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

Based on the analysis of fat distribution by CT scanning, we have proposed a classification of obesity: visceral fat obesity, in which fat accumulation is predominant in the intra-abdominal cavity. This type of obesity is more frequently accompanied by disorders of glucose and lipid metabolism, and also with hypertension, than subcutaneous fat obesity. We also showed that almost 90% of obese patients with ischemic heart disease have visceral fat accumulation. From clinical and basic experiments, aging, imbalance of sex hormone, overintake of sucrose and lack of physical exercise have been suggested to be major factors for visceral fat accumulation. Since intra-abdominal fat (mesenteric and omentum fat) have been show to have high activities of both lipogenesis and lipolysis, its accumulation induces a high content of free fatty acids, a product of lipolysis, in portal circulation which goes into the liver directly. Excess free fatty acid may cause the enhancement of lipid synthesis and gluconeogenesis as well as insulin resistance, resulting in hyperlipidemia, glucose intolerance and hypertension and finally atherosclerosis.
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PMID:Pathophysiology and pathogenesis of visceral fat obesity. 785 91

1. Secondary hyperparathyroidism in chronic renal failure may contribute to abnormalities of lipid metabolism and glucose tolerance. Amelioration of secondary hyperparathyroidism has been reported to mitigate the hyperlipidaemia and improve glucose tolerance experimentally. 2. The effect of the partial suppression of hyperparathyroidism by intravenous calcitriol on lipid levels and glucose tolerance was studied in 15 haemodialysis patients with secondary hyperparathyroidism. All received intravenous calcitriol 1 microgram at the end of haemodialysis thrice weekly for eight weeks. Oral glucose tolerance test and plasma lipid profiles including triglyceride, total cholesterol, high density lipoprotein cholesterol (HDL-C), low density lipoprotein cholesterol (LDL-C), apoprotein A-I and apoprotein B were determined simultaneously before and after eight weeks of therapy. 3. Before calcitriol treatment, uraemic patients with secondary hyperparathyroidism displayed a significant higher triglyceride and a significant lower HDL-C and apoprotein A-I as well as marked glucose intolerance with an increment of the area below the glucose curve when compared with healthy control subjects. 4. After eight weeks of calcitriol treatment, there was a significant decrement in serum intact parathyroid hormone (476.45 +/- 48.33 versus 191.37 +/- 30.17 ng/l, P < 0.001) and plasma triglyceride (2.24 +/- 0.34 versus 1.80 +/- 0.29 mmol/l, P < 0.05) as well as a significant increment of plasma apoprotein A-I (38.13 +/- 2.14 versus 44.19 +/- 2.18 mumol/l, P < 0.05), whereas there was no significant change in serum total cholesterol, LDL-C, HDL-C, and apoprotein B.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of intravenous calcitriol on lipid profiles and glucose tolerance in uraemic patients with secondary hyperparathyroidism. 787 41

Chronic renal failure is characterized by abnormalities in glucose metabolism. In fact there are present a normal fasting plasma glucose level )or mild hyperglycemia) in the presence of hyperinsulinemia, blunted decrease in the plasma glucose concentration in response to exogenous insulin administration, and diminished effect of intravenous insulin on glucose uptake in forearm perfusion studies. The glucose intolerance is not the result of reduced insulin secretion, or circulating insulin antagonists, and does not correlate with the coexisting metabolic acidosis. Glucose intolerance exists because the peripheral insulin-sensitive tissue (muscle, adipose tissue, liver) of the patients with chronic renal failure are insulin resistant. However there are two subgroups of uremic patients with regard to glucose tolerance: about half of uremic patients can augment their insulin secretion sufficiently to maintain normal glucose tolerance despite glucose intolerance. In the other half, insulin secretion following glucose loads is not different from normal values, so that glucose intolerance results. The cause of the peripheral insulin resistance remain unclear. Besides deranged renal function can result in the development of hypoglycemia. The most important predisposing mechanism to hypoglycemia is diminished glucose availability due to substrate limitation; the second important mechanism (alcohol, insulin, propranolol, etc.). Finally, in chronic renal failure persistent hyperinsulinemia can contribute hyperlipemia and to high incidence of cardiovascular disease.
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PMID:[Glucose metabolism and chronic renal insufficiency]. 801 26

