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The effects of canola and olive oils consumption compared to sunflower oil, on lipid profile and hepatic steatosis in women with polycystic ovarian syndrome: a randomized controlled trial.
Yahay, M, Heidari, Z, Allameh, Z, Amani, R
Lipids in health and disease. 2021;(1):7
Abstract
BACKGROUND Polycystic Ovarian Syndrome (PCOS) is one of the most common endocrinopathies and metabolic disorders in women during their reproductive years. It is often associated with dyslipidemia and other risk factors of cardiovascular diseases (CVD). This study was aimed to evaluate dietary intervention effects with canola and olive oils compared to sunflower oil on lipid profile and fatty liver severity among women with PCOS. METHOD This study was a 10-week intervention including 72 women with PCOS. Patients were randomly assigned to three groups for receiving 25 g/day canola, olive, or sunflower oils for 10 weeks. The primary and secondary outcomes were to assess changes in lipid profile and in fatty liver severity, respectively. RESULT At the end of the study, 72 patients with a mean age of 29.31 were analysed. Canola oil consumption resulted in a significant reduction in serum levels of TG (P = 0.002) and TC/HDL (P = 0.021), LDL/HDL (P = 0.047), and TG/HDL (P = 0.001) ratios, however, there was no significant reduction in lipid profile following olive oil consumption. Canola (P < 0.001) and olive oils (P = 0.005) could significantly reduce the fatty liver grade. Moreover, HOMA-IR in both canola (P < 0.001) and olive (P = 0.004) groups was significantly decreased. CONCLUSION In total, compared to olive and sunflower oils, significant improvements in lipid profile, liver function, and HOMA-IR were observed following canola oil consumption in women with PCOS. TRIAL REGISTRATION IR.MUI. RESEARCH REC.1397.315. Registered 30 JUNE 2019 - Retrospectively registered, https://www.irct.ir/trial/38684.
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Circulating PCSK9 is associated with liver biomarkers and hepatic steatosis.
Paquette, M, Gauthier, D, Chamberland, A, Prat, A, De Lucia Rolfe, E, Rasmussen, JJ, Kaduka, L, Seidah, NG, Bernard, S, Christensen, DL, et al
Clinical biochemistry. 2020;:20-25
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Abstract
BACKGROUND In parallel to the increasing prevalence of metabolic syndrome, the prevalence of hepatic steatosis has also increased dramatically worldwide. Hepatic steatosis is a major risk factor of hepatic cirrhosis, cardiovascular disease and type 2 diabetes. Circulating levels of proprotein convertase subtilisin/kexin type 9 (PCSK9) have been positively associated with the metabolic syndrome. However, the association between PCSK9 and the liver function is still controversial. OBJECTIVE The objective of this study is to investigate the association between circulating PCSK9 levels and the presence of hepatic steatosis, as well as with liver biomarkers in a cohort of healthy individuals. METHODS Total PCSK9 levels were measured by an in-house ELISA using a polyclonal antibody. Plasma albumin, alkaline phosphatase, ALT, AST, total bilirubin and GGT were measured in 698 individuals using the COBAS system. The presence of hepatic steatosis was assessed using ultrasound liver scans. RESULTS In a multiple regression model adjusted for age, sex, insulin resistance, body mass index and alcohol use, circulating PCSK9 level was positively associated with albumin (β = 0.102, P = 0.008), alkaline phosphatase (β = 0.201, P < 0.0001), ALT (β = 0.238, P < 0.0001), AST (β = 0.120, P = 0.003) and GGT (β = 0.103, P = 0.007) and negatively associated with total bilirubin (β = -0.150, P < 0.0001). Tertile of circulating PCSK9 was also associated with hepatic steatosis (OR 1.48, 95% CI 1.05-2.08, P = 0.02). CONCLUSION Our data suggest a strong association between PCSK9 and liver biomarkers as well as hepatic steatosis. Further studies are needed to explore the role of PCSK9 on hepatic function.
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Dyslipidemia and Fatty Liver Disease in Overweight and Obese Children.
