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Vascular Disease in Patients with Nonalcoholic Fatty Liver Disease.
Potze, W, Siddiqui, MS, Sanyal, AJ
Seminars in thrombosis and hemostasis. 2015;(5):488-93
Abstract
Nonalcoholic fatty liver disease (NAFLD) is increasingly being diagnosed and is considered to be the most frequent chronic liver disorder in Western countries. It represents a histopathological spectrum ranging from simple hepatic steatosis to steatohepatitis and finally cirrhosis. NAFLD is considered as the hepatic manifestation of the metabolic syndrome and is associated with increased mortality. Increasing evidence now suggests that NAFLD is also associated with higher cardiovascular disease (CVD) morbidity and mortality independent of conventional cardiometabolic risk factors (such as obesity, insulin resistance, and diabetes mellitus). The exact mechanisms linking NAFLD to increased CVD risk are still incompletely understood and likely reflect multiple coexisting pathways. Recent evidence suggests a contributive effect of an altered hemostasis in patients with NAFLD. For example, patients with NAFLD have higher levels of prothrombotic factors (e.g., von Willebrand factor, fibrinogen, factor VII activity, and plasminogen activator inhibitor-1), which correlate with underlying histological severity of the disease. The current review focuses on these hemostatic abnormalities in NAFLD and the link with increased CVD risk.
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Fructose and cardiometabolic disorders: the controversy will, and must, continue.
Wiernsperger, N, Geloen, A, Rapin, JR
Clinics (Sao Paulo, Brazil). 2010;(7):729-38
Abstract
The present review updates the current knowledge on the question of whether high fructose consumption is harmful or not and details new findings which further pushes this old debate. Due to large differences in its metabolic handling when compared to glucose, fructose was indeed suggested to be beneficial for the diet of diabetic patients. However its growing industrial use as a sweetener, especially in soft drinks, has focused attention on its potential harmfulness, possibly leading to dyslipidemia, obesity, insulin resistance/metabolic syndrome and even diabetes. Many new data have been generated over the last years, confirming the lipogenic effect of fructose as well as risks of vascular dysfunction and hypertension. Fructose exerts various direct effects in the liver, affecting both hepatocytes and Kupffer cells and resulting in non-alcoholic steatotic hepatitis, a well known precursor of the metabolic syndrome. Hepatic metabolic abnormalities underlie indirect peripheral metabolic and vascular disturbances, for which uric acid is possibly the culprit.Nevertheless major caveats exist (species, gender, source of fructose, study protocols) which are detailed in this review and presently prevent any firm conclusion. New studies taking into account these confounding factors should be undertaken in order to ascertain whether or not high fructose diet is harmful.
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Roles of the lipid peroxidation product 4-hydroxynonenal in obesity, the metabolic syndrome, and associated vascular and neurodegenerative disorders.
Mattson, MP
Experimental gerontology. 2009;(10):625-33
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Abstract
A rising tide of obesity and type 2 diabetes has resulted from the development of technologies that have made inexpensive high calorie foods readily available and exercise unnecessary for many people. Obesity and the metabolic syndrome (insulin resistance, visceral adiposity and dyslipidemia) wreak havoc on cells throughout the body thereby promoting cardiovascular and kidney disease, and degenerative diseases of the brain and body. Obesity and insulin resistance promote disease by increasing oxidative damage to proteins, lipids and DNA as the result of a combination of increased free radical production and an impaired ability of cells to detoxify the radicals and repair damaged molecules. By covalently modifying membrane-associated proteins, the membrane lipid peroxidation product 4-hydroxynonenal (HNE) may play particularly sinister roles in the metabolic syndrome and associated disease processes. HNE can damage pancreatic beta cells and can impair the ability of muscle and liver cells to respond to insulin. HNE may promote atherosclerosis by modifying lipoproteins and can cause cardiac cell damage by impairing metabolic enzymes. An adverse role for HNE in the brain in obesity and the metabolic syndrome is suggested by studies showing that HNE levels are increased in brain cells with aging and Alzheimer's disease. HNE can cause the dysfunction and degeneration of neurons by modifying membrane-associated glucose and glutamate transporters, ion-motive ATPases, enzymes involved in amyloid metabolism, and cytoskeletal proteins. Exercise and dietary energy restriction reduce HNE production and may also increase cellular systems for HNE detoxification including glutathione and oxidoreductases. The recent development of low molecular weight molecules that scavenge HNE suggests that HNE can be targeted in the design of drugs for the treatment of obesity, the metabolic syndrome, and associated disorders.
