Normal fizyolojik kosullar altinda, glikoz homeostazisi periferik dokularda (iskelet, kalp kasi, adipoz (GLUT 4) ve karacigerde (
GLUT2) ve hepatik glikoz uretiminin inhibisyonunda insulin aracili glikoz alimi ile siki bir sekilde duzenlenir (5).
Regulation of
GLUT2 glucose transporter expression in liver by thyroid hormone, evidence for hormonal regulation of hepatic glucose transport system.
Chen et al., "Inhibition of the intestinal glucose transporter
GLUT2 by flavonoids," FASEB Journal, vol.
Besides, we also observed that the liver
Glut2 mRNA expression was reduced in KD and KD + AE groups, which suggested improved glycemic control in diabetic mice (Figure 6(l)).
Primers used for PCR amplification were ACTB forward GATATCGCTGCGCTCGTC, reverse TCCATATCGTCCCA GTTGG; SOX2 forward TGATGGAGACGGAGCTGAAG, reverse GCTTGCTGATCTCCGAGTTG; NANOG forward GATTTGTGGGCCTGAAGAAAACT, reverse AGGAGA GACAGTCTCCGTGTGAG; ANAPC2 forward CCAGTA CAGGCGGTGATCTT, reverse GCTCTCGTCGTCACTGTC AA; ABL-1 forward AACACCCTAACCTGGTGCAG, reverse CAAGTGGTTCTCCCCTACCA; CDC2 forward GGGGTC AGCTCGTTACTCAA, reverse GATGCTAGGCTTCCTGG TTTC; CDK4 forward CTGACCGGGAGATCAAGGTA, reverse AGCCAGCTTGACTGTTCCAC; CDK6 forward TC CCAGGAGAAGAAGACTGG, reverse GGTCCTGGAAGT ATGGGTGA; INS forward GGGGAACGAGGCTTCTTC TA, reverse AGTTGCAGTAGTTCTCCAGC; PDX1 forward AAGTCTACCAAAGCTCACGC, reverse GTTCAACATGA CAGCCAGCT; and
GLUT2 forward TTGGGCTGAGGAA GAGACTG, reverse AACCCCATCAAGAGAGCTCC.
It is known though that HNF4A regulates expression of genes involved in glucose transport (
GLUT2), glycolysis (aldolase B, liver pyruvate kinase), and lipid metabolism (Apo AII, apoB, and apoCIII) [8].
Sener, "Comparison of GLUT1,
GLUT2, GLUT4 and SGLT1 mRNA expression in the salivary glands and six other organs of control, streptozotocin-induced and Goto-Kakizaki diabetic rats," Cellular Physiology and Biochemistry, vol.
About TSH, there is only one report that shows that TSH can stimulate
GLUT2 gene transcription by activating the p38 MAPK signal pathway [35].
We also analyzed expression levels of the insulin receptor (Insr) and
Glut2 (Slc2a2) genes since Ding et al.
Glucose-stimulated upregulation of
GLUT2 gene is mediated by sterol response element-binding protein-1c in the hepatocytes.
recently showed that genetic deletion of mPGES-2 remarkably enhances liver injury in streptozotocin-treated mice via induction of
GLUT2. (45) The possibility of tissue-specific or particular pathological roles of mPGES-2 has not yet been ruled out.