Hyperlipidemia là gì? Các công bố khoa học về Hyperlipidemia
Hyperlipidemia là một tình trạng mà mức độ lipid (chất béo) trong máu cao hơn mức bình thường. Đây là một yếu tố nguy cơ cho các bệnh tim mạch và cảnh báo về tì...
Hyperlipidemia là một tình trạng mà mức độ lipid (chất béo) trong máu cao hơn mức bình thường. Đây là một yếu tố nguy cơ cho các bệnh tim mạch và cảnh báo về tình trạng cơ thể không thể điều tiết lipid một cách hiệu quả. Có hai loại hyperlipidemia chính: hyperlipidemia gia đình (do di truyền) và hyperlipidemia không gia đình (do chế độ ăn uống và sinh hoạt không lành mạnh). Điều chỉnh chế độ ăn uống, tập thể dục và đôi khi sử dụng thuốc uống có thể giúp kiểm soát và giảm mức độ lipid trong máu.
Hyperlipidemia là một tình trạng mà mức độ lipid (chất béo) trong máu của một người cao hơn mức độ bình thường. Lipid bao gồm cholesterol và triglyceride, hai loại chất béo quan trọng trong cơ thể. Tuy nhiên, mức độ lipid cao có thể gây ra các vấn đề sức khỏe nghiêm trọng, đặc biệt là về hệ tim mạch.
Có ba loại lipid chính trong máu:
1. Cholesterol: Cholesterol có hai dạng, LDL (lipoprotein có mật độ thấp) và HDL (lipoprotein có mật độ cao). LDL cholesterol thường được gọi là "chất béo xấu" vì khi mức độ nó cao, có thể dẫn đến tình trạng mắc bệnh tim mạch. HDL cholesterol, ngược lại, được coi là "chất béo tốt" vì nó giúp loại bỏ cholesterol từ mạch máu và giảm nguy cơ bị các vấn đề tim mạch.
2. Triglyceride: Triglyceride là một loại chất béo chính trong cơ thể và là nguồn năng lượng dự phòng. Mức độ triglyceride cao có thể gây ra các vấn đề tim mạch và bệnh tiểu đường.
3. Lipoprotein (a): Lipoprotein (a) là một thành phần khác của lipid trong máu và cũng có thể gây nguy cơ tim mạch.
Hyperlipidemia có thể là do yếu tố di truyền hoặc do cách sống không lành mạnh. Thực phẩm giàu chất béo, đặc biệt là chất béo bão hòa và cholesterol, có thể góp phần tăng mức độ lipid trong máu. Ngoài ra, không vận động đủ và bị thừa cân cũng có thể gây ra hyperlipidemia.
Việc điều trị hyperlipidemia bao gồm thay đổi lối sống, như tăng cường hoạt động thể chất, ăn một chế độ ăn uống lành mạnh và kiểm soát cân nặng. Trong một số trường hợp nặng, nhà điều dưỡng có thể đưa ra quyết định sử dụng thuốc uống để kiểm soát mức độ lipid trong máu.
Danh sách công bố khoa học về chủ đề "hyperlipidemia":
Hyperlipidemia in Coronary Heart Disease II. GENETIC ANALYSIS OF LIPID LEVELS IN 176 FAMILIES AND DELINEATION OF A NEW INHERITED DISORDER, COMBINED HYPERLIPIDEMIA
Journal of Clinical Investigation - Tập 52 Số 7 - Trang 1544-1568 - 1973
Roux-en-Y Gastric Bypass vs Intensive Medical Management for the Control of Type 2 Diabetes, Hypertension, and Hyperlipidemia
JAMA - Journal of the American Medical Association - Tập 309 Số 21 - Trang 2240 - 2013
Hyperlipidemia and Coronary Disease
Background
Hypercholesterolemia is a risk factor for coronary disease, and platelet reactivity is increased with hypercholesterolemia, suggesting a prethrombotic risk. The aim of this study was to measure mural platelet thrombus formation on an injured arterial wall in a model simulating vessel stenosis and plaque rupture in hypercholesterolemic coronary disease patients before and after cholesterol reduction.