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Metabolic syndrome and Alzheimer's disease: a link to a vascular hypothesis?
Milionis, HJ, Florentin, M, Giannopoulos, S
CNS spectrums. 2008;(7):606-13
Abstract
Current evidence from epidemiological, neuroimaging, pathological, pharmacotherapeutic, and clinical studies indicate an association of Alzheimer's disease with risk factors of vascular atherosclerotic disease either in isolation or in aggregate. "Metabolic syndrome" (MetS) is the name for a clustering of risk factors for cardiovascular disease and type 2 diabetes that are of metabolic origin. These include central obesity, elevated plasma glucose, high blood pressure, atherogenic dyslipidemia, a prothrombotic state, and a proinflammatory state. In this article, we provide an overview of the relevant literature with regard to the relationship of Alzheimer's disease with MetS. Accumulating evidence suggests a "vascular hypothesis" to be related to the pathology of Alzheimer's disease. In the light of this evidence, clinician may consider lifestyle interventions toward an early and effective cardiovascular risk-factor management to reduce the cardiometabolic and the cognitive decline risk, while further research of other preventive strategies may be warranted.
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Glycemic control and prevention of microvascular and macrovascular disease in the Steno 2 study.
Vaag, AA
Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists. 2006;:89-92
Abstract
OBJECTIVE To review key findings and insights from the Steno 2 trial involving 160 patients with type 2 diabetes in Denmark. METHODS The Steno 2 study design, with conventional and intensive treatment arms, is described, and the outcomes are summarized. RESULTS Intensive and target-driven behavior modeling and polypharmacy for 7.8 years induced an absolute risk reduction of 20% in cardiovascular disease events in patients with type 2 diabetes and the metabolic syndrome in comparison with a conventional multifactorial treatment. The relative risk reduction found for microvascular events after 4 years was maintained at a similar level after 7.8 years of intervention: nephropathy 61%, retinopathy 58%, and autonomic neuropathy 63%. CONCLUSION Improving glycemic control in patients with type 2 diabetes may be as important as, or even more important than, treating hypertension and dyslipidemia for the prevention of both microvascular and macrovascular complications, particularly when aggressive treatment is initiated at an early stage of the disease.
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Management of the metabolic syndrome as a strategy for preventing the macrovascular complications of type 2 diabetes: controversial issues.
Aguilar-Salinas, CA, Mehta, R, Rojas, R, Gómez-Pérez, FJ, Olaiz, G, Rull, JA
Current diabetes reviews. 2005;(2):145-58
Abstract
The metabolic syndrome is known to increase cardiovascular morbidity and precede the development of type 2 diabetes. Even before the appearance of hyperglycemia, the components of the metabolic syndrome play a crucial role in the pathogenesis of the macrovascular complications. Thus, the recognition and treatment of the metabolic syndrome may be a strategy to prevent the most likely cause of death (i.e. cardiovascular events) in cases that eventually develop type 2 diabetes. In this review, controversial issues regarding the treatment of the two main components of the metabolic syndrome (i.e dyslipidemia and arterial hypertension) are discussed. Several disparities in the current NCEP-ATPIII recommendations, when applied to patients with the metabolic syndrome, are pointed out. In population-based studies, the number of individuals with the metabolic syndrome who would need LDL cholesterol lowering treatment following these guidelines is remarkably low compared to subjects belonging to the same risk strata (10 year risk 10-20%). Subjects with the metabolic syndrome do not fall into the same risk category, resulting in differing LDL-C targets. Also, the Framingham tables underestimate the cardiovascular risk associated with the metabolic syndrome; hence fewer cases qualify for drug therapy. In addition, LDL-C underestimates the number of atherogenic particles and is therefore not the ideal target for these patients. The selection of antihypertensive medication in the metabolic syndrome is also controversial. Thus, there is sufficient evidence for a review of the current management of the metabolic syndrome as part of a strategy to prevent the macrovascular complications in type 2 diabetes.