Determinants of Physical Activity Engagement in Patients With Nonalcoholic Fatty Liver Disease: The Need for an Individualized Approach to Lifestyle Interventions

2020 ◽  
Author(s):  
Philip O’Gorman ◽  
Ann Monaghan ◽  
Marie McGrath ◽  
Sara Naimimohasses ◽  
John Gormley ◽  
...  

Abstract Objectives Physical activity (PA) is an important non-pharmacological treatment for non-alcoholic fatty liver disease (NAFLD). This study investigated the determinants of PA engagement and awareness of the World Health Organisation (WHO) PA guidelines in patients with NAFLD. Methods Study participants were 101 patients with NAFLD (median age: 54 [IQR = 15] y; 53 women and 48 men) who completed 4 questionnaires: (1) a PA guideline awareness questionnaire; (2) a PA questionnaire assessing PA levels; and (3) 2 questionnaires assessing perceived barriers and motivators for engaging in PA. Binary logistic regression was performed to assess predictors of PA levels. Results Twenty-four percent of participants correctly identified the recommended WHO weekly PA guidelines, and 39% adhered to the guidelines. Lack of willpower, time and energy were the most frequently cited barrier domains. Scores for lack of willpower (odds ratio [OR] = 1.45, 95% CI = 1.088–1.919) and lack of resources (OR = 1.378, 95% CI = 1.003–1.893), and reporting 3 or more ‘significant’ barrier domains (OR = 5.48, 95% CI = 1.792–15.873) were significant predictors of PA levels. Maintaining health and fitness was the most cited motivator domain and was a significant predictor (OR = 2.551, 95% CI = 1.253–5.208) of PA levels. Conclusions This study highlights) the lack of awareness of the WHO PA guidelines and the key determinants of PA participation in patients with NAFLD. Determinants of PA should be identified at the individual level to create a personalized approach for PA maintenance for people with NAFLD to promote lifelong participation in PA. Impact This study closes a gap in the published data on the determinants of PA engagement in patients with NAFLD.

2018 ◽  
Vol 1 (2) ◽  
pp. 24-28
Author(s):  
Tanita Suttichaimongkol

Non-alcoholic fatty liver disease (NAFLD) is a leading cause of death from liver cirrhosis, endstage liver disease, and hepatocellular carcinoma. It is also associated with increased cardiovasculardisease and cancer related mortality. While lifestyle modifications are the mainstay of treatment,only a proportion of patients are able to make due to difficult to achieve and maintain, and so moretreatment options are required such as pharmacotherapy. This review presents the drugs used inmanaging NAFLD and their pharmacologic targets. Therapies are currently directed towards improvingthe metabolic status of the liver, insulin resistance, cell oxidative stress, apoptosis, inflammation orfibrosis. Several agents are now in large clinical trials and within the next few years, the availability oftherapeutic options for NAFLD will be approved.     Keywords: nonalcoholic fatty liver disease, nonalcoholic steatohepatitis, fibrosis, cirrhosis  


2020 ◽  
Vol 21 (6) ◽  
pp. 599-609 ◽  
Author(s):  
Longxin Qiu ◽  
Chang Guo

Aldose reductase (AR) has been reported to be involved in the development of nonalcoholic fatty liver disease (NAFLD). Hepatic AR is induced under hyperglycemia condition and converts excess glucose to lipogenic fructose, which contributes in part to the accumulation of fat in the liver cells of diabetes rodents. In addition, the hyperglycemia-induced AR or nutrition-induced AR causes suppression of the transcriptional activity of peroxisome proliferator-activated receptor (PPAR) α and reduced lipolysis in the liver, which also contribute to the development of NAFLD. Moreover, AR induction in non-alcoholic steatohepatitis (NASH) may aggravate oxidative stress and the expression of inflammatory cytokines in the liver. Here, we summarize the knowledge on AR inhibitors of plant origin and review the effect of some plant-derived AR inhibitors on NAFLD/NASH in rodents. Natural AR inhibitors may improve NAFLD at least in part through attenuating oxidative stress and inflammatory cytokine expression. Some of the natural AR inhibitors have been reported to attenuate hepatic steatosis through the regulation of PPARα-mediated fatty acid oxidation. In this review, we propose that the natural AR inhibitors are potential therapeutic agents for NAFLD.


