Glucose Transport and Glucose Transporters in Muscle and Their Metabolic Regulation

Klip, Amira; Paquet, Marie‐Eve

doi:10.2337/diacare.13.3.228

Cited by 324 publications

(176 citation statements)

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“…In mammals, GLUT1 is the other major GLUT isoform expressed in skeletal muscle, together with GLUT4 (25). The levels of GLUT1 mRNA increased modestly during the in vitro differentiation of trout muscle cells, in contrast to what is known in mammals (2,18,41,48).…”

Section: Discussionmentioning

confidence: 67%

Expression of rainbow trout glucose transporters GLUT1 and GLUT4 during in vitro muscle cell differentiation and regulation by insulin and IGF-I

Dı́az

Vraskou²,

Gutiérrez³

et al. 2009

American Journal of Physiology-Regulatory, Integrative and Comp

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Section: Discussionmentioning

confidence: 67%

Expression of rainbow trout glucose transporters GLUT1 and GLUT4 during in vitro muscle cell differentiation and regulation by insulin and IGF-I

Dı́az

Vraskou²,

Gutiérrez³

et al. 2009

American Journal of Physiology-Regulatory, Integrative and Comp

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“…However, another possibility is that ap3bl INM is mediated by the actin-myosin system. The previously reported inhibition of INM by cytochalasin B (2, 14) does not constitute conclusive evidence for a role of actin microfilaments in INM because cytochalasin B not only interferes with actin microfilament function but also directly inhibits glucose uptake into cells (15).…”

Section: And Refs Therein)mentioning

confidence: 91%

Myosin II is required for interkinetic nuclear migration of neural progenitors

Schenk

Wilsch‐Bräuninger

Calegari

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

146

151

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Interkinetic nuclear migration (INM) is a hallmark of the polarized stem and progenitor cells in the ventricular zone (VZ) of the developing vertebrate CNS. INM is responsible for the pseudostratification of the VZ, a crucial aspect of brain evolution. The nuclear migration toward the apical centrosomes in G2 is thought to be a dyneinmicrotubule-based process. By contrast, the cytoskeletal machinery involved in the basally directed nuclear translocation away from the centrosome in G1 has been enigmatic. Studying the latter aspect of INM requires manipulation of the cytoskeleton without impairing mitosis and cytokinesis. To this end, we have established a culture system of mouse embryonic telencephalon that reproduces cortical development, and have applied it to explore a role of actomyosin in INM. Using the nonmuscle myosin II inhibitor blebbistatin at a low concentration at which neither cell cycle progression nor cytokinesis is impaired, we show that myosin II is required for the apical-to-basal (ap3bl), ab-centrosomal INM. Myosin II activity is also necessary for the nuclear translocation during delamination of subventricular zone (SVZ) cells, a second, telencephalon-specific type of neural progenitor. Moreover, the inhibition of ab-centrosomal INM changes the balance between VZ and SVZ progenitor cell fate. Our data suggest a unifying concept in which the actomyosin contraction underlying ab-centrosomal INM sets the stage for the evolutionary increase in VZ pseudostratification and for SVZ progenitor delamination, a key process in cortical expansion.cell cycle ͉ cerebral cortex ͉ cytoskeleton ͉ neural stem cells ͉ neurogenesis

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“…action effect which is independent of insulin [2]. Insulin stimulates glucose disposal by increasing the translocation and intrinsic activity of the GLUT4 transporter [3,4], whereas hyperglycaemia promotes glucose uptake primarily via the GLUT1 transporter [5] although more recent findings suggest a stimulation/activation of GLUT4 as well [6].…”

