Ezetimibe beneficially influences fasting and postprandial triglyceride-rich lipoproteins in type 2 diabetes

Bozzetto, Lutgarda; Annuzzi, Giovanni; Corte, G. Della; Patti, L.; Cipriano, Paola; Mangione, Anna; Riccardi, Gabriele; Rivellese, Angela Albarosa

doi:10.1016/j.atherosclerosis.2011.03.012

Cited by 65 publications

(45 citation statements)

References 24 publications

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“…Ezetimibe has slight positive effects in lowering plasma fasting TG (8%) [153]. In addition, ezetimibe reduces the cholesterol content of both fasting and postprandial TG -rich lipoproteins, thereby lowering the concentrations of atherogenic remnant particles [154]. Initial experience of ezetimibe/fibrates combination seems promising [155,156].…”

Section: Management Of Hypertriglyceridemiamentioning

confidence: 99%

Hypertriglyceridemia: a too long unfairly neglected major cardiovascular risk factor

Tenenbaum

Klempfner

Fisman

2014

Cardiovasc Diabetol

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The existence of an independent association between elevated triglyceride (TG) levels, cardiovascular (CV) risk and mortality has been largely controversial. The main difficulty in isolating the effect of hypertriglyceridemia on CV risk is the fact that elevated triglyceride levels are commonly associated with concomitant changes in high density lipoprotein (HDL), low density lipoprotein (LDL) and other lipoproteins. As a result of this problem and in disregard of the real biological role of TG, its significance as a plausible therapeutic target was unfoundedly underestimated for many years. However, taking epidemiological data together, both moderate and severe hypertriglyceridaemia are associated with a substantially increased long term total mortality and CV risk. Plasma TG levels partially reflect the concentration of the triglyceride-carrying lipoproteins (TRL): very low density lipoprotein (VLDL), chylomicrons and their remnants. Furthermore, hypertriglyceridemia commonly leads to reduction in HDL and increase in atherogenic small dense LDL levels. TG may also stimulate atherogenesis by mechanisms, such excessive free fatty acids (FFA) release, production of proinflammatory cytokines, fibrinogen, coagulation factors and impairment of fibrinolysis. Genetic studies strongly support hypertriglyceridemia and high concentrations of TRL as causal risk factors for CV disease. The most common forms of hypertriglyceridemia are related to overweight and sedentary life style, which in turn lead to insulin resistance, metabolic syndrome (MS) and type 2 diabetes mellitus (T2DM). Intensive lifestyle therapy is the main initial treatment of hypertriglyceridemia. Statins are a cornerstone of the modern lipids-modifying therapy. If the primary goal is to lower TG levels, fibrates (bezafibrate and fenofibrate for monotherapy, and in combination with statin; gemfibrozil only for monotherapy) could be the preferable drugs. Also ezetimibe has mild positive effects in lowering TG. Initial experience with en ezetimibe/fibrates combination seems promising. The recently released IMPROVE-IT Trial is the first to prove that adding a non-statin drug (ezetimibe) to a statin lowers the risk of future CV events. In conclusion, the classical clinical paradigm of lipids-modifying treatment should be changed and high TG should be recognized as an important target for therapy in their own right. Hypertriglyceridemia should be treated.

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Section: Management Of Hypertriglyceridemiamentioning

confidence: 99%

Hypertriglyceridemia: a too long unfairly neglected major cardiovascular risk factor

Tenenbaum

Klempfner

Fisman

2014

Cardiovasc Diabetol

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“…160,161 Similar results have been noted in type 2 diabetic subjects when the same dose of ezetimibe (10mg/day) was added to a lipid lower treatment with simvastatin 20mg. 162 In addition, it seems that this medication may suppress postprandial endothelial dysfunction, as this has been assessed by brachial artery flow-mediated dilation. 163 In respect to ezetimibe efficacy in ameliorating postprandial hyperlipidemia compared to statin therapy, a multicenter, double-blind, crossover trial in 100 abdominally obese patients with metabolic syndrome showed that adding 10mg ezetimibe to a low dose statin treatment (10mg simvastatin) has an equal effect compared to a high dose statin treatment (simvastatin 80mg) in postprandial plasma lipids as well as in fasting and postprandial change of endothelial function.…”

Section: Ezetimibementioning

confidence: 99%

Postprandial dysmetabolism: Too early or too late?

