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

Diabetes is frequently associated with hyperlipidemia, which results in atherogenic complications. Insulin-dependent diabetes mellitus (IDDM) model BB/Wor//Tky (BB) rats exhibit both hyperglycemia and hyperlipidemia and die within 3 weeks after the onset of diabetes unless insulin therapy is given. We performed insulin gene therapy in BB rats with adenovirus vectors through the tail vein. After infusion, plasma triglyceride levels dropped quickly and maintained low levels for 1 week, whereas blood glucose levels showed a slight decrease. The survival period of diabetic BB rats was prolonged to up to 75 days by infusing insulin gene-expressing adenoviral vectors. We suggest that the control of hyperlipidemia can be a life-saving measure when combined with hyperglycemia control in the treatment of diabetes.
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PMID:Adenoviral insulin gene therapy prolongs survival of IDDM model BB rats by improving hyperlipidemia. 1243 86

The aim of this study was to examine the long-term effect of lung transplantation on Health Related Quality of Life by studying 28 patients who survived at least 55 months after lung transplantation. Measures included the Nottingham Health Profile, questions concerning lung-specific problems, the State-Trait Anxiety Inventory, the Self-rating Depression Scale, the Index of Well-Being, the Karnofsky performance index, and questions concerning activities of daily life. Furthermore, comorbid conditions were measured. Before transplantation patients reported restrictions on almost all quality of life measures. Until approximately 43 months after transplantation there were significant improvements on most dimensions of the Nottingham Health Profile and more patients could walk without dyspnea. Significant improvements occurred with regard to the levels of anxiety, depression, and well being, and the scores on the Karnofsky performance index improved. Activities of daily life could be performed without help by most patients. After approximately 43 months patients experienced more dyspnea, anxiety, depression, and a lower level of well being. The number of patients suffering from a decrease of kidney function, drug treated hyperlipidemia, insulin dependent diabetes mellitus and bronchiolitis obliterans syndrome increased. It may be concluded that patients experience a stable and better overall quality of life after transplantation. Long-term after lung transplantation patients experience a decline on several dimensions of quality of life, which may be explained by an increase of comorbid conditions and Bronchiolitis Obliterans Syndrome.
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PMID:Long-term quality of life in patients surviving at least 55 months after lung transplantation. 1267 22

Type 1 diabetes mellitus is potentially associated with serious microvascular and macrovascular complications, although these are usually subclinical during the pediatric and adolescent years. There is no "grace" period for the beginnings of such complications. Duration of diabetes, glycemic control, age, and pubertal stage are critical factors contributing toward development of such problems. Other risk factors include family history (genetic predisposition), hyperlipidemia, hypertension, and smoking. The Diabetes Control and Complications Trial (DCCT) proved the importance of glycemic control and emphasized the ability of improved glucose control to prevent or decrease retinopathy, nephropathy, and neuropathy using a multidisciplinary same-philosophy-of-care approach plus targeted glucose and hemoglobin A(1c) values. Other natural history and intervention studies support the findings of the DCCT. Although our current tools are not perfect, they allow us to decrease microangiopathic complications very significantly if we educate our patients and their family members. Metabolic control counts.
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PMID:Complications of pediatric and adolescent type 1 diabetes mellitus. 1276 57

Diabetic nephropathy has become the single largest cause of end-stage renal disease (ESRD) worldwide. Until recently, it was thought that once a patient developed overt proteinuria, diabetic nephropathy was irreversible and inevitably progressed to ESRD. However, the reversal of lesions caused by diabetic nephropathy (e.g., glomerular basement membrane thickening and mesangial matrix increase) has been demonstrated in a series of patients who underwent a pancreas transplantation 10 years prior to the reversal. Remission of nephrotic range proteinuria has also been reported in some patients with type 1 diabetes from the Collaborative Study Group during a median follow-up of 3 years of angiotensin-converting enzyme (ACE) inhibitor administration; no deterioration of renal function was observed in these patients. Remission and regression in nephropathy of type 1 diabetes patients have also been reported when blood pressure was controlled aggressively. Recent clinical trials have demonstrated that angiotensin II receptor blocker (ARB) preserved renal function and slowed the progression of nephropathy to ESRD in patients with type 2 diabetes. Since many patients with type 2 diabetes manifest with a metabolic syndrome, multifactorial intensive treatment is necessary; such treatment includes behavior modifications, dietary intervention, exercise, and smoking cessation. In this population, pharmacological therapy targeting hyperglycemia, hypertension (including ARB/ACE inhibitor), and hyperlipidemia in cases of type 2 diabetes is also necessary.
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PMID:Remission and regression of diabetic nephropathy. 1292 17

