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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Non-alcoholic steato-hepatitis (NASH) is related to insulin resistance and, thus, frequently occurs as part of the metabolic changes that accompany obesity, diabetes and hyperlipidemia. In childhood, the overwhelming boost of obesity and its co-morbidities have lead to the extraordinarily increased prevalence of NASH. Establishing effective therapeutic strategies to treat the disease represents the challenge for hepatologists and gastroenterologists in the next decade. Therapeutic approaches have aimed at treating associated conditions (obesity, insulin resistance, hyperlipemia, etc) or reducing liver oxidative damage (vitamin E).
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PMID:Therapeutic strategies for pediatric non-alcoholic fatty liver disease: a challenge for health care providers. 1755 19

Oxidative stress is a continuous level of oxidative damage in animal cells, which is caused by an overabundance of reactive oxygen species or a decline in antioxidant ability against them. Oxidative stress increases with individual risk factors of atherosclerosis such as obesity, hypertension, hyperlipidemia, diabetes and smoking. Thus, oxidative stress is considered to play a key role in the pathogenesis of atherosclerosis. This review discusses the relationship between oxidative stress and atherosclerosis based on findings from our research group. We have found that atherosclerotic lesions are formed in the aorta of mice fed a high-cholesterol and high-linoleic diet, in parallel with elevated serum lipid peroxide levels. This model is useful for primary screening of antiatherosclerotic agents with antioxidative activity. One notable factor in the development of atherosclerosis is oxidized low-density lipoprotein (OxLDL). In order to examine OxLDL levels in blood, we have developed anion-exchange HPLC methods using stepwise elution. Using these methods, we have found that OxLDL markedly increases in a rat model of metabolic syndrome, in animals exposed to cigarette smoke and in smokers in parallel with other oxidative stress markers. These oxidative stress markers have been attenuated by administration of several antioxidants. In addition, we have found that smoking accelerates atherogenesis in the aorta of apoE-deficient mice and this acceleration can be ameliorated by administration of vitamin E. These observations suggest that antioxidant supplementation may be an effective therapeutic strategy for metabolic syndrome and smoking-induced diseases in which elevated oxidative stress plays a pivotal role.
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PMID:[Oxidative stress and atherosclerosis]. 1805 88

During aging there is a tendency towards hyperlipidemia and changes in the distribution of lipoproteins. A decline in the functioning of the body's antioxidant defense system is also observed at this time. The objective of this study was to establish the relationship between serum concentrations of total cholesterol and fractions, triglycerides, and Vitamins C and E. 61 adults over 60 years of age were evaluated from January to March, 2006. Nutritional status was diagnosed by BMI (WHO); serum levels of triglycerides (TG), total cholesterol (TC) and fractions (HDL-c and LDL-c) were determined by enzyme method; Vitamin C (colorimetric method) and Vitamin E by HPLC. ATPIII values were used as a reference for risk of TG, TC, HDL, LDL-c, vitamin C: > 0.9 mg/dL (normal), < 0.9 mg/dL (deficit); vitamin E: = 1300 microg/dL (normal), 1300 = microg /dL (deficit). Consumption of vitamins C and E were estimated by the direct weighing method 3 days per week. According to BMI, 19.7% had nutritional deficit, 39.3% overweight, and 11.5% obesity. TG, TC, LDL-c levels were at risk in females, and HDL-c in both genders. Prevalence of risk for heart disease was: TG (45.2%), HDL-c (51.1%), and LDL-c (52.5%). Consumption and serum levels of vitamin E were low in both genders. There was no association between variables. A significant and positive correlation between TG, TC, LDL-C, serum vitamin E, and BMI was observed. The female group showed overweight, hypertriglyceridemia and hypercholesterolemia, HDL-c and LDL-c at risk, and vitamin E deficiency, all of which are important risk factors for cardiovascular disease in this age group.
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PMID:[Relationship between serum lipids and status of vitamin C and E as antioxidants in Venezuelan elderly people]. 1936 97

