The effect of cannabinoid receptor 1 blockade on adipokine and proinflammatory cytokine concentration in adipose and hepatic tissue in mice with nonalcoholic fatty liver disease

2019 ◽  
Vol 97 (2) ◽  
pp. 120-129 ◽  
Author(s):  
Bojan Jorgačević ◽  
Danijela Vučević ◽  
Milena Vesković ◽  
Dušan Mladenović ◽  
Dušan Vukićević ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Proinflammatory Cytokine ◽  
Fatty Liver Disease ◽  
Cannabinoid Receptor ◽  
Control Diet ◽  
Hepatic Tissue ◽  
Nonalcoholic Fatty Liver ◽  
Ifn Γ

In high-fat diet (HFD) induced nonalcoholic fatty liver disease (NAFLD), there is an increase in the endocannabinoid system activity, which significantly contributes to steatosis development. The aim of our study was to investigate the effects of cannabinoid receptor type 1 blockade on adipokine and proinflammatory cytokine content in adipose and hepatic tissue in mice with NAFLD. Male mice C57BL/6 were divided into a control group fed with a control diet for 20 weeks (C, n = 6) a group fed with a HFD for 20 weeks (HF, n = 6), a group fed with a control diet and treated with rimonabant after 18 weeks (R, n = 9), and a group fed with HFD and treated with rimonabant after 18 weeks (HFR, n = 10). Rimonabant significantly decreased leptin, resistin, apelin, visfatin, interleukin 6 (IL-6), and interferon-γ (IFN-γ) concentration in subcutaneous and visceral adipose tissue in the HFR group compared to the HF group (p < 0.01). Rimonabant reduced hepatic IL-6 and IFN-γ concentration as well as plasma glucose and insulin concentration and the homeostatic model assessment index in the HFR group compared to the HF group (p < 0.01). It can be concluded that the potential usefulness of CB1 blockade in the treatment of HFD-induced NAFLD is due to modulation of the adipokine profile and proinflammatory cytokines in both adipose tissues and liver as well as glucose metabolism.

scholarly journals Rimonabant Improves Oxidative/Nitrosative Stress in Mice with Nonalcoholic Fatty Liver Disease

2015 ◽  
Vol 2015 ◽  
pp. 1-11 ◽  
Author(s):  
Bojan Jorgačević ◽  
Dušan Mladenović ◽  
Milica Ninković ◽  
Milena Vesković ◽  
Vesna Dragutinović ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Nitrosative Stress ◽  
Cannabinoid Receptor ◽  
Control Diet ◽  
Control Group ◽  
Standard Diet ◽  
Nonalcoholic Fatty Liver

The present study deals with the effects of rimonabant on oxidative/nitrosative stress in high diet- (HFD-) induced experimental nonalcoholic fatty liver disease (NAFLD). Male mice C57BL/6 were divided into the following groups: control group fed with control diet for 20 weeks (C;n=6); group fed with HFD for 20 weeks (HF;n=6); group fed with standard diet and treated with rimonabant after 18 weeks (R;n=9); group fed with HFD and treated with rimonabant after 18 weeks (HFR;n=10). Daily dose of rimonabant (10 mg/kg) was administered to HFR and R group by oral gavage for two weeks. Treatment induced a decrease in hepatic malondialdehyde concentration in HFR group compared to HF group(P<0.01). The concentration of nitrites + nitrates in liver was decreased in HFR group compared to HF group(P<0.01). Liver content of reduced glutathione was higher in HFR group compared to HF group(P<0.01). Total liver superoxide dismutase activity in HFR group was decreased in comparison with HF group(P<0.01). It was found that rimonabant may influence hepatic iron, zinc, copper, and manganese status. Our study indicates potential usefulness of cannabinoid receptor type 1 blockade in the treatment of HFD-induced NAFLD.

scholarly journals Low Hepatic Tissue Copper in Pediatric Nonalcoholic Fatty Liver Disease

2017 ◽  
Vol 65 (1) ◽  
pp. 89-92 ◽  
Author(s):  
Michael Mendoza ◽  
Shelley Caltharp ◽  
Ming Song ◽  
Lindsay Collin ◽  
Juna V. Konomi ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Hepatic Tissue ◽  
Nonalcoholic Fatty Liver

scholarly journals Decreasing mitochondrial fission alleviates hepatic steatosis in a murine model of nonalcoholic fatty liver disease

2014 ◽  
Vol 307 (6) ◽  
pp. G632-G641 ◽  
Author(s):  
Chad A. Galloway ◽  
Hakjoo Lee ◽  
Paul S. Brookes ◽  
Yisang Yoon
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Hepatic Steatosis ◽  
Fatty Liver Disease ◽  
Mitochondrial Fission ◽  
Hepatic Tissue ◽  
Mitochondrial Morphology ◽  
Nonalcoholic Fatty Liver ◽  
Nitrative Stress

