“Dehydroabietic acid (DAA) is a food-derived terpenoid wit


“Dehydroabietic acid (DAA) is a food-derived terpenoid with various bioactivities. Our previous study has revealed that DAA activates peroxisome proliferator-activated receptor-gamma (PPAR gamma) in luciferase assay SCH727965 mouse and suppresses chronic inflammation in obese adipose tissues. In this study, we examined the effects of DAA on adipocyte differentiation. DAA treatment stimulated the adipocyte differentiation of 3T3-L1 preadipocytes. The DAA treatment increased

the mRNA expression levels of adipocyte differentiation marker genes such as aP2 lipoprotein lipase (LPL), and PPAR gamma. In particular, the expression level of adiponectin, which is an adipocytokine with stimulatory effects on insulin sensitivity, was increased at both the mRNA and protein levels by the DAA treatment. Moreover, the DAA treatment stimulated insulin-dependent glucose uptake into differentiated 3T3-L1 adipocytes. These findings indicate that DAA stimulates adipocyte differentiation and insulin sensitivity in 3T3-L1 cells, suggesting that DAA is a valuable food-derived compound for the management of metabolic syndrome.”
“BACKGROUND: Apolipoprotein E (APOE) and APOA5 play an important role in lipid transport and metabolism.

GW3965 Polymorphisms in APOE and APOA5 have been reported to be associated with baseline lipid levels and lipid responses to statins in different populations.

OBJECTIVE: This study evaluated associations of APOE and APOA5 genotype with baseline lipid levels and response to rosuvastatin in Chinese patients with hyperlipidemia.

METHODS: A total of 386 patients with hyperlipidemia, including 166 with familial hypercholesterolemia (FH), with good adherence to rosuvastatin 10 mg daily, were genotyped for the APOE e2/e3/e4 and APOA5 – 1131T>C polymorphisms. The lipid profile was examined before and after at least 4 weeks of therapy.

RESULTS: In patients

without FH, there was a trend that e2 carriers had lower and those e4 carriers had higher low-density lipoprotein cholesterol (LDL-C) levels than subjects with the e3/e3 genotype (P>.05). However, an opposite significant association between APOE polymorphisms and LDL-C levels was observed in patients with FH (P=.005). The APOA5 – 1131C variant allele was associated with increased baseline triglycerides levels in both patients Caspase inhibitor with and without FH (P < .005 or both). Neither APOE nor APOA5 polymorphisms showed a significant effect on the lipid responses to rosuvastatin.

CONCLUSIONS: This study demonstrates different associations of APOE polymorphisms with baseline LDL-C concentrations in Chinese patients with or without FH and confirms the strong relation between the APOA5 polymorphism and baseline triglyceride levels. These findings expand our knowledge on the genetic determinants of lipids and lipid response to rosuvastatin in Chinese patients with hyperlipidemia. (C) 2012 National Lipid Association. All rights reserved.

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