scholarly journals Serum Adipokine and Ghrelin Levels in Nonalcoholic Steatohepatitis

2006 ◽  
Vol 2006 ◽  
pp. 1-5 ◽  
Author(s):  
Mehmet Yalniz ◽  
Ibrahim Halil Bahcecioglu ◽  
Huseyin Ataseven ◽  
Bilal Ustundag ◽  
Fulya Ilhan ◽  
...  

Adipokines and ghrelin play role in insulin resistance, the key pathophysiological abnormality in patients with nonalcoholic fatty liver diseases. In the present study, relationship between nonalcoholic steatohepatitis (NASH) and serum adipokine and ghrelin levels was investigated. Thirty seven patients with biopsy-proven NASH and 25 age- and sex-matched controls were enrolled. Ten of NASH patients (27%) had diabetes mellitus (n=5) or impaired glucose tolerance (n=5). Body mass index (BMI) was less than 30 kg/m2in67.6%of patients, while in the remaining32.4%it was more than 30 kg/m2. Serum adiponectin, leptin, TNF-α, and ghrelin were determined. Serum leptin (15.49±4.84vs10.31±2.53) and TNF-α(12.1±2.7vs10.31±2.56) levels were significantly higher in the NASH group compared to in the control group (P<.001for each). Nevertheless, adiponectin (11.1±2.1vs17.3±2.8) and ghrelin (6.46±1.1vs7.8±1.1) levels were lower in the NASH group than in the control group (P<.001for each). Serum levels of the adipokines and ghrelin, however, were comparable in the subgroups of patients regardless of whether BMI was<30or>30or glucose tolerance was impaired or not (P>.05). Additionally, neither adipokines nor ghrelin was correlated with histopathological grade and stage (P>.05). In conclusion; there is a significant relationship between NASH and adipokines and ghrelin independent from BMI and status of the glucose metabolism. These cytokines that appear to have role in the pathogenesis of NASH, however, do not have any effect upon the severity of the histopathology.

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 1093.1-1093
Author(s):  
G. Pellegrino ◽  
K. Stefanantoni ◽  
F. Facioni ◽  
C. Angelelli ◽  
A. Gigante ◽  
...  

Background:Electrocardiographic (ECG) abnormalities are described in 25-75% Systemic Sclerosis (SSc) cases and they are associated with other systemic manifestations as well as with a worse prognosis. There is an increasing need for clinical and laboratory biomarkers to ameliorate the diagnostic and therapeutic approaches to patients with ECG abnormalities, due to their actual low sensitivity and specificity. Adipokines are circulating proteins that appear dysregulated in SSc and leptin in particular is synthesized in response to inflammatory conditions and seems to play a proinflammatory and pro-fibrotic action in SSc. Interesting, many studies in the last years have underlined its role in the cardiac remodeling mechanisms and in the development of cardiac fibrosis in other chronic diseases.Objectives:Aim of our study is to evaluate the role of leptin in the development of cardiac rhythm disorders (CRD) during SSc. Furthermore, by the analysis of the clinical and demographical parameters of our SSc patients, we tried to define other possible features associated with increased serum leptin concentration.Methods:We included eighty-five SSc patients, fulfilling the 2013 ACR/EULAR classification criteria, attending the Regional Rare Disease Center of Policlinico Umberto I of Rome. Fifty presented significant CRD at non-invasive diagnostic techniques (12 Lead ECG, 24-hour Holter ECG). Demographic, clinical, conventional cardiovascular risk factors were examined; instrumental and laboratory assessments were obtained, together with ECG recordings. Thirty-five SSc patients without pathologic finding at ECG traces, matched for demographic and clinical features, were recruited as the control group. In all cases, after obtaining written informed consent, blood samples were taken to measure serum levels of leptin using an ELISA assay (Life Technologies-Italia).Results:The fifty SSc patients with CRD (mean age 51±15 years; F:M 41:9) had pulmonary fibrosis (PF) in 32 cases (64%) and a BMI >25Kg/m2in 22 (44%) while in the control group of thirty-five SSc patients (mean age 49±16 years; F:M 33:2) PF was found in 15 (43%) and a BMI >25Kg/m2in 9 (35%); We detected significantly higher median values of serum leptin in SSc patients with CRD compared to the control group (12027 pg/ml IQR 12314 versus 6392 pg/ml IQR 7103;p 0,0009). Additionally, SSc patients with a BMI> 25 kg/m2(31 cases) as well as those with PF (47 cases) showed a significantly higher median serum leptin levels compared to those with BMI <25 kg/m2(13161 pg/ml IQR 13610 versus 8187 pg/ml IQR 8255;p 0,0008) and those without PF (11740 pg/ml IQR 11940 versus 7616 pg/ml IQR 7855;p 0,0079).Conclusion:To our knowledge this is the first report on high serum levels of leptin in SSc patients with CRD that also confirms its increase in those cases with a BMI >25 kg/m2and with PF, according to scientific literature data. The role of leptin in the pathogenesis of SSc remains unclear although it is already known its involvement in the development of cardiac fibrosis during other chronic diseases. On the basis of these results we speculate on leptin involvement in the pathogenesis of CRD during SSc, although further studies are needed with larger cohort of patients.References:[1]Vacca A et al. Rheumatology, 2014[2]Tyndall AJ et al. Ann Rheum Dis, 2010[3]Muresan L et al. Iran J Pub Health, 2017[4]Sanna T et al. Indian Pacing Electrophysiol J, 2009[5]Riccieri V et al. Clin Exp Rheumatol, 2011[6]Żółkiewicz J et al. Arch Dermatol Res, 2019[7]Huby AC et al. Circulation, 2015[8]Shulze PC et al. Clin Chim Acta, 2005[9]Van de Hoogen F et al. Arthritis Rheum, 2013[10]Gui X et al. Biochem Biophys Res Commun, 2018Disclosure of Interests:Greta Pellegrino: None declared, Katia Stefanantoni Consultant of: ItalfarmacoBoehringer Ingelheim, Fausta Facioni: None declared, Carlotta Angelelli: None declared, Antonietta Gigante: None declared, Roberto Badagliacca: None declared, Carmine Dario Vizza: None declared, Sergio Morelli: None declared, Edoardo Rosato: None declared, Valeria Riccieri: None declared