Deeb, A, Attia, S, Mahmoud, S, Elhaj, G, Elfatih, A
Journal of obesity. 2018;:8626818
Abstract
INTRODUCTION Obesity is a worldwide concern. It is associated with morbidity such as dyslipidemia and liver disease. Childhood obesity has dramatically increased, particularly in the Gulf region. We aim to assess the prevalence of dyslipidemia and fatty liver disease (FLD) in overweight and obese children and analyze the association between different anthropometric measures with dyslipidemia and fatty liver disease. METHODS A descriptive, cross-sectional study conducted on children referred with obesity. BMI percentiles were plotted and standardized waist circumference (WC) was generated. Family history of metabolic syndrome was recorded. Fasting lipid, liver transaminases, and ultrasound scans (US) for those with elevated enzymes were performed. Descriptive statistics were used for quantitative parameters. RESULTS 216 participants were recruited. Mean ± SD age was 10.58 ± 2.996 years. 55.3% had dyslipidemia; 11.7% had high cholesterol, 28.6% high triglyceride, 32.7% high LDL, and 18.0% low HDL. 51 (84%) had either elevated transaminases. All had liver US, and 43 had FLD. WC was strongly associated with dyslipidemia and FLD (P=0.04 and 0.003). CONCLUSION Dyslipidemia is common in overweight, obese children. FLD is prevalent in those with elevated liver transaminases. WC is an easy tool that can be utilized to screen for dyslipidemia and FLD in overweight and obese children.
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Proton pump inhibitors as risk factor for metabolic syndrome and hepatic steatosis in coeliac disease patients on gluten-free diet.
Imperatore, N, Tortora, R, Testa, A, Gerbino, N, Caporaso, N, Rispo, A
Journal of gastroenterology. 2018;(4):507-516
Abstract
BACKGROUND Recent research has shown that patients with coeliac disease (CD) are at risk of developing metabolic syndrome (MS) and hepatic steatosis (HS) after commencing a gluten-free diet (GFD). This study aimed to evaluate the predictive factors for MS and HS in CD after 1 year of GFD. METHODS All consecutive newly diagnosed CD patients were enrolled. We prospectively collected data about BMI; waist circumference; blood pressure; cholesterol; triglycerides, glucose and insulin blood levels; insulin resistance (through the homeostatic model assessment HOMA-IR) and treatment with proton pump inhibitors (PPI). Diagnosis of MS was made in accordance with current guidelines and HS was diagnosed by ultrasonography. The prevalence of MS and HS was re-assessed after 1 year of GFD. A logistic regression analysis was performed to identify risk factors for MS and HS occurrence after 1 year of GFD. RESULTS Of 301 patients with newly diagnosed CD, 4.3% met criteria for diagnosis of MS and 25.9% presented with HS at the time of CD diagnosis; 99 subjects (32.8%) had long-term exposure to PPI during the study period. After 1 year, 72 (23.9%) patients had developed MS (4.3 vs 23.9%; p < 0.001, OR 6.9) and 112 (37.2%) had developed HS (25.9 vs 37.2%; p < 0.01, OR 1.69). At multivariate analysis, high BMI at diagnosis (OR 10.8; p < 0.001) and PPI exposure (OR 22.9; p < 0.001) were the only factors associated with the occurrence of MS; HOMA-IR (OR 9.7; p < 0.001) and PPI exposure (OR 9.2; p < 0.001) were the only factors associated with the occurrence of HS. CONCLUSIONS PPI exposure adds further risk of occurrence of MS and HS for patients with CD on GFD. The use of PPI in patients with CD on GFD should be limited to strict indications.
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Conversion of Sugar to Fat: Is Hepatic de Novo Lipogenesis Leading to Metabolic Syndrome and Associated Chronic Diseases?
Schwarz, JM, Clearfield, M, Mulligan, K
The Journal of the American Osteopathic Association. 2017;(8):520-527
Abstract
Epidemiologic studies suggest a link between excess sugar consumption and obesity, fatty liver disease, metabolic syndrome, and type 2 diabetes mellitus. One important pathway that may link these metabolic diseases to sugar consumption is hepatic conversion of sugar to fat, a process known as de novo lipogenesis (DNL). Mechanistic studies have shown that diets high in simple sugars increase both DNL and liver fat. Importantly, removal of sugar from diets of children with obesity for only 9 days consistently reduced DNL and liver fat and improved glucose and lipid metabolism. Although the sugar and beverage industries continue to question the scientific evidence linking high-sugar diets to metabolic diseases, major health organizations now make evidence-based recommendations to limit consumption of simple sugars to no more than 5% to 10% of daily intake. Clear recommendation about moderating sugar intake to patients may be an important nonpharmacologic tool to include in clinical practice.
