Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0242339 (dyslipidemia)
 13,927 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Weight loss reduces many of the health hazards associated with obesity including insulin resistance, diabetes mellitus, hypertension, dyslipidemia, sleep apnea, hypoxemia and hypercarbia, and osteoarthritis. Potential adverse effects of weight loss include a greater risk for gallstone formation and cholecystitis, excessive loss of lean body mass, water and electrolyte problems, mild liver dysfunction, and elevated uric acid levels. Less consequential problems such as diarrhea, constipation, hair loss, and cold intolerance may also occur. The short-term adverse effects are not severe enough to contraindicate weight loss, nor do they outweigh its short-term benefits.
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PMID:Short-term medical benefits and adverse effects of weight loss. 836 5

Obstructive sleep apnea syndrome (OSAS) is a chronic disease characterized by recurrent episodes of partial or complete upper airway collapse and obstruction during sleep, associated with intermittent oxygen desaturation, sleep fragmentation, and symptoms of disruptive snoring and daytime sleepiness. Increasing focus is being placed on the relationship between OSAS and all-cause and cardiovascular disease-related mortality, but it still largely unclear whether this association is causative or simply speculative and epidemiological. Basically, reliable clinical evidence supports the hypothesis that OSAS might be associated with essential and resistant hypertension, as well as with an incremental risk of developing stroke, cardiac rhythm perturbations (e.g., atrial fibrillation, bradyarrhythmias, supraventricular and ventricular arrhythmias), coronary artery disease, acute myocardial infarction, and heart failure. Although it is still unclear whether OSAS might represent an independent risk factor for several acute or chronic conditions, or rather might trigger cardiovascular disease in the presence of traditional cardiovascular risk factors (e.g., obesity, diabetes, and dyslipidemia), there is a plausible biological background underlying this association, in that most of the mechanisms implicated in the pathogenesis of OSAS (i.e., hypoxia, hypercapnia, negative intrathoracic pressure, micro-arousal, sympathetic hyperactivity, metabolic and hormonal changes, oxidative stress, phlogosis, endothelial dysfunction, hypercoagulability, and genetic predisposition) might also be involved in the pathogenesis of cardiovascular disorders. In this article we discuss the different aspects of the relationship between OSAS and pathogenically different conditions such as systemic hypertension, coronary artery disease, stroke, metabolic abnormalities, arrhythmias, and heart failure, and we also discuss the kaleidoscope of phenomena implicated in the pathogenesis of this challenging disease.
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PMID:Obstructive sleep apnea syndrome and cardiovascular diseases. 2145 62

Obesity compounds the metabolic response to critical illness and augments the consequences of overfeeding. Effective monitoring is essential for the prevention of, or to avoid, worsening of preexistent morbidities associated with obesity during the implementation of specialized nutrition support. This monitoring should guide the clinician toward the selection of appropriate therapeutic options to reduce complications from significant hyperglycemia, dyslipidemia, hypercapnia, fluid overload, and worsening of hepatic steatosis. Conventional nutrition outcome markers should be employed, with their limitations understood, when used for the critically ill obese patient.
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PMID:Monitoring nutrition therapy in the critically ill patient with obesity. 2180 31

Patients with obstructive sleep apnea, who experience episodic hypoxia and hypercapnia during sleep, often demonstrate increased inflammation, oxidative stress, and dyslipidemia. We hypothesized that sleep apnea patients would be predisposed to the development of atherosclerosis. To dissect the mechanisms involved, we developed an animal model in mice whereby we expose mice to intermittent hypoxia/hypercapnia (IHH) in normobaric environments. Two- to three-month-old low-density lipoprotein receptor deficient (Ldlr(-/-)) mice were fed a high-fat diet for 8 or 16 wk while being exposed to IHH for either 10 h/day or 24 h/day. Plasma lipid levels, pulmonary artery and aortic atherosclerotic lesions, and cardiac function were then assayed. Surprisingly, atherosclerosis in the aorta of IHH mice was similar compared with controls. However, in IHH mice, atherosclerosis was markedly increased in the trunk and proximal branches of the pulmonary artery of exposed mice; even though plasma cholesterol and triglycerides were lower than in controls. Hemodynamic analysis revealed that right ventricular maximum pressure and isovolumic relaxation constant were significantly increased in IHH exposed mice and left ventricular % fractional shortening was reduced. In conclusion, 1) Intermittent hypoxia/hypercapnia remarkably accelerated atherosclerotic lesions in the pulmonary artery of Ldlr(-/-) mice and 2) increased lesion formation in the pulmonary artery was associated with right and left ventricular dysfunction. These findings raise the possibility that patients with obstructive sleep apnea may be susceptible to atherosclerotic disease in the pulmonary vasculature, an observation that has not been previously recognized.
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PMID:Intermittent hypoxia and hypercapnia induce pulmonary artery atherosclerosis and ventricular dysfunction in low density lipoprotein receptor deficient mice. 2399 Feb 45

