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Macronutrients and the Adipose-Liver Axis in Obesity and Fatty Liver.
Duwaerts, CC, Maher, JJ
Cellular and molecular gastroenterology and hepatology. 2019;(4):749-761
Abstract
Macronutrient metabolism is a highly orchestrated process, with adipose tissue and liver each playing central roles in nutrient uptake, processing, transport, and storage. These 2 tissues form an important metabolic circuit, particularly as it relates to lipids as the primary storage form of excess energy. The function of the circuit is influenced by many factors, including the quantity and type of nutrients consumed and their impact on the overall health of the tissues. In this review we begin with a brief summary of the homeostatic disposition of lipids between adipose tissue and liver and how these processes can become dysregulated in obesity. We then explore how specific dietary nutrients and nutrient combinations can exert unique influences on the liver-adipose tissue axis.
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2.
Effects of newer antidiabetic drugs on nonalcoholic fatty liver and steatohepatitis: Think out of the box!
Ranjbar, G, Mikhailidis, DP, Sahebkar, A
Metabolism: clinical and experimental. 2019;:154001
Abstract
Nonalcoholic fatty liver disease (NAFLD) is the most common chronic liver disease in Western societies and a major cause of hepatic disease worldwide. Its more severe type, namely nonalcoholic steatohepatitis (NASH), may result in the development of cirrhosis and hepatocellular carcinoma. NAFLD, and especially NASH, are also associated with increased cardiovascular morbidity and mortality. Type 2 diabetes mellitus (T2DM) predisposes to NAFLD development and progression via insulin resistance and hyperglycemia. It has also been reported that the majority of T2DM patients have NAFLD/NASH, thus potentially further increasing their cardiometabolic risk. Current guidelines recommend to screen for NAFLD in all T2DM patients and vice-versa. Lifestyle remains the first-line therapeutic option for NAFLD/NASH. Among antidiabetic drugs, pioglitazone was shown to improve histological features of NASH. More recently, there is an increasing interest regarding the effects of newer anti-diabetic drugs, such as dipeptidyl peptidase 4 inhibitors (DPP-4i), sodium glucose cotransporter 2 inhibitors (SGLT2i), and glucagon-like peptide-1 receptor agonists (GLP-1 RAs) on NAFLD/NASH. The present narrative review considers the up-to-date data on the impact of DPP-4i, SGLT2i, and GLP-1 RAs on biochemical and/or histological markers of NAFLD/NASH. The potential clinical implications of these findings in daily practice are also discussed. Taking into consideration the global increasing prevalence of NAFLD/NASH, therapeutic options that can prevent or treat this disease will exert considerable benefits on human health.
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3.
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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4.
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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5.
Measurement of liver fat fraction and iron with MRI and MR spectroscopy techniques.
Sharma, P, Altbach, M, Galons, JP, Kalb, B, Martin, DR
Diagnostic and interventional radiology (Ankara, Turkey). 2014;(1):17-26
Abstract
Diffuse liver disease is a widespread global healthcare burden, and the abnormal accumulation of lipid and/or iron is common to important disease processes. Developing the improved methods for detecting and quantifying liver lipid and iron is an important clinical need. The inherent risk, invasiveness, and sampling error of liver biopsy have prompted the development of noninvasive imaging methods for lipid and iron assessment. Ultrasonography and computed tomography have the ability to detect diffuse liver disease, but with limited accuracy. The purpose of this review is to describe the current state-of-the-art methods for quantifying liver lipid and iron using magnetic resonance imaging and spectroscopy, including their implementation, benefits, and potential pitfalls. Imaging- and spectroscopy-based methods are naturally suited for lipid and iron quantification. Lipid can be detected and decomposed from the inherent chemical shift between lipid and water signals, whereas iron imparts significant paramagnetic susceptibility to tissue, which accelerates proton relaxation. However, measurements of these biomarkers are confounded by technical and biological effects. Current methods must address these factors to allow a precise correlation between the lipid fraction and iron concentration. Although this correlation becomes increasingly challenging in the presence of combined lipid and iron accumulation, advanced techniques show promise for delineating these quantities through multi-lipid peak analysis, T2 water mapping, and fast single-voxel water-lipid spectroscopy.
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6.
Ectopic fat, insulin resistance, and nonalcoholic fatty liver disease: implications for cardiovascular disease.
