View clinical trials related to Elevated Triglycerides.
Filter by:The objectives of this trial are to assess the effects of adding 2 servings/d of either full-fat or low-fat fermented dairy products to the diet, as a replacement for non-dairy foods with macronutrient composition similar to the low-fat fermented dairy condition, on insulin sensitivity, erythrocyte fatty acid profile and other cardiometabolic health markers in metabolically at-risk adults.
The objective of this study is to assess the effects of replacing energy from SoFAS with energy from avocado on non-high-density lipoprotein cholesterol (non-HDL-C) and other aspects of the cardiometabolic health profile including fasting lipoprotein lipid and particle concentrations, insulin sensitivity and blood pressure in men and women with elevated triglycerides (TG).
In this study, a lipase -sourced from a nonpyrogenic yeast, Candida rugosa, will be investigated to establish optimal TG levels in adults in a 12-week supplementation period. The investigational product provides a lipase formulation that is stable and active in acidic and neutral pH environments, while also fully digesting TGs into free fatty acids and glycerol which is beyond the scope of pancreatic lipase (Schuler et al. 2012). This will be a novel study investigating the effects of C. rugosa lipase on adults with slightly elevated TG levels.
Elevated plasma triglycerides (TG) are due to an excess of TG-rich lipoproteins of several different types, most commonly of very-low-density lipoproteins (VLDL), but also intermediate-density lipoproteins (IDL, or VLDL remnants), chylomicrons, and/or chylomicron remnants. Epidemiologic evidence that a moderate elevation in TG is often associated with increased atherosclerotic cardiovascular disease (ASCVD) risk, and more recent evidence from Mendelian randomization studies has shown that elevated TG associated with genetic variants may be a causal factor for ASCVD and possibly for premature all-cause mortality.[1-6] Fasting plasma TG concentrations may be categorized as: normal (< 150 mg/dL ), borderline (150-199 mg/dL), high TG (HTG, 200-499 mg/dL), and very high TG (VHTG, ≥ 500 mg/dL).[7, 8] Risk of acute pancreatitis is increased in VHTG patients, especially those with TG ≥ 1000 mg/dL.[9] For VHTG, the primary goal of therapy is to reduce TG to < 500 mg/dL,[10] whereas there is no specific treatment goal for HTG nor prescription indication. However, the omega-3 fatty acids, EPA and DHA have well-established efficacy in reducing TG in the range of 150-500 when administered at doses of > or = 3 g/d EPA+DHA (reviewed in Skulas-Ray et al. in press). Importantly, administration of omega-3 fatty acids to people with TG in this range lead to a 25% reduction in major adverse cardiovascular endpoints in the recently completed "Reduction of Cardiovascular Events with EPA Intervention Trial" (REDUCE-IT).[11] The results of REDUCE-IT provide compelling evidence for the use 3 g/d omega-3 fatty acid supplementation to reduce cardiovascular risk among patients with TG 150-500 mg/dL. The concentrated EPA supplement used in REDUCE-IT is just one of three long chain n-3 omega-3 fatty acids that influence lipids and lipoproteins and other aspects of cardiovascular risk. Most research has focused on the evaluation of EPA and DHA, which are the two predominant n-3 FA in fish and in n-3 agents, but docosapentaenoic acid (DPA) is present in fish oil, as well, and accumulates in the blood at similar concentrations. The carbon length of the n-3 FA appears important for physiological effects. EPA has a carbon length of 20, DHA has a carbon length of 22, and DPA, the metabolic intermediate of EPA and DHA, is a 22-carbon n-3 FA. DPA may have significant potential for treating HTG and VHTG,[12, 13] but research on this fatty acid remains limited. In a 2-week open-label crossover comparison of 4 g/d of a DPA concentrate (containing unspecified amounts of free DPA and EPA) vs. 4 g/d EPA concentrate in people with HTG, plasma TG were reduced 33% by the DPA concentrate, which was significantly more than the 11% reduction with EPA.[13] Thus, a recent scientific advisory from the American Heart Association (Skulas-Ray et al, in press) concluded that more research is needed to elaborate the lipid and lipoprotein effects of DPA. Additional biomarker research suggests DPA similarly can influence health outcomes that respond to EPA and DHA. For instance, decreased serum concentrations of DPA and DPA + DHA have been associated with increased risk of risk of acute coronary events[14] and myocardial infarction[15], respectively. Plasma DPA was also inversely associated with incident cardiovascular disease (CVD) in some ethnic groups.[16] In conclusion evidence supports a potential role of DPA in improving health, but results from clinical supplementation studies are needed to clarify the effect of DPA supplementation on lipids and lipoproteins as well as other cardiovascular disease risk factors-relative to supplementation with EPA and DHA-to ascertain whether enrichment of omega-3 concentrates with DPA could offer health benefits above and beyond concentrates that only contain EPA and DHA.
The purpose of this study is to determine whether hepatic de novo lipogenesis (DNL) in response to the ingestion of a mixture of glucose and fructose is greater in South Asians compared to controls (Caucasians).
The aim of this study is to demonstrate whether, along with dietary recommendations, Armolipid Plus ® can improve the profile of patients with elevated plasma LDL-C acting as a change of lifestyle therapy (TLC) according to the definition of Adult Treatment Panel III (ATP III)
The purpose of this study is to determine the effectiveness of two different non-energy restricted controlled carbohydrate programs with the American Diabetes Associations' diet on glycosylated hemoglobin and other diabetes risk factors in obese adolescents with metabolic syndrome, a constellation of symptoms associated with the development of type 2 diabetes and cardiovascular disease.
Dietary fructose potently exacerbates the dyslipidemia associated with obesity, insulin resistance and accelerated atherosclerosis. In a randomized crossover outpatient study of 15 overweight adults, we will measure the increase over 4 hours in serum VLDL triglyceride palmitate made by the liver from each single oral dose of fructose (0.5 g/kg), fructose:glucose 1:1 (1 g/kg) or fructose:glucose 1:1 (2 g/kg). Our hypotheses are that the synthesis of palmitate from dietary fructose will be 1) greater when consumed with glucose and 2) show a dose-response. The lipogenic responses will be compared and correlated with markers of carbohydrate and lipid flux measured after fasting and post-fructose. The results will serve as a guide to the development of a new outpatient probe of the de novo lipogenic pathway in subjects who vary in their lipogenic response to oral fructose. These studies should ultimately yield valuable new information about the mechanisms linking dietary carbohydrate to elevated triglycerides, diabetes and cardiovascular disease.