As described above, glucose uptake

As described above, glucose uptake is mainly dependent on GLUT4 which translocates extracelluar glucose through the cell membrane into the cell [32]. It has been observed that disruption of GLUT4 expression in adipose tissue or muscles results in global insulin resistance [33]. GLUT4 heterozygous Knockout mice developed muscle insulin resistance and diabetes [34] whereas transgenic over-expression of GLUT4 improved glucose utilization rate in-vivo [35]. The expression of GLUT4 has been well reported to be altered under various physiological and pathological states.Thus, GLUT4 is considered to be an important therapeutic target for the treatment of T2DM. The GLUT4 gene promoter is governed by two domains namely the myocyte enhancer factor-2 (MEF2)binding domain and Domain I. When MEF2 binds to the MEF2 binding domain and GLUT4 enhancer factor (GEF) binds to Domain I,transcriptional activity is the most advanced [36–38]. In supportof this, reduced MEF2 expression correlates with reduced GLUT4 expression [39]. Class II HDACs particularly, HDAC 4 and 5 repress transcriptional activity of MEF2 and regulate GLUT4 expression by the virtue of their deacetylase activity which makes the chromatin structure compact such that the transcriptional complex does not have access to DNA [40–42]. Studies also report that over expression of HDAC5 decreases GLUT4 expression in cardiac tissue. Phosphorylation of HDAC5 on serine 259 and 498 by AMPK results in its dissociation from MEF2 domain [43,44].

Kết quả (Việt) 1:

As described above, glucose uptake is mainly dependent on that translocates GLUT4 glucose extracelluar through the cell membrane into the cell [32]. It has been observed that disruption of GLUT4 expression in tissue fat or muscle results in the global insulin resistance [33]. GLUT4 tiger dam muscular mice developed insulin resistance and diabetes [34] while the transgenic expression of GLUT4 on improving road user rate in-vivo [35]. the expression of GLUT4 have also been reported to be changed according to the physiological state and various diseases. Therefore, GLUT4 is considered an important goal of therapy for the treatment of T2DM . GLUT4 gene promoter is managed by two particular domains myocyte enhancer factor-2 (MEF2) binding domain and domain name me. When linked MEF2 binding domain MEF2, and GLUT4 enhancer factor (GEF ) associated with transcriptional activity my domain name is the most advanced [36-38]. In this supportof, reducing MEF2 expression correlates reduced GLUT4 expression [39]. Class II HDACs in particular, HDAC 4 and 5 repress transcriptional activity of MEF2 and GLUT4 expression by adjusting their virtue deacetylase activity that makes compact chromatin structure such that transcriptional complex has no access to DNA [40-42]. the study also reported that over expression of GLUT4 expression in HDAC5 reduce heart tissue. phosphorylation of serine 259 and 498 HDAC5 in AMPK results of its dissociation from MEF2 domain [43,44].

Kết quả (Việt) 2:

As described above, glucose uptake is mainly dependent on that translocates GLUT4 glucose across the cell membrane extracelluar into cells [32]. It has been observed that disruption of GLUT4 expression in tissues or muscular fat results in the global insulin resistance [33]. GLUT4 knockout mice developed allergic muscle insulin resistance and diabetes [34] while the transgenic expression of GLUT4 through improved efficiency in vivo glucose [35]. the expression of GLUT4 was reported also to be changed in many physiological and pathological states.Thus, GLUT4 is considered an important therapeutic target for the treatment of T2DM. the GLUT4 gene promoter is dominated by two specific areas is enhanced myocyte factor-2 (MEF2) binding domain and domain I. When linked MEF2 binding domain of MEF2 and GLUT4 enhancer factor (GEF) associated with the domain name first, work is the most dynamic advanced transcription [36-38]. In this supportof, reducing MEF2 expression correlated with reduced GLUT4 expression [39]. Class II HDACs in particular, HDAC 4 and 5 apply MEF2 transcriptional activity and GLUT4 expression adjusted by virtue of their deacetylase activity that makes the chromosome structure compact complex such that transcription does not have access to the DNA [40-42]. the study also reported that the expression of GLUT4 expression in HDAC5 reduce heart tissue. phosphorylation on serine 259 and 498 HDAC5 by AMPK results in its dissociation from MEF2 domain [43,44].