Transport glukózy
Transport glukózy do buněk
- “glucose transporters”, the membrane-associated carrier proteins
- Increased uptake of glucose to cells
- Malignant cells [1]
- Human breast cancer cells [1]
Estrogens
- Stimulate glucose transport in various target organs [1]
- Altering the expression of genes encoding proteins and enzymes involved in glucose metabolism [1]
- E2 plays an important role in the maintenance of normal insulin sensitivity
- E2 stimulated GLUT-1 expression in breast cancer cells [1]
- This effect was inhibited by tamoxifen [1]
- Nízkoglykemizující strava jako například metabolic balance má hluboký smysl pro ženy po karcinomu prsu !!!
- E2 and epidermal growth factor
- Increased protein levels of GLUT12 intracellularly and at the cell surface, in cultured breast cancer cells [1]
- E2 treatment induced
Progesteron
- Progesterone (P) alone seems to be followed by insulin resistance [1]
Na+-coupled glucose transporters (SGLT)
- SGLT1, SGLT2 = sugar transporters
- SGLT3 = glucose sensor [1]
SGLT1
- Mutation
- Related to the glucose-galactose malabsorption syndrome [1]
Glucose transporter facilitators (GLUT)
- GLUT-1 - GLUT-14 [1]
- Eleven are involved in sugar transport
- Individual isoforms of glucose transporters
- Different substrate specificity
- Kinetic characteristics
- Expression profiles
- Tissue-specific adaptation
GLUT-1
- Glucose transporter 1 deficiency syndrome
- Over-expression of GLUT-1 in breast cancer biopsies positive correlation with:
- Tumor grade
- Extent of proliferation
- Invasiveness [1]
GLUT-2
- Appear to be responsible for glucose sensing in:
- Pancreatic beta-cells
- Neuronal
- Other cells
- Mutacemi
- Fanconi-Bickel syndrome [1]
- Glut-2 also regulated by PPAR-gamma in the liver
- PPAR-gamma bound to the -197-184 region of the promoter of GLUT-2 [1]
- Rosiglitazone enhanced the GLUT-2 mRNA level in the primary cultured hepatocytes [1]
- Contributing to glucose transport into liver in a condition when PAPR-? expression is increased
- Type-2 diabetes
- Severe obesity [1]
- Hindbrain of obese rats
- Decreased expression of GLUT-2 mRNA
- Increased expression of glucokinase [1]
GLUT-4
- Regulated by their subcellular distribution
- Malfunction, x expression, x regulation of GLUT-4
- insulin resistance syndrome [1]
- Decreased expression of GLUT-4
- Early in the development of feline obesity [1]
- ER-alfa is a positive regulator of GLUT-4 expression
- ER-beta has a suppressive role [1]
- ER-alfa i beta necessary for optimal caveolin-1 expression
- Co-localization of caveolin-1 and GLUT-4 not an absolute requirement
- Reduction in GLUT-4 contribute to the insulin resistance in alfa-ERKO mice [1]
- Adipocytes with BPA
GLUT-8
- Regulated by their subcellular distribution
Literatura:
[1] Regulation of Energy Metabolism Pathways by Estrogens and Estrogenic Chemicals and Potential Implications in Obesity Associated with Increased Exposure to Endocrine Disruptors. URL < www.ncbi.nlm.nih.gov/pmc/articles/PMC2747085/?tool=pmcentrez >.