It is not known if vitamin E in hyperlipidemia and hypercholesterolemia of longer duration has any beneficial or adverse effects on electrolytes, and liver and kidney function. The objectives of this study are to determine (i) if long duration of mild hypercholesterolemia has any adverse effects on serum electrolytes, glucose and enzymes related to liver and kidney functions; (ii) if vitamin E has any effects on serum electrolytes, glucose and enzymes related to liver and kidney function in hypercholesterolemia. Blood samples were collected from the rabbits before and at various intervals during administration of a high cholesterol diet (0.25%) for 2 and 4 months, and while on a high cholesterol diet with vitamin E following a high cholesterol diet. Measurements of serum total cholesterol (TC), glucose, aspartate aminotransferase (AST), alkaline phosphatase (ALP), alanine aminotransferase (ALT), gamma-glutamyltransferase (GGT), albumin, creatinine, electrolytes [sodium (Na), potassium (K), chloride (Cl), and carbon dioxide (CO2)] were made. High cholesterol diet for 2 months produced hypercholesterolemia which was associated with reductions in serum glucose, unaltered serum electrolytes, ALT, ALP, GGT, albumin and creatinine, and increased levels of AST. Hypercholesterolemia for 4 months had effects similar to hypercholesterolemia for 2 months except it lowered serum ALP. Vitamin E did not affect any of the parameters except serum glucose and Cl, which decreased compared to the values at month 2. Hypercholesterolemia for short and long term does not have adverse effects on liver or kidney function, and serum electrolytes. Vitamin E during hypercholesterolemia does not affect serum electrolytes or liver and kidney function.
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PMID:Effects of vitamin E on serum enzymes and electrolytes in hypercholesterolemia. 1973 Sep 89

Acetone is considered to be a substance that can disturb cellular oxidative status, being also associated with the production of glucose during its metabolization. The objective of the present study was to determine the effects of chronic treatment with acetone in oxidative stress and metabolic parameters in rats. Twenty male Wistar rats were divided into two groups: control (CG) and chronic acetone group (CAG). After 28 days of acetone ingestion in a 5% aqueous solution (CAG) or water (CG) the animals were euthanized and urine, plasma and liver were collected for the determination of acetone, glucose, lipemia, hepatic fat, malondialdehyde (MDA), reduced glutathione (GSH), and vitamin E. As expected, urinary and plasma acetone levels were higher in CAG. There was no difference in hepatic MDA values between groups, whereas hepatic GSH was lower in CAG than in CG and hepatic vitamin E was higher in CAG than in CG. There was also an increase in glycemia, cholesterolemia and hepatic fat in CAG compared to CG. Chronic treatment with a 5% acetone solution produced an increase in acetonemia that was able to promote changes in hepatic oxidative metabolism and in lipid content in rats similar to those observed in nonalcoholic steatohepatitis.
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PMID:Chronic acetonemia alters liver oxidative balance and lipid content in rats. A model of NASH? 1985 60

Cardiovascular disease (CVD) is the most important adult health problem in the world. Epidemiological studies and laboratory experiments have shown that fruit and vegetable consumption has protective effects against CVD. The purpose of the study was to investigate the effects of consumption of two kiwifruit per day on the lipid profile, antioxidants and markers of lipid peroxidation in hyperlipidemic adult men and women in Taiwan. Forty-three subjects who had hyperlipidemia, including 13 males and 30 females, participated in this study. They were asked to consume two kiwifruit per day for 8 weeks. Anthropometric measurements were made. Before the intervention and at 4 and 8 weeks of the intervention, fasting blood samples were analyzed for total cholesterol, triacylglycerol, low-density lipoprotein (LDL) cholesterol, and high-density lipoprotein cholesterol (HDL-C). Additionally vitamin E and vitamin C, the malondialdehyde + 4-hydroxy-2(E)-nonenal concentration, and the lag time of LDL oxidation were determined. No significant differences from baseline to 8 weeks of the intervention were detected for triacylglycerol, total cholesterol, or LDL cholesterol. However, after 8 weeks of consumption of kiwifruit, the HDL-C concentration was significantly increased and the LDL cholesterol/HDL-C ratio and total cholesterol/HDL-C ratio were significantly decreased. Vitamin C and vitamin E also increased significantly. In addition, the lag time of LDL oxidation and malondialdehyde + 4-hydroxy-2(E)-nonenal had significantly changed at 4 and 8 weeks during the kiwifruit intervention. Regular consumption of kiwifruit might exert beneficial effects on the antioxidative status and the risk factors for CVD in hyperlipidemic subjects.
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PMID:Effects of kiwifruit consumption on serum lipid profiles and antioxidative status in hyperlipidemic subjects. 1991 18

Nicotine, an active ingredient of tobacco smoke, is known to induce hyperlipidemia and disturb the prooxidant-antioxidant status. In our study, ferulic acid, a naturally occurring nutritional compound, was tested for its antioxidant and antihyperlipidemic property in a dose-dependent manner against nicotine-induced toxicity in female Wistar rats. We tested three different doses of ferulic acid-10 mg, 20 mg, and 40 mg/kg body weight-for their protective effects. The activities of biochemical marker enzymes lactate dehydrogenase and alkaline phosphatase, levels of peroxidative indices (thiobarbituric acid reactive substances and hydroperoxides), nitric oxide, and circulatory lipids (cholesterol, triglycerides, free fatty acids, and phospholipids) were increased significantly in the nicotine-treated group when compared to normal, which were brought down in ferulic acid-treated groups. The antioxidant status (superoxide dismutase, catalase, glutathione peroxidase, vitamin E, and reduced glutathione) was found to be decreased in the nicotine-treated group, and was significantly increased in ferulic acid-administered groups. Further, ferulic acid also positively modulated the nicotine-induced changes in the micronutrients (zinc and copper) level. The dose 20 mg/kg body weight was found to be more effective than the other two doses. Our data suggest that FA exerts its preventive effects by modulating the degree of lipid peroxidation, antioxidant status, lipid profiles, and trace element levels during nicotine-induced toxicity.
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PMID:Ferulic Acid modulates altered lipid profiles and prooxidant/antioxidant status in circulation during nicotine-induced toxicity: a dose-dependent study. 2002 Oct 59

