Explore chapters and articles related to this topic
Role of Ascorbate and Dehydroascorbic Acid in Metabolic Integration of the Cell
Published in Qi Chen, Margreet C.M. Vissers, Vitamin C, 2020
Gábor Bánhegyi, András Szarka, József Mandl
At least six members of the GLUT family (GLUT1-4, -8, -10) have been recognized as DHA transporters [18,46,53,61,68,69]. Half of them have been reported in the internal membranes: GLUT1 in the Golgi apparatus [60] and the mitochondrial inner membrane [42], GLUT8 in the lysosomes [3,26], and GLUT10 in the nuclear envelope [20], in the mitochondrial inner membrane [46], in the Golgi apparatus [46], and in the ER [30,71]. Thus, vitamin C can be transported into many intracellular compartments in the form of DHA, with the mediation of GLUT transporters [8].
diabetic embryopathy in the preimplantation embryo
Published in Moshe Hod, Lois G. Jovanovic, Gian Carlo Di Renzo, Alberto de Leiva, Oded Langer, Textbook of Diabetes and Pregnancy, 2018
Of the different glucose transporters existing in the early embryo, GLUT8 was found to be one of the most important.25 This transporter is regulated by insulin. During early differentiation of the mouse blastocyst, there is a significant increase in glucose demand, and insulin causes GLUT8 to move to the plasma membrane, thus increasing the uptake of glucose, which is then converted to lactic acid. It is presumed that, similar to other glucose transporters, hyperglycemia decreases GLUT8, hence reducing the uptake of glucose by the ICM, inducing cell death.
Microbial and metabolic impacts of trehalose and trehalose analogues
Published in Gut Microbes, 2020
Yiming Zhang, Brian J. DeBosch
We hypothesize that part of the bioavailability-independent effects of trehalose and its analogues are accounted by signaling events via specific interactions with the carbohydrate transporters, 4,5 or via downstream intracellular signaling pathways with which these sugars interact.5,6,13 For example, although both LT and trehalose have comparable GLUT8 inhibitory capacity, trehalose is a more potent inhibitor against other class I GLUTs.12 In addition, trehalose activates TFEB and FGF217,13,46,48,49 through yet-incompletely defined mechanisms. Forthcoming work should directly examine structure-function relationships and specific mechanistic actions for these compounds.
Metformin mitigates impaired testicular lactate transport/utilisation and improves sexual behaviour in streptozotocin-induced diabetic rats
Published in Archives of Physiology and Biochemistry, 2021
Victor Udo Nna, Ainul Bahiyah Abu Bakar, Azlina Ahmad, Mahaneem Mohamed
Sertoli cells glucose uptake is made possible through the action of GLUTs located on their plasma membranes (Angulo et al.1998). Studies have particularly implicated GLUT1 and GLUT3 as the transporters involved in importing glucose into SCs (Galardo et al.2008, Oliveira et al.2012, Joshi et al.2017). Besides GLUTs 1 and 3, GLUT8 isoform has been identified in SCs (Piroli et al.2002). However, studies have suggested that GLUT8 is not localised in SCs plasma membrane, and is therefore not expected to contribute to glucose import from the extracellular environment (Piroli et al.2002, Alves et al.2013a), which is why we concentrated on GLUT1 and GLUT3 in our study. In the present study, although GLUT3 mRNA was down-regulated in the untreated diabetic rat testis, intra-testicular glucose level remained high, and GLUT1 mRNA seemed unaffected in our T1DM model. Our findings suggest that SCs have an adaptive response to insulin deficiency (a characteristic feature of T1DM) which ensures that intra-testicular glucose level remains adequate for lactate production. This hypothesis is supported by the increased intra-testicular LDH activity and increased lactate level in the present study. On the other hand, it may not be entirely correct to assume that the glucose, lactate, and LDH activity seen in DC group came from the SCs alone, as other cell types in the testis also contain glucose, lactate, and LDH. Nevertheless, with the central role of SCs as nurse cells, most of the glucose, lactate, and LDH seen in the present study may have come from this cell type. A previous in vitro experiment using human SCs cultured under insulin-deprived state (mimicking T1DM) had reported decreased GLUT3 but increased GLUT1 mRNA transcript levels and decreased lactate production despite having normal glucose consumption with control cells (Oliveira et al.2012). This shows that in conditions of insulin deprivation as is the case in T1DM, lactate utilisation may be impaired.