Antioxidants ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1076
Author(s):  
Guoyi Tang ◽  
Yu Xu ◽  
Cheng Zhang ◽  
Ning Wang ◽  
Huabin Li ◽  
...  

Nonalcoholic fatty liver diseases (NAFLD) represent a set of liver disorders progressing from steatosis to steatohepatitis, fibrosis, cirrhosis, and hepatocellular carcinoma, which induce huge burden to human health. Many pathophysiological factors are considered to influence NAFLD in a parallel pattern, involving insulin resistance, oxidative stress, lipotoxicity, mitochondrial dysfunction, endoplasmic reticulum stress, inflammatory cascades, fibrogenic reaction, etc. However, the underlying mechanisms, including those that induce NAFLD development, have not been fully understood. Specifically, oxidative stress, mainly mediated by excessive accumulation of reactive oxygen species, has participated in the multiple NAFLD-related signaling by serving as an accelerator. Ameliorating oxidative stress and maintaining redox homeostasis may be a promising approach for the management of NAFLD. Green tea is one of the most important dietary resources of natural antioxidants, above which epigallocatechin gallate (EGCG) notably contributes to its antioxidative action. Accumulative evidence from randomized clinical trials, systematic reviews, and meta-analysis has revealed the beneficial functions of green tea and EGCG in preventing and managing NAFLD, with acceptable safety in the patients. Abundant animal and cellular studies have demonstrated that green tea and EGCG may protect against NAFLD initiation and development by alleviating oxidative stress and the related metabolism dysfunction, inflammation, fibrosis, and tumorigenesis. The targeted signaling pathways may include, but are not limited to, NRF2, AMPK, SIRT1, NF-κB, TLR4/MYD88, TGF-β/SMAD, and PI3K/Akt/FoxO1, etc. In this review, we thoroughly discuss the oxidative stress-related mechanisms involved in NAFLD development, as well as summarize the protective effects and underlying mechanisms of green tea and EGCG against NAFLD.


2021 ◽  
Vol Publish Ahead of Print ◽  
Author(s):  
Hamed Ebrahimzadeh Leylabadlo ◽  
Hossein Samadi Kafil ◽  
Safar Farajnia ◽  
Dariush Shanehbandi ◽  
Seyed Yaghoub Moaddab ◽  
...  

2017 ◽  
Vol 36 (4) ◽  
pp. 261-267 ◽  
Author(s):  
Roya Navekar ◽  
Maryam Rafraf ◽  
Aida Ghaffari ◽  
Mohammad Asghari-Jafarabadi ◽  
Manouchehr Khoshbaten

2003 ◽  
Vol 112 (1) ◽  
pp. 91-100 ◽  
Author(s):  
Aimin Xu ◽  
Yu Wang ◽  
Hussila Keshaw ◽  
Lance Yi Xu ◽  
Karen S.L. Lam ◽  
...  