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EJE PRIZE 2015: How does insulin resistance arise, and how does it cause disease? Human genetic lessons.
Semple, RK
European journal of endocrinology. 2016;(5):R209-23
Abstract
Insulin orchestrates physiological responses to ingested nutrients; however, although it elicits widely ramifying metabolic and trophic responses from diverse tissues, 'insulin resistance (IR)', a pandemic metabolic derangement commonly associated with obesity, is usually defined solely by blunting of insulin's hypoglycaemic effect. Recent study of monogenic forms of IR has established that biochemical subphenotypes of IR exist, clustering into those caused by primary disorders of adipose tissue and those caused by primary defects in proximal insulin signalling. IR is often first recognised by virtue of its associated disorders including type 2 diabetes, dyslipidaemia (DL), fatty liver and polycystic ovary syndrome (PCOS). Although these clinically observed associations are confirmed by cross-sectional and longitudinal population-based studies, causal relationships among these phenomena have been more difficult to establish. Single gene IR is important to recognise in order to optimise clinical management and also permits testing of causal relationships among components of the IR syndrome using the principle of Mendelian randomisation. Thus, where a precisely defined genetic defect is identified that directly produces one component of the syndrome, then phenomena that are causally linked to that component should be seen. Where this is not the case, then a simple causal link is refuted. This article summarises known forms of monogenic severe IR and considers the lessons to be learned about the pathogenic mechanisms both upstream from common IR and those downstream linking it to disorders such as DL, fatty liver, PCOS and cancer.
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Systematic review with meta-analysis: non-alcoholic steatohepatitis - a case for personalised treatment based on pathogenic targets.
Younossi, ZM, Reyes, MJ, Mishra, A, Mehta, R, Henry, L
Alimentary pharmacology & therapeutics. 2014;(1):3-14
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BACKGROUND Non-alcoholic fatty liver disease (NAFLD) is an umbrella term, which encompasses simple steatosis and non-alcoholic steatohepatitis (NASH). The entire spectrum of NAFLD has been associated with metabolic syndrome. NASH is associated with increased mortality compared with that of the general population. Many therapeutic options for NASH have been studied. However, there is very little evidence supporting the efficacy of most regimens for the treatment of NASH. AIM: To provide a review focusing on the current therapeutic options available for patients with NASH as well as to briefly introduce possible future interventions. METHODS A MEDLINE, Pubmed and Cochrane Review database search using a combination of keywords, which included non-alcoholic fatty liver disease, non-alcoholic hepatic steatosis, NAFLD, NASH, treatment, therapeutics, vitamin E, orlistat and bariatric surgery. An overall summary of the articles was developed for each section of discussion in this review. RESULTS NASH associated with metabolic syndrome can progress advanced fibrosis and cirrhosis. Weight loss and lifestyle modification have been shown to improve NASH. Other medications used for weight loss and metabolic syndrome have been evaluated, such as orlistat, metformin and thiazolidinediones. Alternative regimens using ursodeoxycholic acid, statins and probiotics as well as bariatric surgery have been evaluated, but have not been recommended as first-line treatment for NASH. Vitamin E for NASH patients without diabetes seems to be promising. The lack of effective treatment for NASH suggests the heterogeneity of patients presenting with the NASH phenotype. The best treatment strategy for these patients may be to identify their pathogenic target and develop personalised treatment protocols. CONCLUSIONS Currently, there are few options available for the management of NASH. Future targeted treatment strategies based on the pathogenic pathways may be needed to develop effective treatment for patients with NASH.
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Omega-3 fatty acids for treatment of non-alcoholic fatty liver disease: design and rationale of randomized controlled trial.
