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)

High fructose consumption is associated with the development of fatty liver and dyslipidemia with poorly understood mechanisms. We used a matrix-assisted laser desorption/ionization-based proteomics approach to define the molecular events that link high fructose consumption to fatty liver in hamsters. Hamsters fed high-fructose diet for 8 weeks, as opposed to regular-chow-fed controls, developed hyperinsulinemia and hyperlipidemia. High-fructose-fed hamsters exhibited fat accumulation in liver. Hamsters were killed, and liver tissues were subjected to matrix-assisted laser desorption/ionization-based proteomics. This approach identified a number of proteins whose expression levels were altered by >2-fold in response to high fructose feeding. These proteins fall into 5 different categories including (1) functions in fatty acid metabolism such as fatty acid binding protein and carbamoyl-phosphate synthase; (2) proteins in cholesterol and triglyceride metabolism such as apolipoprotein A-1 and protein disulfide isomerase; (3) molecular chaperones such as GroEL, peroxiredoxin 2, and heat shock protein 70, whose functions are important for protein folding and antioxidation; (4) enzymes in fructose catabolism such as fructose-1,6-bisphosphatase and glycerol kinase; and (5) proteins with housekeeping functions such as albumin. These data provide insight into the molecular basis linking fructose-induced metabolic shift to the development of metabolic syndrome characterized by hepatic steatosis and dyslipidemia.
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PMID:Proteomic analysis of fructose-induced fatty liver in hamsters. 1864 Mar 90

Carbamoyl-phosphate synthase 1 gene (CPS1) rs1047891 single nucleotide polymorphism (SNP) has been associated with a number of metabolic disorders including obesity, insulin resistance, and hyperhomocysteine (HCY). Studies on association between this SNP and prevalence of dyslipidemia have been few, with no report from Chinese subjects. This study was to investigate association of rs1047891 SNP and several environment factors with serum lipid levels in Chinese Han and Maonan populations. Genotypes of rs1047891 SNP in 810 individuals of Maonan and 795 participants of Han nationality were determined by polymerase chain reaction-restriction fragment length polymorphism and then confirmed by direct sequencing. Frequencies of CC, CA, and AA genotypes were 71.32%, 25.16%, and 3.52% in Han and 61.36%, 31.85%, and 6.79% in Maonan populations (P < 0.01), respectively. The frequency of A allele was 16.10% in Han and 22.72% in Maonan individuals (P < 0.001), respectively. Subjects with CA/AA genotypes had lower high-density lipoprotein cholesterol (HDL-C) and apolipoprotein (Apo) A1 levels in Han. They had higher low-density lipoprotein cholesterol (LDL-C) levels and lower HDL-C levels in Maonan than subjects with CC genotype (P < 0.05-0.01). Subgroup analyses revealed that subjects with CA/AA genotypes had lower HDL-C and ApoA1 levels in Han females, higher LDL-C levels in Maonan males, and lower HDL-C levels in both Maonan males and females than subjects with CC genotype (P < 0.05-0.01). Serum lipid parameters were also correlated with several environmental factors in both ethnic groups. The difference in serum lipid profiles between Han and Maonan populations may partly result from different polymorphisms of CPS1 rs1047891 and SNP-enviromental interactions.
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PMID:Association of CPS1 rs1047891 SNP and serum lipid levels in two Chinese ethnic groups. 3193 13