Body mass index defined as weight (Kg)/height (cm2) and plasma lipids (total lipids-TL, triglycerides-TG and cholesterol-CH) were determined in 131 patients (61 males and 70 females aged between 21 and 63 years) with impaired glucose tolerance (IGT) defined according to WHO criteria. Blood glucose (BG) values and plasma insulin (PI) levels (radioimmunological assay) were determined during 2 hours OGTT with samples obtained before and after 1 h and 2 h after the intake of 75 g glucose. The sum of blood glucose and plasma insulin levels (0 + 1h + 2h) were compared in each of the following 5 groups of subjects: A--25 cases with IGT but without obesity (BMI: 23.2 +/- 2.6) and hyperlipidaemia (PL: 627 +/- 112; TG: 102 +/- 109 and CH: 208 +/- 35 mg/dl); B--35 cases with IGT and obesity (BMI: 31.2 +/- 2.6) but without hyperlipidaemia (PL: 807 +/- 109; TG: 136 +/- 31 and CH: 254 +/- 41 mg/dl); C--23 cases with IGT and hyperlipidaemia (PL: 1013 +/- 217; TG: 214 +/- 85 and CH: 311 +/- 52 mg/dl) but without obesity (BMI: 25.4 +/- 1.9); D--48 cases with IGT and both obesity (BMI: 30.9 +/- 2.8) and hyperlipidaemia (PL: 1457 +/- 155; TG: 597 +/- 188 and CH: 483 +/- 184 mg/dl); a control group of 49 cases without IGT, obesity (BMI: 26.2 +/- 1.9) or hyperlipidaemia (PL: 726 +/- 99 mg/dl).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Insulin resistance: the link between impaired glucose tolerance, body mass index and plasma lipids. 814 75

A higher prevalence of stroke is found in the patient with both diagnosed and undiagnosed diabetes and glucose intolerance. Because of local cerebral acidosis caused by ischemia and hyperglycemia, morbidity and mortality from a stroke are increased. Most studies show that individuals with admission serum glucose > 120 mg/dl (6.7 mM) have a higher morbidity and mortality from a stroke. The prevalence of cerebral infarcts, especially lacunar infarcts, is increased and the prevalence of subarachnoid hemorrhage, cerebral hemorrhage, and transient ischemic attacks are decreased in the diabetic patient. Age, race, hypertension, and the presence of diabetic nephropathy and coronary and peripheral vascular disease are risk factors for stroke in the diabetic patient, whereas obesity, smoking, hyperlipidemia, and glycemic control are not. Investigation and treatment of the diabetic patient with a stroke is discussed.
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PMID:Stroke in the diabetic patient. 817 50

Concerns about the side effects of chronic steroid therapy have prompted increasing interest in steroid-free immunosuppression for renal transplant recipients who are maintained on cyclosporine-based regimens. Studies to date suggest that at least 50% of cyclosporine-treated patients can be managed without steroid therapy. Reported benefits of avoiding or withdrawing steroid therapy have included improvements in hyperlipidemia, hypertension, and glucose intolerance and accelerated growth in children. Whether these effects will increase patient or allograft survival remains to be proved. Furthermore, the benefits of steroid-free immunosuppression must be weighed against the risk of precipitating allograft rejection. Although the elimination of steroids clearly increases the short-term risk of acute rejection, further studies are needed to determine the effects of steroid-free immunosuppression on long-term allograft function and to identify clinical or immunologic factors that can predict a successful outcome after the elimination of steroids.
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PMID:Steroid-free immunosuppression after renal transplantation. 819 89

This review examines the relationship between renal transplantation and two important metabolic consequences: hyperlipidemia and glucose intolerance. Before cyclosporine, hypertriglyceridemia and hypercholesterolemia were common abnormalities that worsened in the cyclosporine era. In addition to obesity, steroid use, and reduced renal function, cyclosporine plays an independent role in elevating cholesterol levels, with particular reference to the modulation of the low-density lipoprotein receptor. Management includes maintaining low levels of steroid, manipulation of cyclosporine appropriately, diets low in fat and cholesterol, and an exercise program. Pharmacologic management in general revolves around the HMG-COA reductase drugs, which can be used safely if liver function tests and muscle enzymes are monitored. The unmasking of clinically important glucose intolerance occurs in 5 to 10% of patients in the cyclosporine era, not different from the earlier experience. Steroids and cyclosporine independently can worsen glucose tolerance to unmask a genetic predisposition to Type II diabetes in some and to even create glucose intolerance in otherwise normal individuals. Management is based on dietary and immunosuppressive drug dosing manipulations and the judicious use of oral hypoglycemic agents. Half of these recipients may ultimately need insulin. In summary, hyperlipidemia and glucose intolerance remain important metabolic consequences of renal transplantation that affect long-term patient survival unless recognized and treated.
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PMID:Hyperlipidemia and glucose intolerance in the post-renal transplant patient. 819 94

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

Carney's complex is an unusual disorder consisting of a variety of endocrinological and urological manifestations. The characteristic gonadal and adrenal features of Carney's complex should become familiar to urologists. A patient was evaluated for obesity, cushingoid features, hyperlipidemia, glucose intolerance, coronary artery disease, a left adrenal mass, bilateral testicular masses and cardiac myxomas. Pathological evaluation revealed the testicular tumors to be of Sertoli cell origin, the adrenal mass to be an adrenocortical adenoma and intracardiac lesions consistent with myxomas. The features of Carney's complex are discussed.
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PMID:Carney's complex in a patient with hormone-producing Sertoli cell tumor of the testicle. 841 42


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