2005 ◽  
Vol 90 (4) ◽  
pp. 2290-2296 ◽  
Author(s):  
Johan Svensson ◽  
Hans Herlitz ◽  
Per-Arne Lundberg ◽  
Gudmundur Johannsson

Abstract In a randomized, placebo-controlled, crossover study under metabolic ward conditions, 10 GH-deficient adults received 1-wk GH replacement therapy (9.5 μg/kg·d). The effect of this treatment on the erythrocyte sodium/lithium countertransport (SLC) activity and on serum levels of adiponectin, resistin, leptin, IGF binding protein-1 (IGFBP-1) and IL-6 was determined. The 1-wk GH replacement impaired glucose homeostasis determined from an oral glucose tolerance test. The other measured variables in serum were unchanged by GH replacement. At baseline, serum adiponectin level was inversely correlated and serum leptin level was positively correlated with measures of glucose tolerance and insulin sensitivity. The changes in serum leptin level and erythrocyte SLC activity were positively correlated, and the change in serum IGFBP-1 level was negatively correlated, correlated with changes in measures of glucose metabolism. In conclusion, short-term GH treatment induced glucose intolerance but did not significantly change the erythrocyte SLC activity and the serum levels of adipokines, arguing against direct effects of GH on these measures. However, baseline values or changes in erythrocyte SLC activity, adiponectin, leptin, and IGFBP-1 correlated with glucose metabolism. This suggests that these factors are of importance for glucose homeostasis in GH-deficient adults, most likely through GH-independent mechanisms.


2019 ◽  
Vol 0 (0) ◽  
Author(s):  
Milica Culafic ◽  
Sandra Vezmar Kovacevic ◽  
Violeta Dopsaj ◽  
Branislav Oluic ◽  
Nemanja Bidzic ◽  
...  

Summary Background The progression of the nonalcoholic fatty liver disease to nonalcoholic steatohepatitis (NASH) is multifactorial, and there is still a lack of approved medications for its treatment. The study aimed to evaluate the impact of combined treatment with Pentoxifylline and Metformin on biochemical parameters in patients with NASH. Setting: Outpatient hepatology clinic. Methods A prospective trial was conducted. The first cohort included patients with biopsy-proven NASH, while the second cohort consisted of patients with biopsy-confirmed NAFLD. Blood tests were checked at baseline and every three months. Pentoxifylline at a dosage of 400 mg t.i.d. and Metformin at the dosage of 500 mg t.i.d. were introduced for six months in NASH group. The impact of the treatment was assessed based on biochemical results after combined treatment with low-cost medications. Results All 33 NASH patients completed 24 weeks of treatment. We observed significant improvement (p<0.05) of median values after treatment for the following parameters: serum uric acid levels decreased by 51.0 micromol/L, calcium decreased for 0.27 mmoL/L, magnesium showed an increase of 0.11 mmoL/L. Insulin resistance improved as a reduction of HOMA – IR by 1.3 was detected. A significant decrease of median in liver enzymes, alanine aminotransferase, aspartate aminotransferase and gammaglutamyltransferase by 24.0 IU/L, 9.1 IU/L, 10.8 IU/L respectively, was noted. Conclusions Pentoxifylline and Metformin may provide possible treatment option in NASH. Some new potential benefit of the therapy in improving liver function whilst decreasing cardiovascular risk was perceived.


2017 ◽  
Vol 7 (1) ◽  
pp. 101-106 ◽  
Author(s):  
Sameh M Abdel Monem

ABSTRACT Aim Nonalcoholic fatty liver disease (NAFLD) is probably the most common liver disorder in the world. A subgroup of NAFLD patients is characterized by injury to the hepatocytes and inflammation in addition to excessive fat (steatohepatitis), the latter condition is nominated nonalcoholic steatohepatitis (NASH). This work aimed to evaluate the role of probiotics on the outcome of NASH in patients admitted to the Tropical Medicine Department, Faculty of Medicine, Zagazig University (inpatients and outpatients). Materials and methods This study was performed on 30 patients (17 males and 13 females), with body mass index from 30 to 35 and average age of 44 years with bright fatty liver in ultrasonography and raised alanine transaminase (ALT) and aspartate transaminase (AST) and positive liver biopsy findings. The patients were divided into group I (case group) that included 15 patients who received probiotics and group II of 15 patients as control group who did not receive probiotics; the study was conducted between November 2014 and April 2016. Clinical assessment, laboratory evaluation, pelvic-abdominal ultrasound, and liver biopsy of all cases were carried out. Results In this study, there was significant decrease in liver enzymes (ALT and AST) and no statistically significant other laboratory findings. Also there was relief for dyspepsia in some patients. Conclusion Probiotics treatment is effective, safe, well-tolerated, inexpensive, appropriate for long-term use, and optimally, works at multiple levels to downregulate inflammatory mediators, and therefore, probiotics could be an option in the treatment of NASH. How to cite this article Monem SMA. Probiotic Therapy in Patients with Nonalcoholic Steatohepatitis in Zagazig University Hospitals. Euroasian J Hepato-Gastroenterol 2017;7(1):101-106.


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