Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To investigate the hypothesis that insulin resistance plays a role in the etiology of hypertension and hyperlipidemia, we measured serum lipid levels, the fasting glucose/insulin ratio, and the insulin response to oral glucose (GTT) in a group of young obese subjects (n = 21) with hypertension and normal glucose tolerance and in normotensive subjects (n = 36) with normal glucose tolerance, matched for age and body mass index. Leisure time physical activity was evaluated by a questionnaire outlining three levels of physical activities during leisure time. Subjects with hypertension had higher fasting serum insulin (19 +/- 2 v 13 +/- 1 microU/mL, P < .01) and lower fasting glucose/insulin ratio (5.3 +/- 0.2 v 7.1 +/- 0.5 mg/dL/microU/mL, P < .01) than normotensive subjects. Subjects with hypertension had higher peak serum insulin and lower plasma glucose area/insulin area ratio in response to glucose (1.8 +/- 0.2 v 2.4 +/- 0.2 mg/dL/microU/mL, P < .05) than normotensive subjects. Serum total cholesterol, low-density cholesterol, and triglycerides were higher in the obese hypertensive subjects than in obese normotensive ones. Blood pressure correlated with either fasting serum insulin, fasting glucose/insulin ratio, or glucose area/insulin area ratio during GTT. The level of leisure time physical activities was lower in obese hypertensive subjects than in obese normotensive ones. There were significant correlations between the levels of physical activity and the fasting plasma glucose/insulin ratio (r = 0.371, P < .01) or the fasting serum insulin concentration (r = -0.282, P < .05). The study provided evidence that a low level of leisure time physical activity is associated with insulin resistance and resultant hyperinsulinemia, which are the key metabolic abnormalities that link hypertension, obesity, and hyperlipidemia in young subjects.
Am J Hypertens 1992 Dec
PMID:Leisure time physical activity and insulin resistance in young obese students with hypertension. 128 41

The progression of atheroarteriosclerosis was shown to be age dependent. This designation covers two separate entities: arteriosclerosis, the progressive and diffuse hardening of the walls of arteries with loss of elasticity, and atheromatous plaque formation, which can start early in life according to nutrition and genetic factors (LDL-receptor expression). Lipoprotein-receptor interactions play a crucial role in lipidic plaque formation. There is, however, no indication that the diffuse hardening of the vascular wall would also be influenced by these mechanisms. We described recently a high-affinity receptor for elastin peptides, present on smooth muscle cells, fibroblasts, and also on monocytes and PMNs. When activated, this receptor will increase intracellular calcium. Circulating elastin peptides were determined by a sensitive Elisa method and found to be between 0.1 and 20 micrograms/ml, in the range of activation of the elastin receptor. They increase in obliterative arteriopathies and type IIb hyperlipidemia. Elastolysis accompanies aging and vascular pathology; the sensitivity of this receptor changes with age, intracellular Ca++ increases, but the receptor appears to be uncoupled from its normal transmission mechanism. These results may well explain the increasing diffuse calcification of the vessel wall. The previously demonstrated potentiation of cholesterol deposition in elastic fibers by calcium is in agreement with simultaneous deposition of calcium and lipids. The recent demonstration of the efficient competition of fibronectin for LDL in proteoglycan-LDL complexes suggests that this reaction may be involved in foam cell formation by the opsonization of LDL for phagocytosis. Fibronectin was shown to accumulate in atherosclerotic plaques. Altogether these recent results confirm the importance of cell-matrix interactions in atherogenesis and lead to a better understanding of the age dependence of these disease processes.
Ann N Y Acad Sci 1992 Dec 26
PMID:Cell-matrix interactions in the genesis of arteriosclerosis and atheroma. Effect of aging. 133 48

The combined syndrome of android (upper body) obesity, diabetes, hyperlipidaemia and hypertension is discussed in terms of a deranged endocrine regulation of metabolism. The syndrome is characterized by insulin insensitivity and an increased control of metabolism by cortisol. The antagonism between the two hormones appears to be partly responsible for the hyperglycaemia, hypertriglyceridaemia and hypercholesterolaemia. The synergism between insulin and cortisol in stimulating energy deposition, associated with a decreased effect of corticotropin-releasing factor in stimulating energy expenditure, is likely to contribute to the development of obesity. The efficacy of D-fenfluramine in treating the obese-diabetic-hyperlipidaemic-hypertensive syndrome probably depends on its actions on the serotoninergic system in the hypothalamus which both decreases food consumption and tends to normalize hormonal balance through the hypothalamic-pituitary-adrenal axis.
Int J Obes Relat Metab Disord 1992 Dec
PMID:Neuroendocrine regulation and obesity. 133 26