Diabetes now accounts for >40% of patients with ESRD. Despite significant progress in understanding diabetic nephropathy, the cellular mechanisms that lead to diabetes-induced renal damage are incompletely defined. For defining changes in protein expression that accompany diabetic nephropathy, the renal proteome of 120-d-old OVE26 transgenic mice with hypoinsulinemia, hyperglycemia, hyperlipidemia, and proteinuria were compared with those of background FVB nondiabetic mice (n = 5). Proteins derived from whole-kidney lysate were separated by two-dimensional PAGE and identified by matrix-assisted laser desorption ionization-time-of-flight (MALDI-TOF) mass spectrometry. Forty-one proteins from 300 visualized protein spots were differentially expressed in diabetic kidneys. Among these altered proteins, expression of monocyte/neutrophil elastase inhibitor was increased, whereas elastase IIIB was decreased, leading to the hypothesis that elastin expression would be increased in diabetic kidneys. Renal immunohistochemistry for elastin of 325-d-old FVB and OVE26 mice demonstrated marked accumulation of elastin in the macula densa, collecting ducts, and pelvicalyceal epithelia of diabetic kidneys. Elastin immunohistochemistry of human renal biopsies from patients with type 1 diabetes (n = 3) showed increased elastin expression in renal tubular cells and the interstitium but not glomeruli. These results suggest that coordinated changes in elastase inhibitor and elastase expression result in increased tubulointerstitial deposition of elastin in diabetic nephropathy. The identification of these coordinated changes in protein expression in diabetic nephropathy indicates the potential value of proteomic analysis in defining pathophysiology.
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PMID:Alterations in the renal elastin-elastase system in type 1 diabetic nephropathy identified by proteomic analysis. 1497 67

Coronary vascular disease is one facet of a generalized disturbance of vascular function present throughout the vascular tree. Dysfunction of the endothelium leads to thickening of the intima and media of the vessel wall of large and medium-sized muscular arteries and large elastic arteries, such as the aorta, carotid, and iliac arteries. Flow-mediated dilatation of the brachial artery is one of several tests used to assess dysfunction of the endothelium using high resolution ultrasound. Endothelial dysfunction has been demonstrated in children with heterozygous familial hypercholesterolemia, type 1 diabetes, morbid obesity, and homozygous homocystinuria and in the offspring of a parent with early coronary disease. High resolution ultrasound has also confirmed postmortem findings that atherogenesis has its beginnings in childhood and adolescence, with the demonstration of increased carotid artery intima-medial thickening in children with familial hypercholesterolemia, familial combined hyperlipidemia, and type 1 diabetes and in the offspring of a parent with early coronary disease. In combination with family history and traditional risk factors, ultrasound evaluation of brachial artery flow-mediated vasodilation and carotid artery intima-medial thickening could be used in a clinical setting to assess coronary risk in high risk pediatric patients.
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PMID:Clinical review 168: What vascular ultrasound testing has revealed about pediatric atherogenesis, and a potential clinical role for ultrasound in pediatric risk assessment. 1524 May 74

Studies of diabetic vascular disease have traditionally used murine models of type 1 diabetes and genetic models of type 2 diabetes. Because the majority of patients with type 2 diabetes have diet induced obesity, we sought to study the effect of diabetes on arterial disease in a mouse model of diet induced obesity/diabetes. C57Bl/6 mice fed a high-fat diet for 9 weeks developed type 2 diabetes characterized by elevated body weight, hyperglycemia, and hyperinsulinemia. Arteries from diabetic mice exhibited a marked decrease in endothelium-dependent vasodilation, a modest decrease in endothelium independent vasodilation, and an increase in sensitivity to adrenergic vasoconstricting agents. Insulin stimulated protein kinase B (akt) and endothelial nitric oxide synthase (eNOS) phosphorylation were preserved in arteries from diabetic mice; however, eNOS protein dimers were markedly diminished. Arterial nitrotyrosine staining indicated that increased levels of peroxynitrite contributed to eNOS dimer disruption in the diabetic mice. The abnormal vasomotion was not an acute response to the high-fat diet, as short term high-fat diet feeding had no effect on endothelium dependent dilation. A trend toward smaller neointimal lesions was noted in high-fat diet fed mice after femoral artery wire denudation injury. In summary, disrupted eNOS dimer formation rather than impaired insulin mediated eNOS phosphorylation contributed to the endothelial dysfunction in diet induced obese/diabetic mice. The lack of an increase in neointimal formation indicates that additional diabetes associated parameters (such as hyperlipidemia and atherosclerotic vascular disease) may need to be present to increase neointimal formation in this model.
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PMID:Diabetes induces endothelial dysfunction but does not increase neointimal formation in high-fat diet fed C57BL/6J mice. 1610 22

