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

In order to clarify lipoprotein abnormality in mild to moderate obesity (BMI > or = 25), plasma was separated by table top ultracentrifugation into VLDL (chylomicron), IDL, LDL and HDL. Chol, TG and ApoB were determined in each fraction by enzymatic and sensitive Latex method. The data were analysed according to glucose intolerance and hyperinsulinemia (HI). In obese subjects, irrespective of glucose intolerance, Chol, TG & ApoB levels were high in plasma, and an increase in VLDL (Chol, TG & ApoB), IDL (Chol & ApoB), LDL (Chol & ApoB), and a decrease in HDL-Chol were observed. These levels were also abnormal in nonDM particularly with HI. In DM, HI did not seem to affect hyperlipidemia. Correlation between Chol, TG and ApoB in three ApoB containing lipoprotein subfractions was noted in obesity. The ratio of Chol/ApoB and TG/ApoB in LDL was significantly lower in obesity implying that LDL particles were smaller in size. Half of nonDM patients had HI, and only 29% of DM patients had HI, and both groups had almost the same lipoprotein abnormality. Hyperlipidemia was severe in nonDMHI(+) compared to nonDMHI(-). Therefore, in hyperlipidemia of obesity, hyperinsulinemia plays a role in nonDM and hyperglycemia in DM. Insulin resistance seems to be an important factor in DM. Although the mechanism may be different, the consequence of hyperlipidemia is similar. Increased numbers of ApoB containing lipoproteins and smaller size of LDL are the characteristic features of hyperlipidemia in mild to moderate obesity. Because these quantitative and qualitative changes appear to be linked to an increased risk for premature arteriosclerosis, intensive therapy should be recommended even in mild to moderate obesity.
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PMID:[Quantitative and qualitative alterations of plasma lipoproteins in obesity]. 837 54

Total body fat and anthropometric assessments of fat distribution were examined in 23 lean and obese rhesus monkeys (Macaca mulatta). In addition, the relationships of central obesity to hyperinsulinemia, insulin resistance, glucose intolerance and hyperlipidemia were studied. Total body fat (as determined by the tritiated water dilution method), plasma glucose, insulin, lipoproteins (triglyceride, cholesterol and HDL- and LDL-cholesterol) and free fatty acids (FFA), and glucose disappearance rate (KG) and peripheral insulin-stimulated glucose uptake (M) were obtained. Results showed that abdominal circumference was the best predictor of body fat (r = 0.90; P < 0.001). There were strong linear relationships between abdominal circumference and plasma insulin (r = 0.66), glucose tolerance (r = -0.53), and M rate (r = -0.59) (all P < 0.05) but not to plasma glucose, lipoprotein fractions, or free fatty acids. When the subjects were grouped according to degree of obesity and insulin resistance (lean normals, obese insulin sensitive, and obese insulin resistant), the obese resistant monkeys had significantly higher plasma insulin levels, lower glucose tolerance, and significantly higher plasma triglyceride levels. We conclude that the spontaneously obese rhesus monkey is an excellent model of central obesity. Furthermore, in this model upper body obesity appears to be facilitative in the development of hyperinsulinemia, glucose intolerance and hypertriglyceridemia but does not appear to be causally related. In the rhesus monkey and in humans as well, we propose that the link between central obesity and these metabolic abnormalities may be peripheral insulin resistance.
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PMID:Central obesity in rhesus monkeys: association with hyperinsulinemia, insulin resistance and hypertriglyceridemia? 838 42

Diabetes mellitus is an important risk factor for coronary heart disease and cerebral vascular disease. Moreover, diabetic patients are frequently hyperlipidemic (our recent study has revealed that approximately 70% of diabetic patients are dyslipidemic) and are at a higher risk when complicated with hyperlipidemia. In addition, abnormalities in lipoprotein metabolism, which may promote arteriosclerosis, are seen even in normolipidemic diabetics. One such alteration is an increased cholesterol level in intermediated-density lipoproteins from normolipidemic diabetic patients. Recently, abnormal particles in low-density lipoprotein (LDL) fraction, glycated-LDL and small, dense LDL, are regarded as atherogenic lipoproteins. Several factors promoting arteriosclerosis in diabetics, such as abnormal lipoprotein metabolism, increase of lipoprotein (a), hyperinsulinemia, enhancement of polyol pathway, dysfunction of platelet, are described here.
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PMID:[Diabetes mellitus as a risk factor for arteriosclerosis]. 841 88

