Active clinical trials for "Hyperlipoproteinemia Type IV"

The study will evaluate safety and tolerance of intravenous delivery of GC304 gene therapy drug as a treatment of primary hypertriglyceridemic patients with previous onset of acute pancreatitis.

The Torcetrapib project was terminated on December 2, 2006 due to safety findings. To assess the safety and efficacy of the fixed combination torcetrapib/atorvastatin in subjects with Fredrickson Type IV Hypertriglyceridemia.

The primary purpose of this trial is to determine if the treatment with rosuvastatin 10 and 20mg/day during 8 weeks in hypertriglyceridemic patients will reduce their triglyceride levels.

The purpose of this study is to determine whether chenodeoxycholic acid decreases de novo hepatic lipogenesis, hepatic fat content, hepatic triglyceride production and plasma triglyceride concentrations and improves hepatic glucose metabolism in patients with the metabolic syndrome, Familial Hypertriglyceridemia and Familial Combined Hyperlipidemia.

Cardiovascular Diseases (CVDs) are the leading causes of death in the world and in Brazil. In 2001, 12.45 million deaths on the globe (21% of the total) were caused by some CVD. The composition of modern man's diet has changed drastically with the industrialization of food, resulting in the transition from a diet rich in fibers and complex carbohydrates to one with a high content of sugars and fats. Since the current dietary pattern is characterized by the consumption of three or more meals a day, containing a quantity of fat in the range of 20 to 70 g, individuals spend a large part of the day in the postprandial state, with continuous fluctuation of lipemia Over 18 hours. Food intake (postprandial state) is the dynamic, unstable response of the body that refers to rapid hormonal and lipoprotein remodeling. It is well established in the literature that high-fat meals (lipid overload) cause an increase in plasma triglycerides. Hypertriglyceridemia and / or elevated triglyceride-rich lipoproteins (LRT) (chylomicrons, VLDL and their remnants) in the postprandial state induces endothelial dysfunction via increased oxidative stress and is an independent risk factor for CVDs. Therefore, Postprandial Lipemia (PPL) is counted as an early marker of atherosclerotic process, metabolic abnormalities and endothelial dysfunction. High-carbohydrate (CHO) diets may promote increased LDL-c, TG, VLDL and HDL-c reduction, as well as PPL, generating a lipid profile associated with an increased risk of CVDs. This effect appears to be more pronounced with the inclusion of simple carbohydrates (mono and disaccharides), although it also occurs with diets rich in complex carbohydrates (polysaccharides). High fructose diets (HFDs) are a known model of induction of insulin resistance, dyslipidemia and DM2 in primates and humans. The chronic effect of fructose consumption has been well studied in the last decades due to its connection with obesity, resistance to Insulin, accumulation of visceral fat and dyslipidemia. As the consumption of fructose is progressively increasing in society and its chronic exposure can generate a phenotypic effect of dyslipidemia and, consequently, the increased risk of CVDs, prevention and treatment strategies should be seen as an important public health issue . Thus, the objective of this study is to understand the effects of exercise on fat metabolism, since there is a lack of robust evidence about the possible cardioprotective and hypolipemic role of the same on HFD.

Fasting blood fat levels (triglycerides) are often used to assess risk of heart disease but the level of fats in the blood after a meal is actually a stronger risk factor. Most of our day is spent digesting the food we eat (which takes hours). Therefore, "after meal" blood fat levels have more of an impact on formation of blockages in our arteries and our risk of heart disease compared to "fasting" blood fat levels. Exercise performed hours before a meal reduces the level of fats that appear in the blood after a meal and can be used to reduce our risk of heart disease. Exercise has this effect because muscle burns fats for hours after an exercise session is over; this helps to remove fats from the blood. Unfortunately, when high-sugar drinks (such as Gatorade) are consumed after exercise, the possible benefits of exercise for reducing blood fat levels after meals is lessened. This is because high-sugar drinks stimulate the release of insulin into the blood. Insulin is a hormone which inhibits fat burning at the muscle. Previous research we did showed that foods that result in a slower rise in blood sugar and lower release of insulin preserve the beneficial effects of exercise for lowering blood fat levels after the next meal. Milk also results in a slow rise in blood sugar and low release of insulin; therefore, it may also have this beneficial effect if consumed as a recovery beverage after exercise. Our proposed research will test the effects of consuming two popular exercise-recovery drinks (Milk vs. Gatorade) on the rise in blood fat levels after a meal given hours later. A total of 20 obese or overweight participants will take part. We predict that milk consumed after an exercise session in the evening will result in a lower increase in insulin, a greater amount of fat-burning at muscle and a lower blood fat level after a meal given the next morning. Milk and Gatorade are both promoted as good beverages to promote recovery after exercise. This study will provide evidence about milk as a healthier choice compared to Gatorade and will allow dairy producers to promote health benefits of dairy products.

To determine prospectively the role of elevated plasma triglyceride (TG) as a risk factor for 20-year coronary heart disease (CHD) mortality in familial combined hyperlipidemia (FCHL) and familial hypertriglyceridemia (FHTG), the familial forms of hypertriglyceridemia. Also, to perform genetic epidemiologic studies of recently identified lipoprotein risk factors for CHD, including Atherogenic Lipoprotein Phenotypes (ALP) based on subclasses of low-density lipoproteins (LDL), Lipoprotein(a) (Lp(a)) and apolipoprotein (apo) B plasma levels, and apo E isoforms.