Expression of glucose transporter isoforms and the insulin receptor during hamster preimplantation embryo development

Tonack, Sarah; Ramin, Nicole; Garimella, Sireesha; Rao, Rajnish P.; Seshagiri, Polani B.; Fischer, Bernd; Santos, Anne Navarrete

doi:10.1016/j.aanat.2009.06.002

Cited by 3 publications

(2 citation statements)

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“…Mammalian embryo has unique metabolic needs that must be met to ensure successful pregnancy and healthy offspring. The family of facilitative glucose transporters (GLUTs) plays a major role in providing metabolic substrates to fetal tissues [44]. Alterations in glucose transport and metabolism at the early stages of development can impact fetal development.…”

Section: Glut2 Is Involved In Metabolic Glucose Sensing By Mediatingmentioning

confidence: 99%

Prenatal Effects of Different Intra-Uterine Milieus on Fetal Glucose Sensing Mechanisms during Gestation in Rats

Kamel¹

2012

J Diabetes Metab

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The intra-uterine milieu programs the health of an individual throughout life. This effect has been called fetal origin of adult disease. The altered maternal metabolism is associated with a diabetogenic effect in the adult offspring. The pancreatic glucose-stimulated insulin secretion (GSIS) and peripheral response to insulin are central in glucose homeostasis in fetal circulation and the modulation of these processes during the fetal development may have a serious complications long-lasting. This study was aimed to delineate the prenatal (at gestational day 17) effects of different maternal health challenges on the fetal glucose sensing mechanisms including GLUT2, glucokinase, mitochondrial transcription factor A (mTFA), uncoupling protein 2 (UCP2), phospho-insulin receptor (Phosho-IR) and glucose transporter 4 (GLUT4). We used hyperglycemic, obese and malnourished beside normal female rats to establish pregnancy that was terminated at GD 17. The fetal pancreas, liver, muscle and adipose tissues were obtained for determination of the studied parameters. The results indicated up-regulation of GLUT2, glucokinase, mtTFA and UCP2 expression in fetal pancreas and liver of hyperglycemic mothers fetuses while maternal obesity mildly up-regulate expression of GLUT2, glucokinase and UCP2 in fetal pancreas, liver and adipose tissues, while malnutrition causes down-regulation of UCP2 in pancreas, it up-regulates GLUT2 and glucokinase in liver. In muscle and adipose tissues the level of phosho-IR was increased under maternal hyperglycemia and malnutrition while GLUT4 level increased under maternal diabetes only.We can conclude that the fetal adverse environments can prenatally affect the expression of genes that linked to the development of type 2 diabetes including genes controlling glucose sensing and metabolism.

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Section: Glut2 Is Involved In Metabolic Glucose Sensing By Mediatingmentioning

confidence: 99%

Prenatal Effects of Different Intra-Uterine Milieus on Fetal Glucose Sensing Mechanisms during Gestation in Rats

Kamel¹

2012

J Diabetes Metab

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“…Both GLUT4 (SLC2A4) and GLUT8 (SLC2A8) were found in bovine and rabbit blastocysts (Navarrete Santos et al 2000, 2004b, Augustin et al 2001. GLUT4 was also detected in rat blastocysts (Korgun et al 2001) and GLUT8 was identified in mouse and hamster blastocysts (Carayannopoulos et al 2000, Pinto et al 2002, Tonack et al 2009. A controversy exists on the expression of GLUT4 in mouse blastocysts (Tonack et al 2004vs Hogan et al 1991, Aghayan et al 1992.…”

Section: Introductionmentioning

confidence: 99%

Adiponectin stimulates glucose uptake in mouse blastocysts and embryonic carcinoma cells

et al. 2020

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Preimplantation embryos are sensitive to maternal hormones affecting embryonic signal transduction and metabolic functions. We examined whether adiponectin, the most abundantly secreted adipokine, can influence glucose transport in mouse embryonic cells. In mouse blastocysts full-length adiponectin stimulated glucose uptake, while no effect of globular adiponectin was found. Full-length adiponectin stimulated translocation of GLUT8 glucose transporter to the cell membrane; we did not detect significant changes in the intracellular localization of GLUT4 glucose transporter in adiponectin-treated blastocysts. To study adiponectin signaling in detail, we used embryoid bodies formed from mouse embryonic carcinoma cell (ECC) line P19. We confirmed the expression of adiponectin receptors in these cells. Similar to mouse blastocysts, full-length adiponectin, but not globular adiponectin, stimulated glucose uptake in ECC P19 embryoid bodies. Moreover, full-length adiponectin stimulated AMPK and p38 MAPK phosphorylation. These results indicate that besides AMPK, p38 MAPK is a potential target of adiponectin in mouse embryonic cells. AMPK inhibitor did not influence the adiponectin-stimulated p38 MAPK phosphorylation, indicating independent action of these two signaling pathways. In mouse embryos adiponectin acts as a hormonal regulator of glucose uptake, which becomes especially important in phases with reduced levels of circulating insulin. Our results suggest that adiponectin maintains the glucose supply for early embryos under hypoinsulinaemic conditions, for example, in mothers suffering from type 1 diabetes mellitus.

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Diabetes in Pregnancy

Dornhorst

2010

Textbook of Diabetes

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Expression of glucose transporter isoforms and the insulin receptor during hamster preimplantation embryo development

Cited by 3 publications

References 57 publications

Prenatal Effects of Different Intra-Uterine Milieus on Fetal Glucose Sensing Mechanisms during Gestation in Rats

Prenatal Effects of Different Intra-Uterine Milieus on Fetal Glucose Sensing Mechanisms during Gestation in Rats

Adiponectin stimulates glucose uptake in mouse blastocysts and embryonic carcinoma cells

Diabetes in Pregnancy

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