Regulation of Hepatic GLUT8 Expression in Normal and Diabetic Models

Gorovits, Naira; Cui, Lingguang; Busik, Julia V.; Ranalletta, Mollie; deMouzon, Sylvie Hauguel; Charron, Maureen J.

doi:10.1210/en.2002-220968

Cited by 51 publications

(43 citation statements)

References 32 publications

(54 reference statements)

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“…This suggests that both GLUT 8 and GLUT4 expression in WAT is insulin sensitive. This is consistent with the earlier study in rat in which hyperinsulinemia was found to be associated with an increased level of GLUT8 protein in adipocytes (Gorovits et al, 2003). Our study demonstrates that GLUT4 and GLUT8 expression is differentially regulated in adipose tissue in response to insulin and suggests that GLUT8 and GLUT4 concentrations in adipose tissue are intimately linked to glucose homeostasis.…”

Section: Effect Of Insulin On Expression Of Phosphorylated Mapks In Wsupporting

confidence: 93%

Regulation of leptin synthesis during adipogenesis in males of a vespertilionid bat, Scotophilus heathi

Roy

Krishna

2011

Journal of Experimental Biology

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SUMMARYThe aim of this study was to elucidate the hormonal regulation of leptin synthesis by the white adipose tissue (WAT) during the period of fat accumulation in male Scotophilus heathi. An in vivo study showed a significant correlation between the seasonal changes in serum insulin level with the circulating leptin level and with the changes in body fat mass in S. heathi. An in vitro study showed insulin induced a significant increase in expression of leptin protein in WAT. The insulin-stimulated increase in leptin expression was associated with increased uptake of glucose in the WAT. Two glucose transporters (GLUT4 and GLUT8) are utilized for transport of glucose in the WAT during adipogenesis in the bat. The bats showed high insulin and glucose levels, but a reduction in insulin receptor protein during the period of fat deposition, suggesting insulin resistance, which improved in late winter (January) when most of the fat has been utilized as a metabolic fuel. The in vitro study confirmed that insulin enhanced leptin and GLUT4 expression in WAT. The in vitro study further showed that the expression of leptin is directly proportional to the amount of glucose uptake by the WAT. The expression of GLUT4 and GLUT8 were also shown to be differentially regulated by insulin during adipogenesis. The insulin-stimulated increase in leptin synthesis by WAT is mediated through phosphorylation of MAPK in S. heathi. The specific role of GLUT4 and GLUT8 in the regulation of leptin synthesis during adipogenesis needs further investigation.

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Section: Effect Of Insulin On Expression Of Phosphorylated Mapks In Wsupporting

confidence: 93%

Regulation of leptin synthesis during adipogenesis in males of a vespertilionid bat, Scotophilus heathi

Roy

Krishna

2011

Journal of Experimental Biology

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“…GLUT8 gene expression decreased following glucose deprivation or hypoxia in cultured, differentiated 3T3-L1 adipocytes; however, the conditions tested were beyond the physiologic range [137]. GLUT8 expression in liver is restricted to a single layer of hepatocytes surrounding central veins similar to GLUT1 [141]. The highly glycolytic nature of pericentral hepatocytes suggests GLUT8 involvement in substrate shuttling through the glycolytic pathway [141].…”

Section: Glut8mentioning

confidence: 99%

“…GLUT8 expression in liver is restricted to a single layer of hepatocytes surrounding central veins similar to GLUT1 [141]. The highly glycolytic nature of pericentral hepatocytes suggests GLUT8 involvement in substrate shuttling through the glycolytic pathway [141]. The zonation of GLUT8 expression is altered in type 1 and type 2 diabetic mice models further pointing to GLUT8 involvement in hepatocyte adaptation to altered glucose homeostasis [141].…”

Section: Glut8mentioning

confidence: 99%

“…The highly glycolytic nature of pericentral hepatocytes suggests GLUT8 involvement in substrate shuttling through the glycolytic pathway [141]. The zonation of GLUT8 expression is altered in type 1 and type 2 diabetic mice models further pointing to GLUT8 involvement in hepatocyte adaptation to altered glucose homeostasis [141]. The history of GLUT8 has just begun, and exploration of its function and regulation in the multiple sites where it is expressed will be the focus of future research.…”

Section: Glut8mentioning

confidence: 99%

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What we know about facilitative glucose transporters: Lessons from cultured cells, animal models, and human studies