Mitochondria produce the majority of cellular ATP through oxidative phosphorylation, and their capacity to do so is influenced by many factors. Mitochondrial morphology is recently suggested as an important contributor in controlling mitochondrial bioenergetics. Mitochondria divide and fuse continuously, which is affected by environmental factors, including metabolic alterations. Underscoring its bioenergetic influence, altered mitochondrial morphology is reported in tissues of patients and in animal models of metabolic dysfunction. In this study, we found that mitochondrial fission plays a vital role in the progression of nonalcoholic fatty liver disease (NAFLD). The development of hepatic steatosis, oxidative/nitrative stress, and hepatic tissue damage, induced by a high-fat diet, were alleviated in genetically manipulated mice suppressing mitochondrial fission. The alleviation of steatosis was recapitulated in primary hepatocytes with the inhibition of mitochondrial fission. Mechanistically, our study indicates that fission inhibition enhances proton leak under conditions of free fatty acid incubation, implicating bioenergetic change through manipulating mitochondrial fission. Taken together, our results suggest a mechanistic role for mitochondrial fission in the etiology of NAFLD. The efficacy of decreasing mitochondrial fission in the suppression of NAFLD suggests that mitochondrial fission represents a novel target for therapeutic treatment of NAFLD.

Clinically Significant Hepatopathology Detected At Cholecystectomy Dramatically Increases Billing

2020 ◽  
Vol 154 (Supplement_1) ◽  
pp. S121-S121
Author(s):  
A Rane ◽  
M Li-cheng Wu
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Medical Training ◽  
De Novo ◽  
Hepatic Tissue ◽  
Nonalcoholic Fatty Liver ◽  
Icd 10 ◽  
Alpha 1 Antitrypsin Deficiency

Abstract Introduction/Objective Incidental hepatic tissue obtained via cholecystectomy is generally minute and inconsequential. For these reasons, the hepatic tissue is bundled with the gallbladder and cannot invoke additional billing. However, hepatic tissue that is very large or that harbors significant hepatopathology has clinical utility and could justify additional billing. We hypothesized that such incidental hepatic tissue would dramatically increase billing because the liver is billed at a higher level of complexity than the gallbladder and requires cytochemistry for evaluation. Methods We retrospectively reviewed pathology reports, slides, and codes from 9 specimens from cholecystectomy that contained hepatic tissue that was grossly evident or that demonstrated significant hepatopathology. Our billing department with decades of experience but without medical training codified the reports using the 10th revision of the International Statistical Classification of Diseases and Related Health Problems (ICD-10) and Current Procedural Terminology (CPT), blinded to our study. Results The patients included 5 women and 4 men, ages 18 to 72 years. Five specimens contained very large pieces of liver 0.8 cm to 2.2 cm long and 0.3 cm to 1.8 cm thick. Diagnoses included nonalcoholic fatty liver disease or steatohepatitis (6 specimens), de novo alpha-1 antitrypsin deficiency (2 specimens), de novo sinusoidal amyloidosis (1 specimen), hemosiderosis (1 specimen), and obstruction (1 specimen). Some specimens demonstrated multiple diagnoses. Only ICD-10 codes K76.0 (6 specimens) and K75.81 (2 specimens) were generated, corresponding to nonalcoholic fatty liver disease and steatohepatitis, respectively. ICD-10 codes were omitted for 1 specimen. Although all specimens generated CPT codes 88312 (20 charges) and 88313 (14 charges), corresponding to cytochemistry, none generated CPT code 88307, corresponding to the liver. Conclusion Incidental hepatic tissue obtained via cholecystectomy dramatically increases billing, but significant hepatic findings and exceptions to coding principles must be clearly conveyed to billing departments to ensure proper coding.

scholarly journals Levels of the Oxidative Stress Marker γ-Glutamyltranspeptidase at Different Stages of Nonalcoholic Fatty Liver Disease

2012 ◽  
Vol 40 (3) ◽  
pp. 924-933 ◽  
Author(s):  
M Irie ◽  
T Sohda ◽  
K Iwata ◽  
H Kunimoto ◽  
A Fukunaga ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Serum Levels ◽  
Oxidative Stress Marker ◽  
Hepatic Tissue ◽  
Nonalcoholic Fatty Liver ◽  
Hepatic Expression

OBJECTIVES: This study investigated oxidative stress in the liver, by determining hepatic expression and serum levels of γ-glutamyltranspeptidase (GGT) and 8-hydroxy-2′-deoxyguanosine (8-OHdG) in different stages of nonalcoholic fatty liver disease (NAFLD), and assessed whether GGT can differentiate between the various stages of NAFLD. METHODS: Expression of GGT and 8-OHdG was examined in biopsy specimens by immunohistochemistry, and serum GGT and 8-OHdG levels were measured by enzyme-linked immunosorbent assays in patients with simple fatty liver ( n = 10), nonalcoholic steatohepatitis (NASH; n = 10) and, as a control, in alcoholic liver disease (ALD; n = 10). RESULTS: Hepatic tissue expression of GGT and 8-OHdG was seen in ALD, NASH and fatty liver patients. The percentage of hepatocytes positive for 8-OHdG expression and serum 8-OHdG levels was significantly higher in patients with NASH than simple fatty liver. Serum GGT levels were increased in all cases with ALD, NASH and fatty liver, and correlated significantly with serum levels of 8-OHdG in ALD and NASH, but not in simple fatty liver. CONCLUSIONS: Levels of GGT in fatty liver patients may compensate for mild oxidative stress by repressing 8-OHdG levels and preventing progression to NASH; however further oxidative stress leads to increased levels of 8-OHdG and the development of NASH.

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