Although controversy exists as to the role that insulin resistance and hyperinsulinemia play in the pathogenesis of hypertension there are ample data from both obese and nonobese subjects strongly suggesting that selective insulin resistance, hyperlipidemia, and essential hypertension are directly related. It is therefore mandatory that the evaluation of both lipid profile and insulin sensitivity needs to be made in all patients with essential hypertension. In addition it appears that childhood obesity is the single marker of the child at risk for the development of cardiovascular disease later in life.
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PMID:Adolescent obesity and hypertension. 841 11

Major cardiovascular risk factors, such as hypertension, hyperlipidemia, and diabetes, often cluster in the same individuals. It has been claimed that obesity, hyperinsulinemia, insulin resistance, and a deranged intracellular handling of ions have pathogenetic importance in the development of this metabolic syndrome. However, a decrease in peripheral blood flow is another factor found in all the different facets of this syndrome. An increased peripheral resistance and a rarefaction of skeletal vessels are often seen in hypertensive subjects. Also, the insulin resistance so commonly seen in hypertension may be a consequence of a decreased blood flow because insulin resistance is associated with a decreased capillarization in skeletal muscle. Furthermore, the activity of skeletal muscle lipoprotein lipase, the key enzyme involved in the removal of triglycerides from the circulation, is known to be related to skeletal muscle vascularization. Because enhanced sympathetic activity has been associated with vascular hypertrophy and rarefaction of vascularization, overactivity in this part of the autonomic nervous system may lead to structural changes that will decrease the blood flow in peripheral tissues and thereby induce the metabolic syndrome of cardiovascular risk factors, particularly in individuals who, for genetic reasons, have decreased capillarization at the onset.
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PMID:Decreased peripheral blood flow in the pathogenesis of the metabolic syndrome comprising hypertension, hyperlipidemia, and hyperinsulinemia. 848 Jun 20

Authors call attention to the insulin-resistance and following hyperinsulinism, as important and may be also the basic factor, which is determining for high cardiovascular morbidity and mortality. Authors analyze the pathogenesis of the Reaven's syndrome X, syndrome 5H and their symptoms--insulin-resistance, hyperinsulinism, hyperlipemia with obesity, hypertension and eventually hirsutism. Authors analyze the congenital and acquired factors, which influence its manifestation and so occurrence of the cardiovascular diseases in the adulthood. In the past paediatricians gave little attention to this problem because they supposed the problem as the problem of the adult medicine. We can see that full 5H syndrome is only the top of the iceberg with basis in childhood. In the prevention of the cardiovascular diseases the task of the paediatricians is therefore not substitutable and in future they need to give to the X syndrome extraordinary attention.
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PMID:[Hyperinsulinism--a new pathogenic cause of cardiovascular diseases]. 849 16

Obesity is a multifactorial heterogenous condition. The location of excess fat on the body determines the risk of morbidity and mortality for significant disease. Visceral, or intraabdominal, fat is the fat depot most highly associated with illness and death from cardiocerebrovascular disease and diabetes. Visceral fat is also associated with a quartet of metabolic disturbances. Referred to as the metabolic syndrome, these abnormalities include hypertension, hyperlipidemia, hyperinsulinemia, and insulin resistance. The metabolic syndrome is also present in Cushing's syndrome, which is characterized by primary hypercortisolism as well as profound visceral adiposity and obesity. The interrelationship between hyperactivation or hypersensitivity of the stress axis and disease can be elucidated by an understanding of the effect of excess glucocorticoids upon energy storage and metabolism. The complex interactions of the stress axis upon the growth and reproductive axes, as well as upon the adipose tissue, suggest that chronic stress, whether psychological and/or physical, exerts an intense effect upon body composition, which, in turn, significantly affects the longevity and survival of the organism.
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PMID:Hypercortisolism and obesity. 859 40