Methods and Results
Thirty-two patients with stable coronary disease were studied. Platelet thrombus formation and serum lipids were measured in 16 hypercholesterolemic patients (cholesterol >5.2 mmol/L) before and after a mean of 2.5 months of pravastatin therapy (40 mg/d) and in 16 normocholesterolemic control patients. Thrombus formation was assessed by exposing porcine aortic media to the patient’s flowing venous blood for 3 minutes at a shear rate of 754 or 2546 s
−1
at 37°C in an ex vivo superfusion chamber. Quantitative morphometric platelet thrombus formation at baseline was higher in the hypercholesterolemic patients at both the high and low shear rates: 4.8±1.0 and 3.3±0.7 μm
2
/mm, respectively, compared with normocholesterolemic patients: 2.1±0.5 and 1.6±0.4 μm
2
/mm (both
P
<.05). In the hypercholesterolemic patients, pravastatin decreased total cholesterol from 6.5±0.2 to 4.5±0.2 mmol/L and LDL cholesterol from 4.5±0.2 to 2.8±0.1 mmol/L (both
P
<.05). Platelet thrombus formation at high and low shear rates decreased to 2.0±0.3 and 1.3±0.3 μm
2
/mm, respectively (both
P
<.05).
Conclusions
Thus, hypercholesterolemia is associated with an enhanced platelet thrombus formation on an injured artery, increasing the propensity for acute thrombosis. Platelet thrombus formation at both high and low shear rates decreased as total and LDL cholesterol levels were reduced with pravastatin. Cholesterol lowering may therefore reduce the risk of acute coronary events in part by reducing the thrombogenic risk.
Ovid Technologies (Wolters Kluwer Health) - Tập 92 Số 11 - Trang 3172-3177 - 1995
Treatment of hyperlipidemia reduces glomerular injury in obese Zucker rats
Kidney International - Tập 33 Số 3 - Trang 667-672 - 1988
Chronic Rapamycin Treatment Causes Glucose Intolerance and Hyperlipidemia by Upregulating Hepatic Gluconeogenesis and Impairing Lipid Deposition in Adipose Tissue
OBJECTIVE
The mammalian target of rapamycin (mTOR)/p70 S6 kinase 1 (S6K1) pathway is a critical signaling component in the development of obesity-linked insulin resistance and operates a nutrient-sensing negative feedback loop toward the phosphatidylinositol 3-kinase (PI 3-kinase)/Akt pathway. Whereas acute treatment of insulin target cells with the mTOR complex 1 (mTORC1) inhibitor rapamycin prevents nutrient-induced insulin resistance, the chronic effect of rapamycin on insulin sensitivity and glucose metabolism in vivo remains elusive.
RESEARCH DESIGN AND METHODS
To assess the metabolic effects of chronic inhibition of the mTORC1/S6K1 pathway, rats were treated with rapamycin (2 mg/kg/day) or vehicle for 15 days before metabolic phenotyping.
RESULTS
Chronic rapamycin treatment reduced adiposity and fat cell number, which was associated with a coordinated downregulation of genes involved in both lipid uptake and output. Rapamycin treatment also promoted insulin resistance, severe glucose intolerance, and increased gluconeogenesis. The latter was associated with elevated expression of hepatic gluconeogenic master genes, PEPCK and G6Pase, and increased expression of the transcriptional coactivator peroxisome proliferator–activated receptor-γ coactivator-1α (PGC-1α) as well as enhanced nuclear recruitment of FoxO1, CRTC2, and CREB. These changes were observed despite normal activation of the insulin receptor substrate/PI 3-kinase/Akt axis in liver of rapamycin-treated rats, as expected from the blockade of the mTORC1/S6K1 negative feedback loop.
CONCLUSIONS
These findings unravel a novel mechanism by which mTORC1/S6K1 controls gluconeogenesis through modulation of several key transcriptional factors. The robust induction of the gluconeogenic program in liver of rapamycin-treated rats underlies the development of severe glucose intolerance even in the face of preserved hepatic insulin signaling to Akt and despite a modest reduction in adiposity.
Diabetes - Tập 59 Số 6 - Trang 1338-1348 - 2010
Familial combined hyperlipidemia is associated with upstream transcription factor 1 (USF1)
Nature Genetics - Tập 36 Số 4 - Trang 371-376 - 2004
Hyperlipidemia in Early Adulthood Increases Long-Term Risk of Coronary Heart Disease
Background—
Many young adults with moderate hyperlipidemia do not meet statin treatment criteria under the new American Heart Association/American College of Cardiology cholesterol guidelines because they focus on 10-year cardiovascular risk. We evaluated the association between years of exposure to hypercholesterolemia in early adulthood and future coronary heart disease (CHD) risk.
