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

The effect of addition of different carbohydrates (starch, glucose, fructose) to the feed was investigated using the experimental animal. Additionally, the admixture of cholesterol and of cholesterol plus cholic acid was tested. Fructose (70% of the feed) causes a slight increase in serum triglyceride concentration and a very slight increase in triglyceride concentration in the liver. Fructose and to a lesser degree glucose cause an increase in pyruvate kinase activity in the liver. The activity of glucose-6-phosphate dehydrogenase is increased slightly following high-dosed glucose, whereas the increase is very pronounced following fuctose-rich feed. The admixture of cholesterol (with cholic acid) causes a decrease in glucose-6-phosphate dehydrogenase activity up to 70%. The activity of glutamate dehydrogenase is decreased also following cholesterol admixture. A fructose-rich diet causes a slight degree of hyperlipemia with a metabolic situation similar to a latent diabetic state. This effect is greatly intensified by the addition of cholesterol and cholic acid to the diet of the rats. Especially striking was the increase in serum-free-fatty-acid concentrations in all groups of animals. This is speculated to be a sign of insulin deficiency. The so-called "carbohydrate-induced hypertriglyceridemia" is obviously intensified within a short period by the admixture of cholesterol plus cholic acid to the experimental diet.
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PMID:[Effect of various dietary carbohydrates on supplementary cholesterol]. 89 66

Effects of fructose feeding in moderate amounts on lipid metabolism of obese versus lean, and diabetic versus nondiabetic Zucker rats, were studied. Forty pairs of male lean and obese animals were assigned to two dietary groups, fructose and glucose. For each diet, one-half of lean and obese animals were injected with streptozotocin intraperitoneally (i.p.) to induce diabetes, and the other half were injected with buffer i.p. as a nondiabetic control group. After 9 wk of feeding, animals were fasted overnight, decapitated and exsanguinated. Organs were removed and weighed. Blood glucose, insulin, lactic acid, triglycerides, cholesterol, total liver lipids and urinary glucose were determined. Hyperphagia was observed in obese, non-diabetic and lean-diabetic animals. Streptozotocin injection drastically reduced insulin levels, and produced an impairment of growth, hyperglycemia, glucosuria, polydipsia and polyuria. Fructose feeding increased organ weights in kidney, liver and retroperitoneal adipose tissue, regardless of diabetic state. However, lactic acid levels were lower in fructose-fed groups than glucose-fed groups. In obese rats serum triglyceride levels were also lower in fructose-fed groups than in glucose-fed groups. Serum cholesterol was not affected by fructose feeding. The results indicated that fructose feeding did not produce hyperlipemia and lactic acidosis in the blood circulation in Zucker rats. However, fructose feeding did not improve glucose intolerance in diabetic animals, rather fructose feeding produced hyperinsulinemia in nondiabetic, obese animals.
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PMID:Effects of fructose feeding on lipid parameters in obese and lean, diabetic and nondiabetic Zucker rats. 390 Mar 13

The effects of fructose loading on the integrated cardiovascular function in vivo, glycemic control, glucose tolerance, and plasma lipid levels in nondiabetic and streptozotocin (STZ) diabetic rats were investigated. Endothelial morphology of the thoracic aorta was also assessed with scanning electron microscopy. Fructose-loaded nondiabetic rats exhibited elevated blood pressure and pulse rate, and signs of arterial atherogenesis, such as focal adherence of leukocytes and fibrin to the endothelium. Intraperitoneal glucose tolerance tests revealed a greater increase in plasma insulin in response to glucose challenge in these animals than in the control. Compared with the untreated STZ-diabetic animals, fructose-loaded diabetic rats had significantly greater hyperglycemia, glucose intolerance, and hyperlipidemia and higher blood pressure, but had a similar degree of hypoinsulinemia, cardiac dysfunction, and cardiac enlargement. They also showed signs of early atherogenesis. The central venous pressure and the susceptibilities of the rats to the induction of ventricular arrhythmias by intravenous infusion of aconitine were not significantly affected by either STZ injection or fructose loading. It is concluded that prolonged intake of an excessive amount of fructose has detrimental effects on the cardiovascular system, glucose metabolism, and plasma lipid levels in both nondiabetic and STZ-diabetic rats.
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PMID:Fructose loading induces cardiovascular and metabolic changes in nondiabetic and diabetic rats. 782 85