Byrne, CD, Targher, G
Arteriosclerosis, thrombosis, and vascular biology. 2014;(6):1155-61
Abstract
Ectopic fat accumulation in the liver causes nonalcoholic fatty liver disease (NAFLD), which is the most common cause of chronic liver disease in Western countries. Ectopic liver lipid, particularly diacylglycerol, exacerbates hepatic insulin resistance, promotes systemic inflammation, and increases risk of developing both type 2 diabetes mellitus and cardiovascular disease. Increasing evidence suggests that NAFLD is an emerging risk factor for cardiovascular disease, and although there are currently no licensed treatments for NAFLD per se, current evidence suggests that statin treatment is safe in NAFLD. Presently, there is insufficient evidence to indicate that statins or other cardioprotective agents, such as angiotensin receptor blockers, are effective in treating NAFLD. In this brief narrative review, we discuss the diagnosis of NAFLD and the role of ectopic liver fat to cause insulin resistance and to increase risk of both type 2 diabetes mellitus and cardiovascular disease. For this review, PubMed was searched for articles using the key words non-alcoholic fatty liver disease or fatty liver combined with diabetes risk, cardiovascular risk, and cardiovascular mortality between 1990 and 2014. Articles published in languages other than English were excluded.
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7.
Impact of coffee on liver diseases: a systematic review.
Saab, S, Mallam, D, Cox, GA, Tong, MJ
Liver international : official journal of the International Association for the Study of the Liver. 2014;(4):495-504
Abstract
Coffee is one of the most commonly consumed beverages in the world. Its health benefits including improved overall survival have been demonstrated in a variety of disease states. To examine the association of coffee consumption with liver disease, a systematic review of studies on the effects of coffee on liver associated laboratory tests, viral hepatitis, nonalcoholic fatty liver disease (NAFLD), cirrhosis and hepatocellular carcinoma (HCC) was performed. Coffee consumption was associated with improved serum gamma glutamyltransferase, aspartate aminotransferase and alanine aminotransferase values in a dose dependent manner in individuals at risk for liver disease. In chronic liver disease patients who consume coffee, a decreased risk of progression to cirrhosis, a lowered mortality rate in cirrhosis patients, and a lowered rate of HCC development were observed. In chronic hepatitis C patients, coffee was associated with improved virologic responses to antiviral therapy. Moreover, coffee consumption was inversely related to the severity of steatohepatitis in patients with non-alcoholic fatty liver disease. Therefore, in patients with chronic liver disease, daily coffee consumption should be encouraged.
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8.
The role of medications for the management of patients with NAFLD.
Mazzella, N, Ricciardi, LM, Mazzotti, A, Marchesini, G
Clinics in liver disease. 2014;(1):73-89
Abstract
The article is intended to provide an overview of the strengths and limits of controlled trials of pharmacologic treatment of nonalcoholic fatty liver disease. No drug has so far been approved, although validated on histologic outcomes. Several new drugs are under scrutiny, acting with different mechanisms along the chain of events from fatty liver to fibrosis, cirrhosis, and hepatocellular carcinoma. The article investigates which drug, if any, should be preferred for a tailored intervention in individual patients, according to age, comorbidities, and disease severity, and if treatment should be continued lifelong, to prevent disease progression and long-term occurrence of cirrhosis.
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9.
Coffee and non-alcoholic fatty liver disease: brewing evidence for hepatoprotection?
Chen, S, Teoh, NC, Chitturi, S, Farrell, GC
Journal of gastroenterology and hepatology. 2014;(3):435-41
Abstract
Coffee is one of the most popular beverages in the world. Several studies consistently show that coffee drinkers with chronic liver disease have a reduced risk of cirrhosis and a lower incidence of hepatocellular carcinoma regardless of primary etiology. With the increasing prevalence of non-alcoholic fatty liver disease (NAFLD) worldwide, there is renewed interest in the effect of coffee intake on NAFLD severity and positive clinical outcomes. This review gives an overview of growing epidemiological and clinical evidence which indicate that coffee consumption reduces severity of NAFLD. These studies vary in methodology, and potential confounding factors have not always been completely excluded. However, it does appear that coffee, and particular components other than caffeine, reduce NAFLD prevalence and inflammation of non-alcoholic steatohepatitis. Several possible mechanisms underlying coffee's hepatoprotective effects in NAFLD include antioxidative, anti-inflammatory, and antifibrotic effects, while a chemopreventive effect against hepatocarcinogenesis seems likely. The so-far limited data supporting such effects will be discussed, and the need for further study is highlighted.
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10.
Should we lower lipids in nonalcoholic fatty liver disease?
Farrell, G
Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association. 2014;(1):152-5