Gorovits

Charron

2003

Biochem Molecular Bio Educ

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Glucose uptake by all cells in the organism by glucose transport proteins is among the most essential processes in life. The process of glucose uptake into tissues is performed by glucose transporters. This review focuses on the biology of facilitative glucose transporters (GLUTs). The knowledge that has accumulated for more than a decade with respect to the regulation of GLUT expression and function in various experimental conditions points to the great potential for GLUTs to be utilized as targets for designing therapies for treatment of diseases related to impaired regulation of glucose homeostasis including type 2 diabetes.Keywords: Glucose uptake, GLUT, insulin action, diabetes.The entry of glucose into cells is a crucial step in lifesupporting processes since glucose is the main monosaccharide in nature that provides carbon and energy for almost all cells. The passage of glucose into cells depends on different parameters, including expression of the appropriate glucose transporters in the target tissues and hormonal regulation of their function. Single cell eucaryotes such as Saccharomyces cerevisiae possess 20 genes encoding glucose or glucose-like transporters and express the glucose transporters most appropriate for the amount of glucose available [1]. In mammalian cells a tight regulation of blood glucose levels is needed to meet the energetic demands of the brain, a tissue that uses glucose as its primary energy source [2,3]. Adequate glucose flux into tissues provides maintenance of glucose homeostasis that is critical in well being. Transport of glucose across the plasma membrane is accomplished by two families of glucose transporters: sodium-glucose co-transporters (SGLT 1 1-3), mainly expressed in the apical membrane of renal and intestinal absorptive epithelial cells that transport glucose against its concentration gradient and utilize ATP (for a review, see Ref. 4), and facilitative glucose transporters (GLUTs) that are expressed in all cells that transport glucose down a concentration gradient [5][6][7]. Until now the search for the mammalian facilitative glucose transporters has yielded 12 carriers including GLUT1-5 and the recently discovered GLUT6 -12. GLUT1-4 share greater than 40% homology [8], and GLUT5, which is a fructose transporter, exhibits 42, 40, 38, and 41.6% identity with GLUT1, GLUT2, GLUT3, and GLUT4, respectively [9]. All GLUTs have been predicted to have 12 membrane-spanning domains (helices) connected by hydrophilic loops, the first of which is exofacial and contains an N-glycosylation site in GLUT1-5 (Fig. 1) [8,10]. Both the amino and carboxyl termini of GLUTs reside on the cytoplasmic side of the cell membrane [11]. The carboxyl termini of all GLUTs have unique amino acid sequences that have been utilized for development of reagents. The common sensitivity of the GLUT family to the inhibitory action of the fungal metabolite cytochalasin B has been reported widely and is utilized in studies of hexose transporters [12]. Substrate selectivity of GLUTs is dictated by conserve...

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“…We have shown that surface SLC2A8 expression is regulated by the insulin/ insulin-like growth factor-1 (IGF1) signaling pathways through the IGF1 receptor in the mouse blastocyst (Carayannopoulos et al 2000, Pinto et al 2002. In different diabetic models, hepatic SLC2A8 has shown altered expression patterns (Gorovits et al 2003). We have also reported that SLC2A9 protein expression was significantly increased in the kidney and liver from STZinduced diabetic mice compared with non-diabetic mice (Keembiyehetty et al 2006).…”

Section: Introductionmentioning

confidence: 99%

Paternal effect on embryo quality in diabetic mice is related to poor sperm quality and associated with decreased glucose transporter expression

Kim

Moley

2008

Reproduction

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The objective of this study was to determine whether sperm quality, fertilization capacity, and subsequent embryo development are altered in diabetic male mice and whether differences in facilitative glucose transporter (GLUT; now known as solute carrier family 2, SLC2A) expression in the testis and sperm exist. Using two type 1 diabetic mouse models, SLC2A expression in the testis and sperm was determined by western immunoblotting and immunofluorescence staining. To address sperm quality and fertilization capacity, computer-assisted sperm analysis and in vitro fertilization were performed. SLC2A1, SLC2A3, and SLC2A5 did not change in expression in the testes or sperm between diabetic and non-diabetic mice. SLC2A8 and SLC2A9b were less expressed in the testes of both diabetic models versus controls. SLC2A9a was not expressed in the Akita testis or sperm when compared with strain-matched controls. 3b-hydroxysteroid dehydrogenase (HSD3B) expression was significantly decreased in the Leydig cells from the diabetic mice. Sperm concentration and motility were significantly lower in both the diabetics when compared with the control. These parameters normalized in Akita diabetic males treated with insulin. In addition, fertilization rates were significantly lower in the Akita group (17.9%) and the streptozotocin (STZ)-injected male group (43.6%) when compared with the normal group (88.8%). Interestingly, of the fertilized zygotes, embryo developmental rates to the blastocyst stage were lower in both diabetic models (7.1% Akita and 50.0% STZ) when compared with controls (71.7%). Male diabetes may cause male subfertility by altering steroidogenesis, sperm motility, and SLC2A expression. This is the first study to link a paternal metabolic abnormality to a sperm effect on cell division and subsequent embryonic development. Reproduction (2008) 136 313-322

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Regulation of Hepatic GLUT8 Expression in Normal and Diabetic Models

Cited by 51 publications

References 32 publications

Regulation of leptin synthesis during adipogenesis in males of a vespertilionid bat, Scotophilus heathi

Regulation of leptin synthesis during adipogenesis in males of a vespertilionid bat, Scotophilus heathi

What we know about facilitative glucose transporters: Lessons from cultured cells, animal models, and human studies

Paternal effect on embryo quality in diabetic mice is related to poor sperm quality and associated with decreased glucose transporter expression

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