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confidence: 99%

Studies on the mass action effect of glucose in NIDDM and IDDM: evidence for glucose resistance

et al. 1997

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Tissue glucose uptake occurs via a facilitated transport system [1]. The major factors that regulate glucose uptake in vivo are the prevailing plasma glucose and insulin concentrations. Following glucose ingestion the plasma glucose concentration rises, insulin secretion is stimulated and the combination of hyperglycaemia and hyperinsulinaemia contributes to the increase in glucose utilization. Plasma glucose concentration influences glucose utilization by a mass Diabetologia (1997) Summary The ability of hyperglycaemia to enhance glucose uptake was evaluated in 9 non-insulin-dependent (NIDDM), 7 insulin-dependent (IDDM) diabetic subjects, and in 6 young and 9 older normal volunteers. Following overnight insulin-induced euglycaemia, a sequential three-step hyperglycaemic clamp (+ 2.8 + 5.6, and + 11.2 mmol/l above baseline) was performed with somatostatin plus replacing doses of basal insulin and glucagon, 3-3 H-glucose infusion and indirect calorimetry. In the control subjects as a whole, glucose disposal increased at each hyperglycaemic step (13.1 ± 0.6, 15.7 ± 0.7, and 26.3 ± 1.1 m mol/kg ⋅ min). In NIDDM (10.5 ± 0.2, 12.1 ± 1.0, and 17.5 ± 1.1 m mol/kg ⋅ min), and IDDM (11.2 ± 0.8, 12.9 ± 1.0, and 15.6 ± 1.1 m mol/kg ⋅ min) glucose disposal was lower during all three steps (p < 0.05-0.005). Hepatic glucose production declined proportionally to plasma glucose concentration to a similar extent in all four groups of patients. In control subjects, hyperglycaemia stimulated glucose oxidation (+ 4.4 ± 0.7 m mol/kg ⋅ min) only at + 11.2 mmol/l (p < 0.05), while non-oxidative glucose metabolism increased at each hyperglycaemic step (+ 3.1 ± 0.7; + 3.5 ± 0.9, and + 10.8 ± 1.7 m mol/kg ⋅ min; all p < 0.05). In diabetic patients, no increment in glucose oxidation was elicited even at the highest hyperglycaemic plateau (IDDM = + 0.5 ± 1.5; NIDDM = + 0.2 ± 0.6 m mol/kg ⋅ min) and non-oxidative glucose metabolism was hampered (IDDM = + 1.8 ± 1.5, + 3.1 ± 1.7, and + 4.3 ± 1.8; NIDDM = + 0.7 ± 0.6, 2.1 ± 0.9, and + 7.0 ± 0.8 m mol/kg ⋅ min; p < 0.05-0.005). Blood lactate concentration increased and plasma non-esterified fatty acid (NEFA) fell in control (p < 0.05) but not in diabetic subjects. The increments in blood lactate were correlated with the increase in non-oxidative glucose disposal and with the decrease in plasma NEFA. In conclusion: 1) the ability of hyperglycaemia to promote glucose disposal is impaired in NIDDM and IDDM; 2) stimulation of glucose oxidation and non-oxidative glucose metabolism accounts for glucose disposal; 3) both pathways of glucose metabolism are impaired in diabetic patients; 4) impaired ability of hyperglycaemia to suppress plasma NEFA is present in these patients. These results suggest that glucose resistance, that is the ability of glucose itself to promote glucose utilization, is impaired in both IDDM and NIDDM patients. [Diabetologia (1997) 40: 687-697] Keywords Hyperglycaemia, mass action effect, glucose-mediated glucose metabolism, glucose oxidation, non-oxidative glucose metabol...

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Glucose Transport and Glucose Transporters in Muscle and Their Metabolic Regulation

Cited by 324 publications

References 0 publications

Expression of rainbow trout glucose transporters GLUT1 and GLUT4 during in vitro muscle cell differentiation and regulation by insulin and IGF-I

Expression of rainbow trout glucose transporters GLUT1 and GLUT4 during in vitro muscle cell differentiation and regulation by insulin and IGF-I

Myosin II is required for interkinetic nuclear migration of neural progenitors

Studies on the mass action effect of glucose in NIDDM and IDDM: evidence for glucose resistance

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