value 1.000), TG 180.98 ± 96.46 mg/dl (p value 0.974), HDL-C 32.13 ± 5.88 mg/dl (p value 0.000), LDL-C 116.41 ± 41.002 mg/dl (p value 0.000), and VLDL-C was 43.47 ± 34.34 mg/dl (p value 0.000). Conclusions: In current study, variable changes in lipid profile observed amongst NAFLD (non-alcoholic fatty liver disease) patients who diagnosed on ultrasound. Early diagnosis and treatment of non alcoholic fatty liver with abnormal lipids can prevent from long-term complication of fatty liver.

铁死亡在非酒精性脂肪性肝病发病中作用的研究进展

铁死亡是近年提出的一种新型细胞死亡方式,其主要特征为铁过载及脂质过氧化。铁死亡参与非酒精性脂肪性肝病的发生发展。铁过载可通过芬顿反应产生大量活性氧,在脂氧合酶的作用下,肝细胞膜上的不饱和脂肪酸发生脂质过氧化,从而诱导肝细胞死亡,导致非酒精性脂肪性肝病/非酒精性脂肪性肝炎的发生。阻断铁死亡可能成为保护肝细胞的治疗策略之一。

A study on mitochondrial respiratory dysfunction and lipid peroxidation in the liver after radiation,burn,and combined radiation-burn injuries in mice

Male mice were subjected to 6 Gy total body irradiation,20% TBSAfull-thickness burns,or combined radiation-burn injury and lipid peroxides(LPO),vita-min E,sulfhydryl group,respiratory control ratio(RCR),ADP/O ratio,and cytochromeoxidase activity of the liver mitochondria were determined in the first 9 d postinjury.Theresults are as follows:(1)LPO level increased in the early postinjury stage after combinedradiation-burn injury,on the 5th-7th day after irradiation and on the 7th day postburn.(2)Vitamin E level decreased significantly in the two groups of radiation and burn inju-ries but showed no significant decrease after combined injury.(3)The sulfhydryl groupshowed a tendency to increase in all the 3 groups.(4)The activity of cytochrome oxidaseincreased significantly on the 7th day after radiation but decreased considerably in theburn and combined injury groups.(5)RCR and ADP/O ratio decreased more significantlyin the combined injury group than in either the radiation group or the burn group.These facts suggest that the respiratory dysfunction of the liver mitochondria results mostprobably from the damage on the mitochondrial membrane due to lipid peroxidation.

达格列净联合水飞蓟宾治疗2型糖尿病合并非酒精性脂肪肝患者疗效分析

目的探讨达格列净联合水飞蓟宾对2型糖尿病合并非酒精性脂肪肝(NAFLD)患者的治疗效果。方法收集2021年1月—2022年12月新疆医科大学第五附属医院内分泌科诊治2型糖尿病合并NAFLD患者104例作为研究对象,按随机数字表法分为对照组52例和研究组52例,2组患者均给予常规治疗及二甲双胍降血糖治疗,研究组在此基础上给予达格列净联合水飞蓟宾治疗,治疗6个月后,比较2组患者治疗前后糖脂代谢指标、肝功能、肝脏硬度、肿瘤坏死因子-α(TNF-α)、超氧化物歧化酶(SOD)以及脂联素(APN)水平变化。结果治疗后2组患者糖化血红蛋白、空腹血糖、餐后2 h血糖以及胰岛素抵抗指数(HOMA-IR)较治疗前下降,且研究组低于对照组(t/P=3.411/<0.001,2.926/0.005,3.578/<0.001,2.672/0.015),研究组患者治疗后体质量指数(BMI)、腰臀比、内脏脂肪面积、总胆固醇(TC)、三酰甘油(TG)以及低密度脂蛋白胆固醇(LDL-C)明显低于治疗前,且低于对照组(t/P=2.873/0.008,2.435/0.013,4.878/<0.001,3.997/<0.001,2.265/0.025,1.997/0.038);研究组患者治疗后天冬氨酸氨基转移酶(AST)、丙氨酸氨基转移酶(ALT)以及总胆红素较治疗前明显下降,且研究组患者低于对照组(t/P=5.737/<0.001,4.971/<0.001,3.258/<0.001);治疗后研究组患者TNF-α降低,SOD及APN升高,且研究组降低/升高幅度大于对照组(t/P=2.453/0.021,3.842/<0.001,3.927/<0.001);治疗期间2组患者恶心呕吐、腹泻、腹胀、便秘、体质量增加、贫血以及低血糖等不良反应发生率比较,差异均无统计学意义(P>0.05)。结论在二甲双胍降糖治疗基础上给予达格列净联合水飞蓟宾可明显改善2型糖尿病合并NAFLD患者胰岛素抵抗水平以及肝功能,降低炎性因子水平和氧化应激损伤,提高APN水平。