The JCR:LA-corpulent rat is a strain exhibiting marked obesity and metabolic derangements characterized by hyperlipidemia due to hypersecretion of very-low-density lipoprotein (VLDL) and severe insulin resistance. The corpulent male rats spontaneously develop atherosclerosis and ischemic myocardial lesions. Male corpulent rats were treated with acarbose in the presence and absence of sugar-supplemented diets. The acarbose-treated rats had lower body weights at 3 months of age with unaltered food consumption, and a similar effect was seen with a high-fructose diet. Fasting insulin concentrations were decreased significantly in acarbose-treated animals at both 3 and 9 months of age, and the rate of plasma glucose disappearance increased at 3 months of age. Acarbose treatment did not affect whole-serum triglyceride concentrations, but there were modest decreases in cholesterol levels. Sugar-supplemented diets caused no significant changes in insulin or glucose concentrations, and caused small increases in nonesterified cholesterol only. Fructose- but not sucrose-supplemented diets were associated with a significantly decreased frequency of old scarred myocardial lesions. The frequency of occurrence of such lesions was also decreased by acarbose treatment. This effect of acarbose treatment may reflect improvement in insulin and glucose metabolism in treated rats. The decrease in myocardial lesions in fructose-fed rats may be secondary to increased carbohydrate metabolism via the pathways leading from fructose to triglyceride.
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PMID:Beneficial effects of acarbose in the atherosclerosis-prone JCR:LA-corpulent rat. 847 19

Diabetic polyneuropathy is the most frequent neuropathy in western countries. In Germany, there are 3.5 to 4 million diabetic patients. Diagnosis should rule out other polyneuropathies and assess two out of the five diagnostic criteria: neuropathic symptoms, neuropathic deficits, pathological nerve conduction studies, pathological quantitative sensory testing and pathological quantitative autonomic testing. So far, the pathophysiology of diabetic neuropathy remains to be fully understood. Among the various pathophysiological concepts are the Sorbitol-Myo-Inositol hypothesis attributing Myo-Inositol depletion to the accumulation of Sorbitol and Fructose, the concept of deficiency of essential fatty acids with reduced availability of gamma-linolenic-acid and prostanoids, the pseudohypoxia- and hypoxia-hypothesis attributing endothelial and axonal dysfunction and structural lesions to increased oxidative stress and free radical production. Obviously, the hyperglycemia induced generation of advanced glycation end products (AGEs) also contributes to structural dysfunctions and lesions. Elevated levels of circulating immune complexes and activated T-lymphocytes as well the identification of autoantibodies against vagus nerve or sympathetic ganglia support the concept of an immune mediated neuropathy. The reduction of neurotrophic factors such as nerve growth factor, neurotrophin-3 or insulin-like growth factors also seems to further diabetic neuropathy. The symmetrical, distally pronounced and predominantly sensory neuropathy is far more frequent than the symmetrical neuropathy with predominant motor weakness or the asymmetrical neuropathy. The painless neuropathy manifests with impaired light touch sensation, position sense, vibratory perception and diminished or absent ankle deep tendon reflexes. The painful sensory diabetic neuropathy primarily affects small nerve fibers and accounts for decreased temperature perception and paresthesias. The proximal, diabetic amyotrophy evolves subacutely or acutely, induces motor weakness of the proximal thigh and buttock muscles and is painful. Cranial nerve III-neuropathy is also painful and has an acute onset. Truncal radiculopathy follows the distribution of truncal roots and frequently causes intense pain. Autonomic neuropathy occurs with and without somatic neuropathy. The most important therapy is to attempt optimal blood glucose control, to reduce body weight and hyperlipidemia. Symptomatic therapy includes alpha-lipoic acid treatment, as the antioxidant seems to improve neuropathic symptoms. Aldose reductase inhibitors might reduce sorbitol and fructose production and normalize myo-inositol levels. However, there are no aldose reductase inhibitors available in Europe as yet. Evening primrose oil, containing gamma-linolenic acid, might improve nerve conduction velocities, temperature perception, muscle strength, tendon reflexes and sensory function. Substitution of nerve growth factor showed promising results in pilot studies but failed in a large-scale multicenter study. Symptomatic pain treatment can be achieved with tricyclic antidepressants, selective serotonin reuptake inhibitors, anticonvulsants such as carbamazepine, gabapentin or lamotrigine, or anti-arrhythmic drugs such as mexiletine. Topical capsaicin application should reduce neuropathic pain but also induces local discomfort in the beginning of therapy. Vasoactive substances, so far have not proven to be of major benefit in diabetic neuropathy. Physical therapy and thorough footcare are of primary importance and allow prevention of secondary complications such as foot amputations.
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PMID:[Diabetic somatic polyneuropathy. Pathogenesis, clinical manifestations and therapeutic concepts]. 1092 53