Obstructive sleep apnoea syndrome (OSAS) is characterized by recurrent partial or complete pharyngeal collapses during sleep. The pathophysiology of OSAS is complex and multifactorial. Factors influencing upper airway patency include a reduction in upper airway dimensions that can result from both anatomical and functional alterations (obesity, fluid shift or maxillo-facial structural changes), and increased pharyngeal collapsibility owing to reduced neuromuscular compensation and lack of the pharyngeal protective reflex during sleep. Severe OSAS is associated with a high cardiometabolic risk. Obstructive apnoeic events incorporate a range of stressors that activate mechanisms contributing to the initiation and progression of cardiac, vascular and metabolic diseases. Obstructed breathing induces markedly negative intrathoracic pressure and also provokes hypoxia and hypercapnia. The hypoxaemic stress is further amplified by the subsequent reoxygenation (intermittent hypoxia), resulting in the generation of reactive oxygen species (ROS), sympathetic activation and inflammation. OSAS is able to increase the number of fatal and non-fatal cardiovascular events, including arrhythmias, myocardial infarction and stroke. OSAS is associated with dyslipidemia, type 2 diabetes, its poor control and non-alcoholic fatty liver disease. Screening, diagnosis and integrated care of OSAS should be included in an aggressive management of risk reduction in chronic cardiovascular and metabolic diseases.
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PMID:[Pathophysiology of obstructive sleep apnea syndrome and its cardiometabolic consequences]. 2812 3

Hypertension and metabolic disorders evidenced in adults who have been exposed to nutritional insults during early life may be sex-dependent. We evaluated if blood pressure (BP), cardiorespiratory control, and metabolic parameters are affected in female offspring (FO) from dams fed a dyslipidaemic diet during pregnancy and lactation. FO was obtained from dams who received control (CTL) or dyslipidaemic diets during pregnancy and lactation. The effects of a maternal dyslipidaemic diet on BP, cardiorespiratory control, and biochemical parameters were assessed at 30 and 90 days of age. The experimental protocol based on a dyslipidaemic diet intervention was effective in developing maternal dyslipidemia. At 30 days of age, the FO from dyslipidaemic dams displayed disordered respiratory pattern, enhanced ventilatory response to hypercapnia (P < 0.05), and increased serum levels of total cholesterol and triglycerides (P < 0.05) when compared with CTL female offspring. At 90 days of age, FO from dyslipidaemic dams had augmented BP (P < 0.05), exacerbated cardiorespiratory responses to hypercapnia (P < 0.05), enhanced pressor responses to peripheral chemoreflex activation (P < 0.05), impaired baroreflex (P < 0.05), and larger delta variations in arterial pressure after ganglionic blockade (P < 0.05). Furthermore, during oral glucose and insulin tolerance tests, FO from dyslipidaemic dams exhibited altered glucose tolerance and insulin sensitivity (P < 0.05) when compared with FO from CTL dams. Altered breathing linked to enhanced central and peripheral chemosensitivity, impaired baroreflex, and augmented sympathetic tone may be predisposing factors for increased BP and metabolic disorders in female offspring from dyslipidaemic dams.
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PMID:Maternal dyslipidemia during pregnancy and lactation increases blood pressure and disrupts cardiorespiratory and glucose hemostasis in female rat offspring. 3064 94