Janczyk, W, Socha, P, Lebensztejn, D, Wierzbicka, A, Mazur, A, Neuhoff-Murawska, J, Matusik, P
BMC pediatrics. 2013;:85
Abstract
BACKGROUND Non-alcoholic fatty liver disease (NAFLD) is a liver manifestation of metabolic syndrome since obesity and insulin resistance are the main pathogenic contributors for both conditions. NAFLD carries increased risk of atherosclerosis and cardiovascular diseases. There is an urgent need to find effective and safe therapy for children and adults with NAFLD. Data from research and clinical studies suggest that omega-3 fatty acids may be beneficial in metabolic syndrome-related conditions and can reduce the risk of cardiovascular disease. METHODS/DESIGN We are conducting a randomized, multicenter, double-blind, placebo-controlled trial of treatment with omega-3 fatty acids in children with NAFLD. Patients are randomized to receive either omega-3 fatty acids containing docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) or placebo for 24 weeks. The dose of omega-3 (DHA+ EPA) ranges from 450 to 1300 mg daily. Low calorie diet and increased physical activity are advised and monitored using validated questionnaires. The primary outcome of the trial is the number of patients who decreased ALT activity by ≥ 0,3 of upper limit of normal. The main secondary outcomes are improvement in the laboratory liver tests, liver steatosis on ultrasound, markers of insulin resistance and difference in fat/lean body mass composition after 6 months of intervention. DISCUSSION Potential efficacy of omega-3 fatty acids in the treatment of NAFLD will provide needed rationale for use of this safe diet supplement together with weight reduction therapy in the growing population of children with NAFLD. TRIAL REGISTRATION NCT01547910.
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Calorie-sweetened beverages and fructose: what have we learned 10 years later.
Bray, GA, Popkin, BM
Pediatric obesity. 2013;(4):242-8
Abstract
BACKGROUND Sugar-sweetened drinks and the fructose they provide are associated with several health problems. METHODS Data from the Nielsen Homescan and product content were analysed for sweetener type using the Gladson Nutrition Database. Meta-analyses and randomized clinical trials were used to evaluate outcomes of beverage and fructose intake. RESULTS Over 70% of all foods contain some amounts of added sugar, and consumption of soft drinks has increased fivefold since 1950. Meta-analyses suggest that consumption of sugar-sweetened beverages is related to the risk of diabetes, the metabolic syndrome and cardiovascular disease in adults and in children. Drinking two sugar-sweetened beverages per day for 6 months induced features of the metabolic syndrome and fatty liver. Randomized, controlled trials in children and adults lasting from 6 months to 2 years have shown that lowering the intake of soft drinks reduced weight gain. Genetic factors influence the weight gain when drinking soft drinks. CONCLUSION Consumption of calorie-sweetened beverages and the fructose they contain has continued to increase and may play a role in the epidemic of obesity, the metabolic syndrome and fatty liver disease. Reducing intake of soft drinks is associated with less weight gain and metabolic improvement as well.
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Dyslipidemia in patients with nonalcoholic fatty liver disease.
Chatrath, H, Vuppalanchi, R, Chalasani, N
Seminars in liver disease. 2012;(1):22-9
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Abstract
Patients with nonalcoholic fatty liver disease (NAFLD) often have dyslipidemia along with other features of metabolic syndrome such as obesity, diabetes mellitus, and hypertension. The dyslipidemia in NAFLD is characterized by increased serum triglycerides, increased small, dense low-density lipoprotein (LDL nontype A) particles, and low high-density lipoprotein (HDL) cholesterol. The pathogenesis of dyslipidemia in NAFLD is not well understood, but it is likely related to hepatic overproduction of the very low-density lipoprotein particles and dysregulated clearance of lipoproteins from the circulation. There is unequivocal evidence that cardiovascular disease is the most common cause of mortality in patients with NAFLD. Aggressive treatment of dyslipidemia plays a critical role in the overall management of patients with NAFLD. Statins are the first-line agents to treat high cholesterol and their dosage should be adjusted based on achieving therapeutic targets and tolerability. Although all statins appear to be effective in improving cholesterol levels in patients with NAFLD, there is more experience with atorvastatin in patients with NAFLD; furthermore, it is the only statin to date to show a reduced cardiovascular morbidity in patients with NAFLD. The risk for serious liver injury from statins is quite rare and patients with NAFLD are not at increased risk for statin hepatotoxicity. Omega-3 fatty acids are perhaps the first choice to treat hypertriglyceridemia because of their safety, tolerability, and efficacy in improving serum triglycerides, as well as their potential to improve liver disease.