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Articles by Zhen-Shan Zhang
Total Records ( 2 ) for Zhen-Shan Zhang
  Zhen-Shan Zhang , Li-Jun Wang , Dong Li , Shu-Jun Li and Necati Ozkan
  Flaxseed oil is rich in linolenic acid, and being accepted in diet by more and more people. The characteristics of flaxseed oil from two different varieties, namely fibre-flax seed and oil-flax seed, were evaluated. It was shown that fatty acids of flaxseed oil were mainly constituted by linolenic, oleic, linoleic, stearic, and palmitic acids, and the oil-flax seed oil contained more linolenic acid (58.03%) compared with the fibre-flax seed oil (47.37%). The fibre-flax seed oil showed a higher absorbance at 290−800 nm. Thermogravimetric curves showed that the oil-flax seed oil was more stable than the fibre-flax seed oil. Thermal profiles indicated that the fibre-flax seed oil had higher melting peak temperature and larger enthalpy. Rheological studies indicated that the apparent viscosity of the fibre-flax seed oil was higher than that of the oil-flax seed oil. It can be concluded that the oil-flax seed oil is better than the fibre-flax seed oil in terms of edibility.
  Tao Pang , Zhen-Shan Zhang , Min Gu , Bei-Ying Qiu , Li-Fang Yu , Peng-Rong Cao , Wei Shao , Ming-Bo Su , Jing-Ya Li , Fa-Jun Nan and Jia Li
  AMP-activated protein kinase (AMPK) serves as an energy sensor and is considered a promising drug target for treatment of type II diabetes and obesity. A previous report has shown that mammalian AMPK α1 catalytic subunit including autoinhibitory domain was inactive. To test the hypothesis that small molecules can activate AMPK through antagonizing the autoinhibition in α subunits, we screened a chemical library with inactive human α1394 (α1, residues 1-394) and found a novel small-molecule activator, PT1, which dose-dependently activated AMPK α1394, α1335, α2398, and even heterotrimer α1β1γ1. Based on PT1-docked AMPK α1 subunit structure model and different mutations, we found PT1 might interact with Glu-96 and Lys-156 residues near the autoinhibitory domain and directly relieve autoinhibition. Further studies using L6 myotubes showed that the phosphorylation of AMPK and its downstream substrate, acetyl-CoA carboxylase, were dose-dependently and time-dependently increased by PT1 with-out an increase in cellular AMP:ATP ratio. Moreover, in HeLa cells deficient in LKB1, PT1 enhanced AMPK phosphorylation, which can be inhibited by the calcium/calmodulin-dependent protein kinase kinases inhibitor STO-609 and AMPK inhibitor compound C. PT1 also lowered hepatic lipid content in a dose-dependent manner through AMPK activation in HepG2 cells, and this effect was diminished by compound C. Taken together, these data indicate that this small-molecule activator may directly activate AMPK via antagonizing the autoinhibition in vitro and in cells. This compound highlights the effort to discover novel AMPK activators and can be a useful tool for elucidating the mechanism responsible for conformational change and autoinhibitory regulation of AMPK.
 
 
 
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