Methods and Results—
We examined Framingham Offspring Cohort data to identify adults without incident cardiovascular disease to 55 years of age (n=1478), and explored the association between duration of moderate hyperlipidemia (non–high-density lipoprotein cholesterol≥160 mg/dL) in early adulthood and subsequent CHD. At median 15-year follow-up, CHD rates were significantly elevated among adults with prolonged hyperlipidemia exposure by 55 years of age: 4.4% for those with no exposure, 8.1% for those with 1 to 10 years of exposure, and 16.5% for those with 11 to 20 years of exposure (
P
<0.001); this association persisted after adjustment for other cardiac risk factors including non–high-density lipoprotein cholesterol at 55 years of age (hazard ratio, 1.39; 95% confidence interval, 1.05–1.85 per decade of hyperlipidemia). Overall, 85% of young adults with prolonged hyperlipidemia would not have been recommended for statin therapy at 40 years of age under current national guidelines. However, among those not considered statin therapy candidates at 55 years of age, there remained a significant association between cumulative exposure to hyperlipidemia in young adulthood and subsequent CHD risk (adjusted hazard ratio, 1.67; 95% confidence interval, 1.06–2.64).
Conclusions—
Cumulative exposure to hyperlipidemia in young adulthood increases the subsequent risk of CHD in a dose-dependent fashion. Adults with prolonged exposure to even moderate elevations in non–high-density lipoprotein cholesterol have elevated risk for future CHD and may benefit from more aggressive primary prevention.
Ovid Technologies (Wolters Kluwer Health) - Tập 131 Số 5 - Trang 451-458 - 2015
Pharmacologic treatment of hyperlipidemia reduces glomerular injury in rat 5/6 nephrectomy model of chronic renal failure. The role of lipid abnormalities in the pathogenesis of focal glomerulosclerosis was investigated in the rat remnant kidney model of chronic renal failure. Rats subjected to right nephrectomy and two-thirds segmental infarction of the left kidney (5/6 nephrectomy) were treated for 10 weeks with the lipid-lowering agent clofibric acid. Both serum cholesterol and urine albumin excretion were significantly reduced by clofibric acid. At 10 weeks, the percent of glomeruli with focal glomerulosclerosis was 5 +/- 2% in clofibric acid-treated and 24 +/- 5% in untreated 5/6 nephrectomy rats (p less than 0.01). Inulin clearance was greater in clofibric acid-treated than in untreated 5/6 nephrectomy rats (0.28 +/- 0.02 versus 0.22 +/- 0.02 ml/min 100 g body wt, p less than 0.05). Body weight, kidney weight, and systemic blood pressure were not significantly altered by clofibric acid. Micropuncture studies, performed in separate groups of clofibric acid-treated and untreated 5/6 nephrectomy rats, demonstrated elevated single nephron glomerular filtration rates and glomerular capillary pressures 4 weeks after surgery. However, clofibric acid did not significantly alter single nephron glomerular filtration rates (95 +/- 2.1 nl/min in treated versus 97.0 +/- 6.2 nl/min in untreated, p greater than 0.05) or glomerular capillary pressures (56.6 +/- 1.5 mm Hg in treated versus 57.8 +/- 0.8 mm Hg in untreated, p greater than 0.05) in 5/6 nephrectomy rats. In a separate set of experiments, 5/6 nephrectomy rats were treated with the specific cholesterol synthesis inhibitor, mevinolin. Mevinolin improved serum lipid levels and reduced albuminuria in 5/6 nephrectomy rats without causing significant alterations in blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)
Circulation Research - Tập 62 Số 2 - Trang 367-374 - 1988
Analysis of the degree of undertreatment of hyperlipidemia and congestive heart failure secondary to coronary artery disease
American Journal of Cardiology - Tập 83 Số 9 - Trang 1303-1307 - 1999
Erectile Dysfunction Is Associated with a High Prevalence of Hyperlipidemia and Coronary Heart Disease Risk
European Urology - Tập 44 Số 3 - Trang 355-359 - 2003
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