Decreased glucose transporter 1 gene expression and glucose uptake in fetal brain exposed to ethanol

Acute ethanol exposure in pregnancy alters the insulin-like growth factor axis of fetal and maternal sheep

“…Ethanol may also impair fetal tissue uptake of nutrients from the fetal circulation, for example by decreasing the expression and activity of glucose transporters. Ethanol administration to adult rats rapidly decreases plasma membrane abundance of GLUT1 and GLUT3 in the cerebral cortex (19), and GLUT1 expression and in vivo and in vitro glucose uptake are reduced in brain tissue of ethanol-exposed fetal rats (37,38). These studies suggest that both impaired placental transport of nutrients and impaired fetal tissue uptake of nutrients may contribute to fetal growth restriction caused by acute ethanol exposure.…”

Novel Molecular Targets for the Prevention of Fetal Alcohol Syndrome

“…Results from our laboratory have demonstrated that alcohol induces an altered monosaccharide uptake and increases the levels of the glucose transporter GLUT1 in primary cultures of rat astrocytes [45,46]. The GLUT1 increase after alcohol exposure has also been observed in rat [43] and chick brain [140]. Taking into account the large functional relevance of astrocytes in glucose metabolism and in brain energy availability, even slight alteration in the regulation of glucose uptake and/or transport by glial cells would significantly compromises neuronal function and brain development [141,142].…”

“…Glucose is a crucial source of energy and its availability for neurons is highly regulated by neighbor glial (in particular astrocytes) and endothelial cells. The effect of alcohol on glucose uptake and on glucose transporters (GLUTs) has been widely studied in several cell types, although with disparate results [44,43]. The varying results could be attributable to differences in cell lines used and to the variety of experimental designs such as alcohol treatments (chronic or acute).…”

“…These processes include neurogenesis, gliogenesis, synaptogenesis, myelination, proliferation, migration, differentiation and survival of cells [10][11][12][13][14][15][16][17][18]. In order to target these cell-specific processes, alcohol may engage simultaneous or sequentially different molecular mechanisms such as acetaldehyde formation [19][20][21], oxidative stress [22][23][24][25][26][27], cell-cell interaction and cell-adhesion disassembly [28][29][30], deregulation of neurotransmission systems [15,[31][32][33][34], growth-factor and trophic support alteration [35][36][37][38][39][40], aberrant glycosylation and glucose uptake [41][42][43][44][45][46][47] and the interference with several cellsignalling pathways (Ca 2+ -dependent, cyclic-nucleotide dependent [18,48], and other signaling pathways [49][50][51][52]. The severity of alco...…”

Dynamic and Persistent Effects of Ethanol Exposure on Development: An In Vivo Analysis During and After Embryonic Ethanol Exposure in Caenorhabditis elegans

“…Combining data from our previous report on larval EtOH exposure (Davis et al., ) with the current study on embryonic exposure, we have shown that growth retardation occurs regardless of exposure timing in C. elegans . This is not surprising because growth retardation has been shown in a wide range of animal species including fruit flies, fish, frog, chicken, mice, rat, sheep, monkey, and human (Abel and Dintcheff, ; Blader and Strahle, ; Boyd et al., ; Carver et al., ; Cutler et al., ; Davis et al., ; Jones and Chernoff, ; Nakatsuji, ; Pennington et al., ; Potter et al., ; Ranganathan et al., ; Scott and Fradkin, ; Singh et al., ; Wang et al., ). This supports the hypothesis that EtOH probably acts on highly conserved mechanisms to inhibit body growth.…”