There has been wide recognition in the past decade of the increasing frequency of type 2 diabetes in youth, largely but not exclusively in North America. In some American locations and populations, incidence and prevalence of type 2 diabetes are much higher than those of type 1 diabetes, because of increased calorie and fat intake, and decreased exercise. The increasing prevalence of type 2 diabetes in the United States has closely paralleled the increase in childhood obesity noted there, but now across the Western world. Besides obesity, the other youth risk factors for type 2 diabetes are: ethnicity, puberty, family history, metabolic syndrome, polycystic ovary syndrome, acanthosis nigricans. Any feature or condition associated with insulin resistance/hyperinsulinemia should alert to screen youth at increased risk for (pre)type 2 diabetes. Treatment goals are to decrease weight and increase exercise, to normalize insulinemia, glycemia and HbA1c, to control hypertension and hyperlipidemia. The aim of the pharmacological therapy is to decrease insulin resistance, namely by metformin. Sometimes, insulin therapy is necessary.
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PMID:[Weight of obesity in (pre)type 2 diabetes in children and adolescents: how and when to screen for?]. 1628 80

It is well known that humans with diabetes have more atherosclerosis and its complications. The causes of this relationship are, however, unclear. Although recent data show that improved glycemic control reduces arterial disease in type 1 diabetes, other studies have shown that subjects with "prediabetes" have more cardiovascular disease before the development of hyperglycemia. Thus, either hyperglycemia and/or lack of insulin actions are toxic to arteries, or metabolic derangements exclusive of hyperglycemia are atherogenic. For >50 years animal models of diabetes and atherosclerosis have been used to uncover potential mechanisms underlying diabetes associated cardiovascular disease. Surprisingly, diabetes alone increases vascular disease in only a few select animal models. Increased atherosclerosis has been found in several animals and lines of genetically modified mice; however, diabetes often also leads to greater hyperlipidemia. This makes it difficult to separate the toxic effects of insulin lack and/or hyperglycemia from those caused by the lipids. These studies are reviewed, as well as more recent investigations using new methods to create diabetic-atherosclerotic models.
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PMID:Diabetic vascular disease: an experimental objective. 1676 60

Approximately one-third of patients with type 1 diabetes develop a variety of complications as a result of mechanisms that are not completely understood. However, insufficient metabolic control seems to play a major role. Other factors such as magnesium (Mg) could also be of importance. We designed this study to elucidate the effect of oral magnesium administration on plasma lipid profile and mesenteric fat in male Wistar rats. Animals were divided into 4 groups (n=10 in each group): one group served as control, while the other groups were made diabetic with a single i.v. injection of 40 mg/kg streptozocin. Animals in which the diabetic state lasted for 10 days were referred as acute diabetic rats, whereas those in which the diabetes lasted for 8 weeks were defined as chronic diabetics. Mg-treated chronic diabetic received 10 g/l of MgSO(4) added to the drinking water (0.46 g/24 h) for eight weeks following which the left common carotid artery was cannulated for continuous recording of blood pressure. Blood glucose, magnesium and lipid profiles levels were also determined. Diabetes induction caused plasma glucose, high density lipoprotein (HDL), low density lipoprotein (LDL), very low density lipoprotein (VLDL), total cholesterol and triglyceride concentrations to increase, however plasma Mg level was decreased. Administration of MgSO(4) for eight weeks caused the return of the above factors to their normal levels. Mg concentrations also increased but failed to reach normal levels. Diabetes induction caused mesenteric fat/body weight ratio to increase, but administration of MgSO(4) reduced the ratio to normal levels. In addition, Mg administration returned systolic blood pressure to the normal level. Our results support the hypothesis that Mg may play a part in the management of diabetes and the prevention of its vascular complications in streptozocin-induced diabetic rats and it may be useful in the treatment of hyperlipidaemia in diabetic case.
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PMID:Effect of oral magnesium sulfate administration on blood pressure and lipid profile in streptozocin diabetic rat. 1729 79


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