Results acquired using global positioning system (GPS) data taken over a large part of SE-Asia, indicate that Sundaland, i.e. Indochina along with the western and central part of Indonesia, constitutes a stable tectonic block moving approximately east with respect to Eurasia at a velocity of 12 þ 3 mm yr 31 . With respect to India and Australia this block moves due south. Significant motion has not been detected along the northern boundary to South China i.e. along the Red River Fault, whereas nearly 50 mm yr 31 of right lateral motion has to be accommodated between India and Sundaland in the Andaman^Burma region. ß
Using three months of GPS satellite‐to‐satellite tracking and accelerometer data of the CHAMP satellite mission, a new long‐wavelength global gravity field model, called EIGEN‐1S, has been prepared in a joint German‐French effort. The solution is derived solely from analysis of satellite orbit perturbations, i.e. independent of oceanic and continental surface gravity data. EIGEN‐1S results in a geoid with an approximation error of about 20 cm in terms of 5 × 5 degree block mean values, which is an improvement of more than a factor of 2 compared to pre‐CHAMP satellite‐only gravity field models. This impressive progress is a result of CHAMP's tailored orbit characteristics and dedicated instrumentation, providing continuous tracking and direct on‐orbit measurements of non‐gravitational satellite accelerations.
Fibroblast growth factor 21 (FGF21), a recently identified member of the FGF superfamily, is mainly secreted from the liver and adipose tissues and plays an important role in improving metabolic syndrome and homeostasis. The aim of this study is to evaluate the role of FGF21 in alcoholic fatty liver disease (AFLD) and to determine if it has a therapeutic effect on AFLD. In this paper, we tested the effect of FGF21 on alcohol-induced liver injury in a murine model of chronic ethanol gavage and alcohol-treated HepG2 cells. Male KM mice received single dose of 5 g/kg ethanol gavage every day for 6 weeks, which induced significant fatty liver and liver injury. The alcohol-induced fatty liver cell model was achieved by adding ethanol into the medium of HepG2 cell cultures at a final concentration of 75 mM for 9 days. Results showed that treatment with recombinant FGF21 ameliorated alcoholic fatty liver and liver injury both in a murine model of chronic ethanol gavage and alcohol-treated HepG2 cells. In addition, FGF21 treatment down-regulated the hepatic expression of fatty acid synthetic key enzyme, activated hepatic AMPK-SIRT1 pathway and significantly down-regulated hepatic oxidative stress protein. Taken together, FGF21 corrects multiple metabolic parameters of AFLD in vitro and in vivo by activation of the AMPK-SIRT1 pathway.
The aim of this study is to evaluate the role of fibroblast growth factor 21 (FGF21) in nonalcoholic fatty liver disease (NAFLD) and seek to determine if its therapeutic effect is through induction of autophagy. In this research, Monosodium L-glutamate (MSG)-induced obese mice or normal lean mice were treated with vehicle, Fenofibrate, and recombinant murine FGF21, respectively. After 5 weeks of treatment, metabolic parameters including body weight, blood glucose and lipid levels, hepatic and fat gene expression levels were monitored and analyzed. Also, fat-loaded HepG2 cells were treated with vehicle or recombinant murine FGF21. The expression levels of proteins associated with autophagy were detected by western blot, real-time PCR, and transmission electron microscopy (TEM). Autophagic flux was monitored by laser confocal microscopy and western blot. Results showed that FGF21 significantly reduced body weight (P < 0.01) and serum triglyceride, improved insulin sensitivity, and reversed hepatic steatosis in the MSG model mice. In addition, FGF21 significantly increased the expression of several proteins related to autophagy both in MSG mice and fat-loaded HepG2 cells, such as microtubule associated protein 1 light chain 3, Bcl-2-interacting myosin-like coiled-coil protein-1 (Beclin-1), and autophagy-related gene 5. Furthermore, the evidence of TEM revealed an increased number of autophagosomes and lysosomes in the model cells treated with FGF21. In vitro experimental results also showed that FGF21 remarkably increased autophagic flux. Taken together, FGF21 corrects multiple metabolic parameters on NAFLD in vitro and in vivo by inducing autophagy.
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