Effects of dehydroepiandrosterone on rat apolipoprotein AI gene expression in the human hepatoma cell line, HepG2

Deleon, Mary Jeanne; Horani, Mohamad Hosam; Haas, Michael J.; Wong, Norman C.W.; Mooradian, Arshag D.

doi:10.1053/meta.2002.30524

Cited by 10 publications

(2 citation statements)

References 22 publications

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“…Glucorticoids, thyroxin and sex steroids have significant effects on the apo A-I promoter. Estradiol and phytoestrogens increase HDL and in some cases increase hepatic apo A-I production, while high levels of dehydroepiandrosterone (DHEA) and testosterone suppress it [96,97].…”

Section: Apo A-i Gene Expressionmentioning

confidence: 99%

Regulation of high‐density lipoprotein by inflammatory cytokines: establishing links between immune dysfunction and cardiovascular disease

Haas

Mooradian

2010

Diabetes Metabolism Res

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Coronary artery disease is a primary co-morbidity in metabolic diseases such as metabolic syndrome, diabetes and obesity. One contributing risk factor for coronary artery disease is low high-density lipoprotein-cholesterol (HDLc). Several factors influence steady-state HDLc levels, including diet, genetics and environment. Perhaps more important to coronary artery disease is factors that attribute to the dynamics of reverse cholesterol transport, storage, and excretion of excess cholesterol. HDLc biogenesis, clearance and innate ability to serve as a cholesterol acceptor and transporter all contribute to HDLc's function as a negative regulator of cardiovascular disease. With the recent failure of torcetrapid, focus is being placed on HDLc biology and its role in various metabolic diseases. Low HDLc levels are often associated with an increased state of background inflammation. Recently, several syndromes with clear pro-inflammatory components have been shown to be inversely correlated with low HDLc levels in the absence of obesity, diabetes and metabolic syndrome. Early studies with HDLc during the acute-phase response suggest that HDLc is substantially physically modified during acute infection and sepsis, and recent studies show that HDLc is physically modified by chronic pro-inflammatory disease. In this review, several of these connections are described and cytokine signalling related to HDLc is examined.

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Section: Apo A-i Gene Expressionmentioning

confidence: 99%

Regulation of high‐density lipoprotein by inflammatory cytokines: establishing links between immune dysfunction and cardiovascular disease

Haas

Mooradian

2010

Diabetes Metabolism Res

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“…Some studies have reported small, nonsignificant decreases in low-density lipoprotein cholesterol (LDL-C) 30,42 and high-density lipoprotein cholesterol (HDL-C). 42 However, other studies have reported that DHEA significantly lowers HDL-C. 30,31,44,45 Likewise, some trials found nonsignificant changes in serum LDL-C, apolipoprotein A1, and triglyceride concentrations, while others reported statistically significant decreases. [30][31][32]45 Results reported on the effects of prasterone on complement levels have also varied.…”

Section: Adverse Effects and Toxicitiesmentioning

confidence: 99%