2015 ◽  
Vol 32 (2) ◽  
pp. 71-77 ◽  
Author(s):  
Shahinul Alam ◽  
Mahabubul Alam ◽  
Sheikh Mohammad Noor E Alam ◽  
Ziaur Rahman Chowdhury ◽  
Jahangir Kabir

Fatty liver is a common cause of chronic liver disease in developed as well as developing countries.We have designed this study to estimate the prevalence and predictors for non alcoholic steatohepatitis (NASH) in non alcoholic fatty liver disease (NAFLD). We have included 493 patients with sonographic evidence of fatty change in liver and 177 of them had done liver biopsy for histopathological study. Other causes of liver disease and alcohol consumption were excluded. Metabolic syndrome and biochemical and anthropometric evaluation was done. Females were predominating 250 (57.0 %). Centrally obese 422 (96.2 %) was more than over all obesity330 (75.1%). NASH was absent in 10 (5.6%) cases and diagnostic of NASH was 75 Journal of Bangladesh College of Physicians and Surgeons Vol. 32, No. 2, April 2014 (42.4 %).Presence of diabetes could significantly (p = 0.001) predicted NASH. Age, sex, BMI, waist circumference, Serum HDL,triglyceride, insulin resistance index, hypertension, metabolic syndrome could not predict NASH. Serum GGT level was significantly (p = 0.05) higher in NASHwith a sensitivity of 45 % and specificity of 68 % only. Serum ALT and AST level could not detect NASH. Females were predominant sufferer of NAFLD in Bangladesh. Prevalence of NASH was much higher42.4%. Diabetes was the main predictor of NASH. GGT was the only biochemical indicator of NASH. We recommend liver biopsy in NAFLD with diabetes and raised GGT.J Bangladesh Coll Phys Surg 2014; 32: 71-77


2021 ◽  
Vol 12 ◽  
Author(s):  
Hongguo Guan ◽  
Yiyan Wang ◽  
Huitao Li ◽  
Qiqi Zhu ◽  
Xiaoheng Li ◽  
...  

Background: 11β-Hydroxysteroid dehydrogenase one is responsible for activating inert glucocorticoid cortisone into biologically active cortisol in humans and may be a novel target for the treatment of nonalcoholic fatty liver disease.Methods: A series of benzylidene cyclopentanone derivatives were synthesized, and the selective inhibitory effects on rat, mouse and human 11β-hydroxysteroid dehydrogenase one and two were screened. The most potent compound [5-bis-(2,6-difluoro-benzylidene)-cyclopentanone] (WZS08), was used to treat nonalcoholic fatty liver disease in mice fed a high-fat-diet for 100 days.Results: WZS08 was the most potent inhibitor of rat, mouse, and human 11β-hydroxysteroid dehydrogenase 1, with half maximum inhibitory concentrations of 378.0, 244.1, and 621.1 nM, respectively, and it did not affect 11β-hydroxysteroid dehydrogenase two at 100 μM. When mice were fed WZS08 (1, 2, and 4 mg/kg) for 100 days, WZS08 significantly lowered the serum insulin levels and insulin index at 4 mg/kg. WZS08 significantly reduced the levels of serum triglycerides, cholesterol, low-density lipoprotein, and hepatic fat ratio at low concentration of 1 mg/kg. It down-regulated Plin2 expression and up-regulated Fabp4 expression at low concentration of 1 mg/kg. It significantly improved the morphology of the non-alcoholic fatty liver.Conclusion: WZS08 selectively inhibits rat, mouse, and human 11β-hydroxysteroid dehydrogenase 1, and can treat non-alcoholic fatty liver disease in a mouse model.