Pappas¹,

Kandaraki²,

Tsirona³

et al. 2016

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postprandial dysmetabolism is a postprandial state characterized by abnormal metabolism of glucose and lipids and, more specifically, of elevated levels of glucose and triglyceride (Tg) containing lipoproteins. Since there is evidence that postprandial dysmetabolism is associated with increased cardiovascular mortality and morbidity, due to macro-and microvascular complications, as well as with conditions such as polycystic ovary syndrome (pCOS) and nonalcoholic fatty liver disease (NaFlD), it is recommended that clinicians be alert for early detection and management of this condition. management consists of a holistic approach including dietary modification, exercise and use of hypoglycemic and hypolipidemic medication aiming to decrease the postprandial values of circulating glucose and triglycerides. This review aims to explain glucose and lipid homeostasis and the impact of postprandial dysmetabolism on the cardiovascular system as well as to offer suggestions with regard to the therapeutic approach for this entity. however, more trials are required to prevent or reverse early and not too late the actual tissue damage due to postprandial dysmetabolism.

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“…A more prominent effect is observed in ameliorating postprandial lipaemia and lowering TRL remnants in spite of background statin [97,98] . In a 6-wk trial of simvastatin-ezetimibe vs. simvastatin monotherapy, fasting and postprandial plasma triglyceride and apoB-48 concentrations were lowered in type 2 diabetic patients [99] . However, intensive lipid lowering with a statin plus ezetimibe may not consistently lower subclinical carotid atherosclerosis in type 2 diabetes, although progression of carotid artery intima-media thickness was inhibited with the combination [100,101] .…”

Section: Dietary and Lifestyle Modificationsmentioning

confidence: 99%

Origin and therapy for hypertriglyceridaemia in type 2 diabetes

Pang

Chan

Watts

2014

WJD

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Hypertriglyceridaemia (HTG) is a risk factor for cardiovascular disease (CVD) in type 2 diabetes and is caused by the interaction of genes and non-genetic factors, specifically poor glycaemic control and obesity. In spite of statin treatment, residual risk of CVD remains high in type 2 diabetes, and this may relate to HTG and atherogenic dyslipidemia. Treatment of HTG emphasises correcting secondary factors and adverse lifestyles, in particular, diet and exercise. Pharmacotherapy is also required in most type 2 diabetic patients. Statins are the first-line therapy to achieve recommended therapeutic targets of plasma low-density lipoprotein cholesterol and non-high-density lipoprotein cholesterol. Fibrates, ezetimibe and n-3 fatty acids are adjunctive treatment options for residual and persistent HTG. Evidence for the use of niacin has been challenged by non-significant CVD outcomes in two recent large clinical trials. Further investigation is required to clarify the use of incretin-based therapies for HTG in type 2 diabetes. Extreme HTG, with risk of pancreatitis, may require insulin infusion therapy or apheresis. New therapies targeting HTG in diabetes need to be tested in clinical endpoint trials. The purpose of this review is to examine the current evidence and provide practical guidance on the management of HTG in type 2 diabetes.© 2014 Baishideng Publishing Group Co., Limited. All rights reserved. Key words: Diabetes; Triglyceride; TherapyCore tip: Diabetic dyslipidemia relates collectively to hyperglycaemia, insulin resistance, hyperinsulinaemia, abdominal visceral adipose disposition, increased liver fat content, and dysregulated fatty acid metabolism. Insulin resistance in diabetes induces hypertriglyceridaemia by increasing the enterocytic production of chylomicrons and an impaired clearance capacity is also involved. Usual care for diabetic dyslipidemia is statin treatment, but a significant proportion of patients have residual dyslipidemia, related to hypertriglyceridaemia and atherogenic dyslipidemia. Current evidence supports the use of fenofibrate in type 2 diabetics with high triglyceride levels.Pang J, Chan DC, Watts GF. Origin and therapy for hypertriglyceridaemia in type 2 diabetes.

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Ezetimibe beneficially influences fasting and postprandial triglyceride-rich lipoproteins in type 2 diabetes

Cited by 65 publications

References 24 publications

Hypertriglyceridemia: a too long unfairly neglected major cardiovascular risk factor

Hypertriglyceridemia: a too long unfairly neglected major cardiovascular risk factor

Postprandial dysmetabolism: Too early or too late?

Origin and therapy for hypertriglyceridaemia in type 2 diabetes

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