Current treatment of obesity seems to be focused mainly on the success of losing body weight, which can be achieved, in order of increasingly drastic manoeuvres: by simple nutritional advice; professional follow-up of a negative energy balance; drugs with effects on appetite regulation, energy absorption or expenditure; total seclusion with control of every administered calorie; surgical intervention; or even jaw-wiring. The only treatment of this sort that has been convincingly shown to have long-lasting effects is surgical intervention in the gastrointestinal tract, but this can only be accepted for use in severe cases. Thus, the problem of treatment of moderate obesity is to find an effective therapeutic modality which iss efficient in maintaining a reduced weight. Obesity treatment also seems to have focused too much on the mass of excess body fat, which is not necessarily an indicator of the medical hazards of the condition. It is important to realize that the risk factor clusters following obesity are often efficiently treated by successful reduction of the obese condition. Instead of specific treatment of each of these complications by, for example, multi-pharmacological therapy, a sufficiently efficient obesity treatment would be a preferable substitute. This goal may, if necessary, be achieved by treatment with a single drug with a useful therapeutic profile, including efficiency in the long-term to prevent relapse. Chronic treatment might then be considered acceptable in the same way as chronic pharmacological treatment of hypertension and hyperlipidemia, for example. No drug has as yet proven to have these characteristics.(ABSTRACT TRUNCATED AT 250 WORDS)
Int J Obes Relat Metab Disord 1992 Dec
PMID:Treatment of obesity. 133 27

Abdominal obesity is closely associated with risk factors for cardiocerebrovascular disease and NIDDM and the precipitation of these diseases. Together, they seem to constitute a metabolic syndrome where hyperinsulinaemia, insulin resistance, hyperlipidaemia, hypertension, visceral fat accumulation, cardiocerebrovascular disease and NIDDM are the individual constituents. The background to this syndrome might be a primary aberration expressing itself as an increased sensitivity of the hypothalamo-adrenal axis, and subsequent inhibition of sex steroid hormone secretions. This in turn will probably be followed by metabolic derangements, primarily peripheral insulin resistance, as well as by visceral fat accumulation by mechanisms which are partially visualized by recent work in the field. Visceral fat accumulation may then amplify the metabolic aberrations via hepatic effects of excessive concentrations of portal FFA, producing hyperproteinaemia, hyperglycaemia, hyperinsulinaemia and, perhaps, hypertension. The background to the central endocrine aberration remains more speculative, but factors leading to increased cortisol production, including specific stress reactions, tobacco smoking and alcohol may turn out to be important. The tentative conclusion provides a hypothesis for further work, and has recently obtained considerable support from further observations in humans in other than the endocrine and metabolic areas, as well as from studies in experimental animal models, where such factors can be studied under fully controlled conditions, which is not possible in humans for ethical reasons.
Int J Obes Relat Metab Disord 1992 Dec
PMID:Regional fat distribution--implications for type II diabetes. 133 83

Isotretinoin, a retinoid derivative, is in wide use as a treatment for severe acne and other dermatologic conditions. Its effects on serum lipids, most notably the induction of hypertriglyceridemia, have been well documented. We present a case of a young woman with a previous history of gestational hyperlipidemia who developed hypertriglyceridemia and pancreatitis after initiation of isotretinoin therapy. A history of gestational hyperlipidemia may serve as a marker to help identify patients who are at increased risk for developing severe hypertriglyceridemia while receiving isotretinoin. Her case emphasizes the need to consider the possibility of pancreatitis in patients who develop abdominal pain while receiving this drug.
Am J Gastroenterol 1992 Dec
PMID:Marked hyperlipidemia and pancreatitis associated with isotretinoin therapy. 144 57

