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SREBP-1Sterol Regulatory Element-Binding Protein-1
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The results showed that adiponectin overexpression significantly (p<0.01) up-regulated the mRNA expression levels of AdipoR2, ACC, FAS, and SREBP-1 (Figure 8), which were 1.85, 4.55, 4.88, and 4.25 times higher, respectively, than those of the control group.
This regulation was supported by the expression of downstream genes controlled by FXR, including SHP-1 as the nuclear receptor induced by FXR and involved in bile acid biosynthesis (19), SREBP-1, which is associated with lipid metabolism and negatively regulated by FXR (20), PPARa, which controls SREBP activity and lipid synthesis (21), CYP7A1, which acts as another important regulator of bile acid metabolism inhibited by both FXR and SHP (19,22), and also PEPCK, which regulates the rate-limiting step of hepatic gluconeogenesis and is activated by FXR (23).
Mason, "KGF induces lipogenic genes through a PI3K and JNK/ SREBP-1 pathway in H292 cells," Journal of Lipid Research, vol.
* Mechanism may be related to accelerating cholesterol and bile acid efflux and suppressing the expression of SREBP-1 in the liver.
Acrp30: Adiponectin; HAART: Highly Active Antiretroviral Therapy; HIV: Human Immunodeficiency Virus; NRTI: Nucleoside Reverse Transcriptase Inhibitor; NNRTI: Non-Nucleoside Reverse Transcriptase Inhibitor; InSTI: Integrase Strand Transfer Inhibitor; PI's: Protease Inhibitors; d4T: Stavudine; EVG: Elvitegravir; RPV: Rilpivirine; NVP: Nevirapine; EFV: Efavirenz; LPV/r: Lopinavir/ ritonavir; PPAR-[gamma]: Peroxisome-Proliferator Activated Receptor gamma; SREBP-1: Sterol Regulatory Element Binding Protein-1; C/ EBP-[alpha]: CCAAT Enhancer Binding Protein alpha; FABP-4: Fatty Acid Binding Protein 4; TNF-[alpha]: Tumor Necrosis Factor alpha.
The low-GI group also had significant decreases in total average area of sebaceous glands, and decreased expression of sterol response element-binding protein-1 (SREBP-1), which stimulates lipogenesis in sebocytes.
Recent studies have shown that elevated levels of serum IGF-I correlate with overproduction of sebum and acne [17] as a result of IGF-I and insulin induced lipogenesis of sebaceous glands, probably by induction of sterol response element-binding protein-1 (SREBP-1) [12].
A low fish oil inhibits SREBP-1 proteolytic cascade, while a high-fish-oil feeding decreases SREBP-1 mRNA in mice liver: relationship to anti-obesity.
Second-hand smoke stimulates lipid accumulation in the liver by modulating AMPK and SREBP-1. J Hepatol.
The researchers also identified the mechanism underlying this effect in the liver, involving the control of the transcription factor SREBP-1 and its downstream targets-regulators of lipid synthesis.
(26) Therefore, the increase in triglycerides caused by ritonavir could be related to the enhancement in the production of hepatic lipoprotein, by inhibiting the proteasome-mediated degradation of Apo B and SREBP-1 in the liver.
If ritonavir impairs proteasome function, SREBP-1 may accumulate in the cell nucleus, which in turn may lead to excessive activity of the genes normally regulated by this protein (Riddle et al.