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)

Cardiovascular diseases are the major causes of morbidity and mortality in people with diabetes. Macroangiopathy in diabetes is manifested by more accelerated and progressive atherosclerosis, which is more widely distributed. The pathogenesis of this accelerated atherosclerosis is multifactorial and includes very complex interactions. Several abnormalities - such as hyperglycemia, dyslipidemia, hypertension, endothelial dysfunction, renin-angiotensin system activation and chronic subclinical inflammation - all appear to play important roles in the development of diabetes-induced atherosclerosis. Treatment of the residual risk, other than glycemia, blood pressure and low-density lipoprotein cholesterol, remains important as the rate of diabetes increases worldwide. A synergistic multifactorial approach against both conventional cardiovascular risk factors and emerging risk factors, such as vasoactive systems, the AGE-RAGE axis, novel proteins, such as TRAIL, and the complement system, as well as oxidative stress and inflammation, may be a promising way to prevent macrovascular disease in diabetes. In this review we focus on the major causes and mechanisms of atherosclerotic disease in patients with diabetes and highlight emerging targets for therapeutic intervention.
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PMID:Linking diabetes and atherosclerosis. 3078 Jul 86

Over consumption of fructose may lead to obesity and dyslipidemia and cause fructosylation-induced alterations in the structure and function of proteins. The aim of this study was to investigate the role of fructosylated-HSA-AGE in the pathogenesis of fatty liver (NAFLD and NASH) by biochemical, immunological and histological studies. Immunogenicity of fructosylated-HSA-AGE was probed by inducing antibodies in rabbits. Fructosylated-HSA-AGE was found to be highly immunogenic. Furthermore, fructosylated-HSA-AGE caused mild fibrosis with steatosis and portal inflammation of hepatocytes in experimental animals. Liver function test and dyslipidemic parameters in immunized animals were also found to be raised. Ultrasonography, which should form part of the assessment of chronically raised transaminases, shows fatty infiltration. Interestingly, alanine aminotransferase (ALT), aspartate aminotransferase (AST), bilirubin, total cholesterol (TC) and triglyceride (TG) profiles confirms USG images of overweight, obese patients. Thus, present study demonstrates that fructosylated-HSA-AGE is hepatotoxic, immunologically active and may cause dyslipidemia.
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PMID:A study on hepatopathic, dyslipidemic and immunogenic properties of fructosylated-HSA-AGE and binding of autoantibodies in sera of obese and overweight patients with fructosylated-HSA-AGE. 3111 79


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