Clinical goals in patients with non-insulin-dependent (type II) diabetes are to control glucose levels and prevent microvascular complications (eye, kidney, and nerve damage) while improving risk factors associated with cardiovascular disease (obesity, smoking, hyperlipidemia, hypertension, and hyperinsulinemia or insulin resistance). A wide array of medications and approaches is available to treat type II diabetes. Still, establishing an effective treatment regimen can be difficult, because patients have varying degrees of insulin secretory defects and insulin resistance and different conditions that must be factored in. Therefore, an individualized plan centered on self-management is the key to successful therapy in type II diabetes.
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PMID:Treatment of type II diabetes: what options have been added to traditional methods? 863 24

Hypertriglyceridemia is the most frequent form of hyperlipidemia seen in diabetes. Because hypertriglyceridemia and hyperinsulinemia often coexist in the general population and because patients with NIDDM generally are hyperinsulinemic, we have undertaken a series of in vivo studies to examine the effects of hyperinsulinemia on VLDL production. These studies showed that chronic hyperinsulinemia is accompanied by increased VLDL production and that this occurs even when plasma free fatty acid (FFA) levels have fallen. By contrast, acute hyperinsulinemia is accompanied by a reduction in VLDL production, and this reduction is, at least in part, mediated by an associated reduction in the availability of plasma FFAs as a substrate for VLDL-triglyceride (TG). The studies also raise the possibility that the difference in the dependence of VLDL production on plasma FFAs in acute versus chronic hyperinsulinemia results from an increase in hepatic lipogenic enzymes and from the availability of an alternate substrate such as fructose. The overall effect of hyperinsulinemia on VLDL production is postulated to reflect both the effect of insulin on apolipoprotein B production and the hepatic synthesis of TG from either plasma FFAs or newly made fatty acids.
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PMID:Hyperinsulinemia and triglyceride-rich lipoproteins. 867 84

Rats with lesions to the ventromedial hypothalamus (VMH) manifest obesity, hyperphagia, and hyperinsulinemia, and fetal VMH transplantation into the third cerebroventricle of VMH-lesioned rats reduces the development of obesity caused by the lesion. The aim of this study was to determine whether the hyperphagia, hyperlipidemia, and hyperinsulinemia of obsese Zucker rats could be corrected by the transplantation of lean fetal Zucker hypothalamic tissue into the third cerebral ventricle of Zucker obese rats. After the fetal hypothalamic transplant (obese-HY), the rate of weight gain was significantly diminished compared with the unoperated Zucker obese rats and the obese rats that received the transplantation of a similar amount of frontal cortical tissue from the same fetus (obese-FC). Food intake was significantly lower, and plasma triacylglycerol and insulin concentrations were also significantly reduced in the obese-HY rats compared with the obese and obese-FC rats. The weight of the adrenal glands, the plasma adrenocorticotropic hormone concentration, the liver weight, and the liver lipid content in obese-HY were significantly less than those observed in the obese and obese-FC animals. There were no significant differences between the obese and the obese-FC animals or between unoperated Zucker lean rats and lean rats transplanted with lean fetal hypothalamus in all the parameters we determined in this study. Neovascularization and normal cellular morphology of the transplanted fetal hypothalamic tissue suggest that the transplanted neural and glial cells were viable and physiologically functional. In conclusion, this study offers evidence suggesting that the hypothalamic-pituitary-adrenal function is defective in Zucker obese rats, resulting in excessive weight gain, hyperphagia, hyperlipidemia, and hyperinsulinemia. The hypothalamic dysfunction in the Zucker obese rats is corrected by the transplantation of lean fetal hypothalamus.
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PMID:Transplantation of lean fetal hypothalamus restores hypothalamic function in Zucker obese rats. 876 Feb 4


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