2016 ◽  
Vol 36 (suppl_1) ◽  
Author(s):  
Takhar Kasumov

Objectives: Nonalcoholic fatty liver disease (NAFLD) is associated with an increased rate of cardiovascular disease (CVD) related mortality. HDL protects against CVD through reverse cholesterol transport, anti-oxidant and anti-inflammatory functions. HDL functions and the proteome composition are altered in CVD. We used 2 H 2 O metabolic labeling approach to test hypothesis that altered HDL proteome dynamics is involved in HDL dysfunction in NAFLD. Methods: The kinetics of HDL proteins were measured in patients NAFLD (n=12) and healthy controls (n=8). Each subject consumed 2 H 2 O in their drinking water and blood samples were collected at different time points during one week. 2 H-enrichment of tryptic peptides from HDL proteins were analyzed by mass spectrometry. Oxidase activity of HDL-associated ceruloplasmin (Cp) and HDL’s inflammatory index were quantified using spectrophotometric assays. Results: Compared to control, NAFLD had higher BMI, Hba1c, HOMA-IR, plasma AST, ALT and triglycerides, but similar LDL and HDL cholesterol. NAFLD also had higher inflammatory index (1.8±0.5 vs 1.2±0.2 RUF/mgHDLc/min, p<0.05) and oxidase activity of Cp (93.7±61.2 vs 61.2 U/L, p<0.005). This was associated with increased serum actvity of MPO (6.2±1.2 vs 8.4±1.6, p<0.05), a nutrophile-derived protein involved in HDL dysfunction. HDL NAFLD was significantly enriched with proteins involved in the acute phase response (complement 3, Cp) but depleted in apoAII and PON1. These changes were associated with increased fractional catabolic rates (FCRs) of apoAI (1.6±0.2 vs 1.1±0.3 %/h), apoAII (1.6±0.2 vs 1.1±0.3 %/h), apoAIV (2.6±0.8 vs 3.9±0.7%/h) and increased relative production rate (RPR) of complement 3 (>4 fold). Oxidase activity of Cp was positively associated with FCR of apoAI (r=0.53, p=0.002) and RPR of C3 (r=0.32, p=0.03). Conclusions: HDL dysfunction in NASH could be related to the altered turnover of HDL proteins, including increased degradation of apoAI, apoAII, apoAIV and increased production of C3.


2019 ◽  
Vol 8 (7) ◽  
pp. 1013 ◽  
Author(s):  
Jang ◽  
Lee ◽  
Lee ◽  
Kim

The aim of the current study was to examine the independent association of physical activity with nonalcoholic fatty liver disease (NAFLD) and aminotransferases while adjusting for obesity and diet. Cross-sectional data from 32,391 participants aged ≥ 20 years in the Korea National Health and Nutrition Examination Surveys (KNHANES) was analyzed by logistic regression models and general linear models. Physical activity was assessed from the questionnaire by health-enhancing physical activity (HEPA). The physical activity was negatively associated with NAFLD and lean NAFLD after adjustment for multiple factors with an odds ratio of 0.7 (95% CI, 0.6–0.8) and 0.5 (95% CI, 0.4–0.7) comparing the most active (HEPA active) and the least active (inactive) participants. Among the participants with NAFLD, physical activity also showed an independent negative association with alanine aminotransferase (ALT) levels but not with aspartate aminotransferase levels. These independent associations were not observed when comparing the minimally active and inactive participants except for the risk of lean NAFLD. Physical activity is independently associated with the degree of hepatocellular injury in patients with NAFLD as well as the risk of NAFLD and lean NAFLD in the general population. Sufficiently active physical activity greater than a minimally active level may be needed to lower the risk of NAFLD and ALT levels.


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