Absence of meal-induced insulin sensitization (AMIS) results in a predictable progression of dysfunctions, including postprandial hyperglycemia, compensatory hyperinsulinemia, resultant hyperlipidemia, increased oxidative stress, and obesity, progressing to syndrome X and diabetes. To test the 'AMIS syndrome' hypothesis we used 3 known means of producing graded and progressive changes in meal-induced insulin sensitization in rats. We used an aging model (9, 26, and 52 weeks), associated with a slow development of AMIS; a low-dose sucrose supplement model to accelerate the development of AMIS; and an antioxidant cocktail (S-adenosylmethionine, vitamin E, and vitamin C) to protect against the effect of the sucrose on meal-induced insulin sensitization. Adiposity was assessed from weighed regional fat masses and bioelectrical impedance. AMIS developed with age, was increased by sucrose supplementation, and was inhibited by the antioxidant cocktail. AMIS correlated with postprandial hyperglycemia, hyperinsulinemia, hyperlipidemia, and with adiposity (r2 = 0.7-0.8) regardless of age or nutrient status. The range of degrees of AMIS, established over time with these models, afforded the tool with which to test the AMIS syndrome and further the argument that AMIS is the first metabolic defect that cumulatively leads to a predictable series of homeostatic disturbances and dysfunctions, including obesity and type 2 diabetes.
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PMID:Obesity, syndrome X, and diabetes: the role of HISS-dependent insulin resistance altered by sucrose, an antioxidant cocktail, and age. 2005 13

Absence of meal-induced insulin sensitization (AMIS) results in a predictable progression of dysfunctions, including postprandial hyperglycemia, compensatory hyperinsulinemia, resultant hyperlipidemia, increased oxidative stress, and obesity, progressing to syndrome X and diabetes. To one year of age, rats show a slow development of AMIS, but this can be potentiated by addition of a low-dose sucrose supplement to the diet. Provision of a synergistic antioxidant cocktail consisting of S-adenosylmethionine, vitamin E, and vitamin C (Samec) attenuates the rate and extent of development of AMIS in both normal aging animals and in aging animals on the sucrose diet. Adiposity, assessed from weighed regional fat masses and from bioelectrical impedance to estimate whole-body adiposity, correlated strongly with AMIS (r2 = 0.7-0.8). Rats given the sucrose supplement had accelerated AMIS and developed fasting hyperinsulinemia and postprandial hyperglycemia, hyperlipidemia, hyperinsulinemia, and adiposity. Samec completely compensated for the negative impact of this sucrose supplement and attenuated development of the associated dysfunctions. AMIS is explained by the HISS (hepatic insulin-sensitizing substance) hypothesis, which is outlined in the paper.
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PMID:Attenuation of age- and sucrose-induced insulin resistance and syndrome X by a synergistic antioxidant cocktail: the AMIS syndrome and HISS hypothesis. 2039 96

Oxidative stress in diabetes co-exists with a reduction in the antioxidant status, which can further increase the deleterious effects of free radicals. Hyperlipidaemia is one of the major risk factors of cardiovascular complications in diabetes. A study was undertaken to evaluate the antioxidant and antihyperlipidaemic activity of protocatechuic acid (PCA) on streptozotocin (STZ)-induced diabetic rats. The levels of thiobarbituric acid reactive substances (TBARS) and lipid hydroperoxides (LOOH) were increased and the level of enzymatic and non-enzymatic antioxidants decreased except vitamin E. Lipid profile increased in diabetic rats, whereas HDL-C level decreased. These alterations reverted to near control levels after the diabetic rats were treated with PCA. Histopathological studies also revealed the protective effects of PCA on liver and kidney. These findings suggest that PCA treatment exerts a therapeutic property by decreasing the oxidative stress and lipid profile. The effect of PCA was comparable to glibenclamide, a well-known hypoglycaemic drug.
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PMID:Antioxidant and antihyperlipidaemic activity of protocatechuic acid on streptozotocin-diabetic rats. 2050 Sep 88


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