ArticleWorld journal of gastroenterology2011
Serum Bcl-2 concentrations in overweight-obese subjects with nonalcoholic fatty liver disease.
Article in World journal of gastroenterology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 69 citations in OpenAlex.
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- Upregulation of BCL-2 by acridone derivative through gene promoter i-motif for alleviating liver damage of NAFLD/NASH.Nucleic acids research · 2020Article
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- High Intrinsic Aerobic Capacity Protects against Ethanol-Induced Hepatic Injury and Metabolic Dysfunction: Study Using High Capacity Runner Rat Model.Biomolecules · 2015Article
- Hepatoprotective effect of herb formula KIOM2012H against nonalcoholic fatty liver disease.Nutrients · 2015Article
- Diabetic foot syndrome: Immune-inflammatory features as possible cardiovascular markers in diabetes.World journal of orthopedics · 2015Review
- Nonalcoholic fatty liver disease and aging: epidemiology to management.World journal of gastroenterology · 2014Review
- Targeting inflammation in diabetes: Newer therapeutic options.World journal of diabetes · 2014Review
- Pathogenesis of liver cirrhosis.World journal of gastroenterology · 2014Review
- Non-alcoholic fatty liver disease, diet and gut microbiota.EXCLI journal · 2014Review
- Pathogenesis of hepatic steatosis: the link between hypercortisolism and non-alcoholic fatty liver disease.World journal of gastroenterology · 2013Review
- Oxidized metabolites of linoleic acid as biomarkers of liver injury in nonalcoholic steatohepatitis.Clinical lipidology · 2013Article
- What is the role of adiponectin in obesity related non-alcoholic fatty liver disease?World journal of gastroenterology · 2013Review
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimTo shed some light on the relationship between anti-apoptotic serum Bcl-2 concentrations and metabolic status, anthropometric parameters, inflammation indices, and non-alcoholic fatty liver disease severity were investigated in 43 young individuals with fatty liver (FL) and 41 with nonalcoholic steatohepatitis (NASH).
methodsCirculating levels of Bcl-2 were detected in 84 patients with ultrasonographic findings of "bright liver" and/or hyper-transaminasemia of unknown origin and/or increase in γ-glutamyl-transpeptidase (γ-GT) strictly in the absence of other acute or chronic liver disease, whose age was not advanced, who gave consent to liver biopsy and were then divided on the basis of the histological results into two groups (43 with FL and 41 with NASH). Twenty lean subjects, apparently healthy and young, were chosen as controls.
resultsSerum Bcl-2 concentrations were significantly higher in the FL group than in the NASH group. Insulin resistance and γ-GT activity were significantly higher in NASH subjects. Apoptotic hepatocytes were significantly more numerous in NASH patients. NASH patients presented with larger spleens and augmented C-reactive protein (CRP) concentrations than healthy subjects. Steatosis grade at histology was similar in both NASH and FL populations. The number of apoptotic cells was significantly related to anti-apoptotic Bcl-2 protein values in FL patients. Bcl-2 serum levels positively correlated to body mass index (BMI) values (P ≤ 0.0001) but not to age of the population. Triglycerides/HDL ratio correlated well to waist circumference in males (P = 0.0008). γ-GT activity was associated with homeostatic metabolic assessment (HOMA) (P = 0.0003) and with serum ferritin (P = 0.02). Bcl-2 concentrations were not related to either spleen size or CRP values. NASH patients presented a weak negative correlation between lobular inflammation and Bcl-2 levels. A prediction by low values of serum Bcl-2 towards a greater presence of metabolically unhealthy overweight/obese patients (MUOs) was evidenced. HOMA, BMI and uric acid, in that sequence, best predicted serum Bcl-2 concentrations.
conclusionMUOs could be detected by Bcl-2 levels. By favoring the life span of hepatocytes, and enhancing triglyceride formation, the anti-apoptotic process inhibits free fatty acids toxicity in FL.
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