ABSTRACT
Insulin resistance is the pathophysiological basis of many diseases. Overcoming early insulin resistance highly significant in prevention diabetes, non-alcoholic fatty liver, and atherosclerosis. The present study aimed at evaluating the therapeutic effects of baicalin on insulin resistance and skeletal muscle ectopic fat storage in high fat diet-induced mice, and exploring the potential molecular mechanisms. Insulin resistance in mice was induced with a high fat diet for 16 weeks. Animals were then treated with three different doses of baicalin (100, 200, and 400 mg·kg(-1)·d(-1)) for 14 weeks. Fasting blood glucose, fasting serum insulin, glucose tolerance test (GTT), insulin tolerance test (ITT), and skeletal muscle lipid deposition were measured. Additionally, the AMP-activated protein kinase/acetyl-CoA carboxylase and protein kinase B/Glycogen synthase kinase 3 beta pathways in skeletal muscle were further evaluated. Baicalin significantly reduced the levels of fasting blood glucose and fasting serum insulin and attenuated high fat diet induced glucose tolerance and insulin tolerance. Moreover, insulin resistance was significantly reversed. Pathological analysis revealed baicalin dose-dependently decreased the degree of the ectopic fat storage in skeletal muscle. The properties of baicalin were mediated, at least in part, by inhibition of the AMPK/ACC pathway, a key regulator of de novo lipogenesis and activation of the Akt/GSK-3ß pathway, a key regulator of Glycogen synthesis. These data suggest that baicalin, at dose up to 400 mg·kg(-1)·d(-1), is safe and able to attenuate insulin resistance and skeletal muscle ectopic fat storage, through modulating the skeletal muscle AMPK/ACC pathway and Akt/GSK-3ß pathway.
Subject(s)
Adipose Tissue/metabolism , Diet, High-Fat , Flavonoids/pharmacology , Glycogen Synthase Kinase 3 beta/physiology , Insulin Resistance , Muscle, Skeletal/metabolism , Proto-Oncogene Proteins c-akt/physiology , Signal Transduction/physiology , AMP-Activated Protein Kinases/metabolism , Acetyl-CoA Carboxylase/metabolism , Animals , Male , Mice , Mice, Inbred C57BLABSTRACT
BACKGROUND/AIMS: Obesity-associated fatty liver disease affects millions of individuals. This study aimed to evaluate the therapeutic effects of baicalin to treat obesity and fatty liver in high fat diet-induced obese mice, and to study the potential molecular mechanisms. METHODS: High fat diet-induced obese animals were treated with different doses of baicalin (100, 200 and 400 mg/kg/d). Whole body, fat pad and liver were weighed. Hyperlipidemia, liver steatosis, liver function, and hepatic Ca(2+)/CaM-dependent protein kinase kinase ß (CaMKKß) / AMP-activated protein kinase (AMPK) / acetyl-CoA carboxylase (ACC) were further evaluated. RESULTS: Baicalin significantly decreased liver, epididymal fat and body weights in high fat diet-fed mice, which were associated with decreased serum levels of triglycerides, total cholesterol, LDL, alanine transaminase and aspartate transaminase, but increased serum HDL level. Pathological analysis revealed baicalin dose-dependently decreased the degree of hepatic steatosis, with predominantly diminished macrovesicular steatosis at lower dose but both macrovesicular and microvesicular steatoses at higher dose of baicalin. Baicalin dose-dependently inhibited hepatic CaMKKß/AMPK/ACC pathway. CONCLUSION: These data suggest that baicalin up to 400 mg/kg/d is safe and able to decrease the degree of obesity and fatty liver diseases. Hepatic CaMKKß/AMPK/ACC pathway may mediate the therapeutic effects of baicalin in high fat diet animal model.
Subject(s)
AMP-Activated Protein Kinases/metabolism , Acetyl-CoA Carboxylase/metabolism , Calcium-Calmodulin-Dependent Protein Kinase Kinase/metabolism , Diet, High-Fat/adverse effects , Fatty Liver/drug therapy , Flavonoids/pharmacology , Obesity/drug therapy , Adipose Tissue/drug effects , Adipose Tissue/metabolism , Alanine Transaminase/blood , Animals , Aspartate Aminotransferases/blood , Body Weight/drug effects , Fatty Liver/blood , Fatty Liver/metabolism , Male , Mice , Mice, Inbred C57BL , Mice, Obese , Obesity/blood , Obesity/metabolism , Signal Transduction/drug effects , Triglycerides/bloodSubject(s)
DNA Fingerprinting , Ethnicity/genetics , Genetics, Population , Microsatellite Repeats , China , Gene Frequency , Humans , Male , Polymerase Chain ReactionABSTRACT
The 20% concentration Eu3+-based red-emitting phosphor, nano-sized La6MoO12:Eu3+ was prepared by the Pechini method. X-ray diffraction (XRD), thermogravimetric and differential thermal analysis (TG-DTA), scanning electron microscopy (SEM), photoluminescence (PL), and decay curves were used to characterize the resulting samples. The phosphor can be efficiently excited by near UV light and exhibits an intense red luminescence corresponding to the electric dipole transition 5D0 --> 7F2 at 615 nm. When the phosphor was mixed into poly(vinyl alcohol) aqueous solution, the fluorescent nanofibers could be prepared by electrospinning process. It was suggested that the La6MoO12:Eu3+ phosphor would be a promising red component for solid-state lighting devices based on InGaN or GaN light-emitting diodes.
ABSTRACT
Allele and haplotype frequencies for the 12 Y-specific short tandem repeats (STR) loci DYS19, DYS385a/b, DYS389I/II, DYS390, DYS391, DYS392, DYS393, DYS437, DYS438, DYS439 (PowerPlex Y System STR Amplification Kit, Promega) were determined in a population sample of 187 unrelated China Han in northeast China.