Recent findings indicate that in addition to its hyperlipemic effect, a high fructose diet has a pro-oxidant effect in rats compared with a starch-based diet. Oligofructose (OFS) has already been shown to decrease plasma lipids in rats. We assessed the impact of fructose on oxidative stress by supplementing a high fructose diet with OFS. Rats were fed either a high fructose diet or a starch-based diet, with or without supplementation of 10 g/100 g oligofructose for 4 wk. Regardless of the type of carbohydrate, OFS in the diet produced an enlargement of the cecum and led to a significant increase in the SCFA cecum pool. Fructose feeding was associated with significantly higher insulin plasma concentrations (+63%) in the control groups, whereas insulin plasma concentrations did not differ in rats fed the fructose diet supplemented with OFS. Plasma leptin concentration was significantly lower (approximately 50%) in the OFS-supplemented fructose group compared with the other three groups. Fructose feeding in rats also significantly increased plasma (P < 0.001) and liver (P < 0.001) triglyceride (TG) concentrations and the addition of OFS prevented the TG accumulation induced by fructose in the liver (P < 0.05) and hyperlipemia (P < 0.05). OFS consumption prevented (P < 0.05) the lower plasma vitamin E/TG ratio in rats fed the fructose diet. Control rats fed the fructose diet had high plasma TBARS values compared with rats fed the starch diet, whereas TBARS values remained unchanged when rats were supplemented with OFS. Control rats fed the fructose diet had higher TBARS urine values and higher heart tissue susceptibility to peroxidation compared with rats fed the starch diet, and this effect was significantly reduced by OFS consumption. Further studies are required to identify the mechanisms underlying the protective effect of OFS against the pro-oxidant effect of fructose. However, the potential nutritional benefits of OFS supplementation in fructose-rich diets are suggested.
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PMID:Oligofructose protects against the hypertriglyceridemic and pro-oxidative effects of a high fructose diet in rats. 1277 37

Fructose intake and the prevalence of obesity have both increased over the past two to three decades. Compared with glucose, the hepatic metabolism of fructose favors lipogenesis, which may contribute to hyperlipidemia and obesity. Fructose does not increase insulin and leptin or suppress ghrelin, which suggests an endocrine mechanism by which it induces a positive energy balance. This review examines the available data on the effects of dietary fructose on energy homeostasis and lipid/carbohydrate metabolism. Recent publications, studies in human subjects, and areas in which additional research is needed are emphasized.
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PMID:Dietary fructose: implications for dysregulation of energy homeostasis and lipid/carbohydrate metabolism. 1597 9

