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)

Increased Very Low Density Lipoprotein (VLDL) production is a major feature of diabetic dyslipidemia with consequences on the metabolism of other lipoproteins such as Low Density Lipoproteins (LDL) and High Density Lipoproteins (HDL). More precisely, we observe, in patients with type 2 diabetes, an increased production of VLDL(1) particles that is potentially detrimental by generating atherogenic remnants, small dense LDL particles and triglyceride-rich HDL particles. Several pathophysiological factors are responsible for increased VLDL production, in type 2 diabetes. Among those, insulin resistance plays an important role. Indeed, defective activation of PI3-kinase, secondary to insulin resistance, is associated with a reduction of apoB degradation in the hepatocytes, a rise in MTP expression (by increasing nuclear transcription factors Fox01 and Foxa2) and an increased activity of phospholipase D1 and ARF-1, which are involved in VLDL(1) formation. Moreover, peripheral insulin resistance is responsible for increased lipolysis of adipose tissue leading to augmented portal flux of FFA to the liver and, as a consequence, activation of VLDL production. In addition, increased de novo lipogenesis is observed in type 2 diabetes. This is secondary to increased activation of SREBP-1c (Sterol Regulatory Element-Binding Protein-1c), mainly by Endoplasmic Reticulum stress, and of ChREBP (Carbohydrate Responsive Element Binding Protein), mainly by hyperglycemia. Furthermore, decreased plasma adiponectin observed in type 2 diabetes, may also play a role in increased VLDL production by decreasing liver AMP-kinase activation and by increasing plasma FFA levels as a consequence of reduced muscle FFA oxidation.
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PMID:Abnormal hepatic apolipoprotein B metabolism in type 2 diabetes. 2018 75

Coronary artery disease is common in patients with chronic obstructive pulmonary disease (COPD). Previous studies have shown that patients with COPD have a higher risk of mortality than those without COPD after coronary artery bypass grafting (CABG). However, most of the previous studies were small, single-center studies with limited case numbers (or their only focus was mortality). The aim of our study was to focus on readmission, acute myocardial infarction (AMI), acute respiratory failure (ARF), cerebrovascular accident, and venous thromboembolism rates after CABG in an Asian COPD population.We conducted a nationwide case-control study in Taiwan using the claims database of hospitalization between January 1, 2009 and December 31, 2013. Patients with COPD before CABG were defined as the case groups. Each case was propensity score-matched by age, sex, hypertension, diabetes, dyslipidemia, cardiovascular disease, cerebrovascular disease, and chronic kidney disease, with 2 controls selected from CABG patients without COPD. The outcomes of interest were mortality, wound infection, and the readmission rate over 30 days for the following diseases: AMI, pneumonia, ARF, cerebrovascular accident, and venous thromboembolism.There were 14,858 patients without COPD and 758 patients with COPD who underwent CABG. After propensity score matching, the 30-day mortality and 30-day readmission rates and AMI were higher in the non-COPD group. The incidences of pneumonia and ARF after CABG were higher in the COPD group.Chronic obstructive pulmonary disease does not necessarily lead to mortality, readmission, or AMI after CABG, and the major respiratory complications associated with CABG in patients with COPD were pneumonia and ARF.
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PMID:Postoperative Complications After Coronary Artery Bypass Grafting in Patients With Chronic Obstructive Pulmonary Disease. 2693 39