There is evidence that increased reactivity of blood plasma to thrombogenic surfaces (hypercoagulability) may contribute to the risk of thrombotic occlusion of a coronary artery in coronary heart disease. The Northwick Park Heart Study found raised levels of factor VII coagulant (VIIc) activity and fibrinogen in men at high risk of a coronary event. Several other European studies have confirmed the latter finding, but the Northwick Park Heart Study is the only study to report formally on VIIc to date. Plasma VIIc is increased in the presence of hyperlipidemia and on a high fat diet, and falls with lipid-lowering therapy and a reduction in fat intake. Fibrinogen concentration is raised in smokers and decreases when the habit is given up. Thus, these markers of thrombogenic risk are readily controlled by standard preventive measures against coronary heart disease. Unresolved issues include: (1) whether the distinctive features of the Northwick Park VII bioassay improve the value of VIIc as a predictor of coronary heart disease; (2) the separate extent to which activation of factor VII and increases in factor VII concentration account for the raised VIIc in hyperlipidemia; (3) the basis of the raised fibrinogen in men at high coronary heart disease risk, even among nonsmokers; and (4) the usefulness of plasma levels of activation peptides of factors IX, X, and prothrombin as markers of thrombogenic risk.
Arch Pathol Lab Med 1992 Dec
PMID:Hemostasis and cardiovascular risk. The British and European experience. 145 78

In September 1988, the U.S. Air Force instituted routine centrifuge training for aircrew involved in high performance, high G aircraft. As of June 1991, 6,078 aircrew members have been trained. This report documents an anterolateral myocardial infarction that occurred in a 37-year-old pilot immediately after his centrifuge training profile. The individual had a history of elevated lipids and smoking, and was on a waiver from the USAF for Flying Class II duties for hyperlipidemia treated with cholestyramine.
Aviat Space Environ Med 1992 Dec
PMID:Myocardial infarction occurring at the conclusion of centrifuge training in a 37-year-old aviator. 814 98

To investigate whether the lowering of triglyceride levels has beneficial effects on glucose metabolism, we studied 13 nondiabetic men with combined hyperlipidemia (phenotype IIB) before and after 2 months of treatment with a slow-release formulation of bezafibrate (400 mg daily). The rates of whole body glucose disposal were quantitated by the euglycemic hyperinsulinemic clamp technique (insulin infusion rate of 80 mU/m2/min). In an oral glucose tolerance test, fasting glucose level decreased slightly (5.0 +/- 0.2 versus 4.8 +/- 0.2 mmol/L; p < 0.05) during bezafibrate treatment. Glucose and insulin levels after an oral glucose load remained unchanged. Rates of whole body glucose disposal did not change during bezafibrate treatment (39.5 +/- 3.3 mumol/kg/min before treatment versus 40.6 +/- 2.7 mumol/kg/min after treatment; difference not significant). Basal hepatic glucose output also remained unchanged (8.2 +/- 0.2 mumol/kg/min before treatment versus 8.3 +/- 0.2 mumol/kg/min after treatment; difference not significant). Our findings show that bezafibrate has a triglyceride-lowering effect without any significant influence on insulin sensitivity.
Clin Pharmacol Ther 1992 Dec
PMID:Effects of bezafibrate on insulin sensitivity and glucose tolerance in subjects with combined hyperlipidemia. 145 71

The concern about long-term toxicity of oral synthetic retinoids has developed because many patients, especially those with genodermatoses, require lifelong therapy. Several organ systems are at risk, especially the hepatic, skeletal, and cardiovascular systems. Although acute hepatotoxicity is a rare side effect of etretinate and acitretin therapy, prospective studies have not demonstrated chronic liver toxicity. The frequency of bone changes induced by retinoids is difficult to estimate, because this adverse effect is usually asymptomatic and requires x-ray or scintigraphic examination for detection. Atherosclerosis develops in many patients who receive long-term retinoid therapy, but the extent to which the process is aggravated by drug-induced hyperlipidemia is not known. Many patients have now been treated with either etretinate or isotretinoin continuously for as many as 15 years and have not developed any signs of severe chronic toxicity. However, continued intense surveillance is recommended for patients expected to require lifelong therapy.
J Am Acad Dermatol 1992 Dec
PMID:Long-term safety of retinoid therapy. 146 Jan 22


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>