This study was performed to investigate whether the plasma concentration of phosphatidylcholine hydroperoxide (PCOOH), which is a marker of oxidized stress in the blood, increased in cholesterol-fed rabbits, and fructose ingestion promoted this process and aggravated atherosclerosis. Male Japanese white rabbits (age: 12 weeks, and body weight: around 2.0 kg, n = 15) were divided into three groups, (1) a NN group as a normal control fed a standard diet (n = 5), (2) a CN group fed 1.0% cholesterol, and (3) a CF group given both 1.0% cholesterol and 10% fructose-containing tap water. During 8 weeks, plasma PCOOH levels increased significantly in the CN and CF groups compared to the NN group and fructose further raised the PCOOH level. The atherosclerosis was significantly promoted and the deposition of advanced glycation end products (AGEs) was marked in the CF group compared to the CN group. Fructose worsened the atheromatous lesions caused by cholesterol feeding. The mechanism is most likely through lipid peroxidation, which was increased by cholesterol feeding-induced hyperlipidemia, and the formation of AGEs.
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PMID:Fructose ingestion enhances atherosclerosis and deposition of advanced glycated end-products in cholesterol-fed rabbits. 1620 22

Fructose supplementation produced cardinal features of Syndrome-X including significant elevations in seum cholesterol, triglyceride, glucose and insulin and also in body weight. While treatment with methanolic extract of dried rhizomes of Zingiber officinale produced a significant reduction in fructose induced elevation in lipid levels, bodyweight, hyperglycemia and hyperinsulinemia, treatment with ethyl acetate extract of Z officinale did not poduce any significant change in either of the last two parameters. However, it produced a significant reduction in elevated lipid levels and body weight The concentration of 6-gingerol was found to be higher in methanolic extract and less in ethyl acetate extract. The results suggest that the methanolic extract of Z officinale produces better effects as compared to ethyl acetate extract in fructose induced hyperlipidemia associated with insulin resistance. The extent of activity appears to be dependent on the concentration of 6-gingerol present in the extracts.
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PMID:Beneficial effects of Zingiber officinale Roscoe on fructose induced hyperlipidemia and hyperinsulinemia in rats. 1635 28

Fructose is a monosaccharide which is abundant in nature. It is the sweetest naturally occurring carbohydrate. The availability of fructose increased substantially when it became possible in the 1960s to economically produce high fructose syrups from corn starch and other starches. Such high fructose syrups are now used to sweeten soft drinks, fruit drinks, baked goods, jams, syrups and candies. The most recent data available suggest that fructose consumption is increasing worldwide. Fructose presently accounts for about 10% of average total energy intake in the United States. Studies in both healthy and diabetic subjects demonstrated that fructose produced a smaller postprandial rise in plasma glucose and serum insulin than other common carbohydrates. Substitution of dietary fructose for other carbohydrates produced a 13% reduction in mean plasma glucose in a study of type-1 and type-2 diabetic subjects. However, there is concern that fructose may aggravate lipemia, particularly in men. In one study, daylong plasma triglycerides (estimated by determining the area under response curves) in healthy men was 32% greater during a high fructose diet than during a high glucose diet. There is also concern that fructose may be a factor contributing to the growing worldwide prevalence of obesity. Increasing fructose consumption is temporally associated with the increase in obesity. Moreover, on theoretical grounds, dietary fructose might increase energy intake. Fructose stimulates insulin secretion less than does glucose and glucose-containing carbohydrates. Since insulin increases leptin release, lower circulating insulin and leptin after fructose ingestion might inhibit appetite less than consumption of other carbohydrates and lead to increased energy intake. However, there is not yet any convincing experimental evidence that dietary fructose does increase energy intake. Although evidence that fructose has adverse effects is limited, adding fructose in large amounts to the diet may be undesirable, particularly for men. Fructose that occurs naturally in fruits and vegetables is a modest component of energy intake and should not be of concern.
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PMID:Is fructose the optimal low glycemic index sweetener? 1682 Jul 33


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