Transport of 2-deoxy-D-glucose by isolated protoplasts of the yeast, Kluyveromyces lactis

1982 ◽  
Vol 28 (7) ◽  
pp. 901-906 ◽  
Author(s):  
Paulette W. Royt ◽  
Averett S. Tombes

Protoplasts of succinate- and glucose-grown Kluyveromyces lactis were generated by incubating cells with β-mercaptoethanol and β-glucuronidase in the presence of MgSO4 as osmotic stabilizer. Transport of 2-deoxyglucose by the protoplasts was comparable with that of the walled cells. Only protoplasts of succinate-grown cells exhibited a lag in glucose utilization. Removal of the wall by this technique does not result in loss of the inducible component of the glucose carrier via degradation or release.

1991 ◽  
Vol 261 (2) ◽  
pp. R265-R275
Author(s):  
T. Otsuka ◽  
L. Wei ◽  
D. Bereczki ◽  
V. Acuff ◽  
C. Patlak ◽  
...  

The effects of pentobarbital sodium on local cerebral glucose utilization (LCGU) and 3-O-methylglucose (3-MG) influx were measured by quantitative autoradiography in 52 brain areas of control and treated rats. Pentobarbital (50 mg/kg ip) lowered LCGU to a relatively uniform rate (approximately 35 mumol.100 g-1.min-1) in 24 of 25 forebrain areas. Among the 18 hindbrain areas, LCGU was decreased by pentobarbital by 15-55% (range 50-157 and 28-110 mumol.100 g-1.min-1 in control and treated rats, respectively). In contrast, pentobarbital lowered the 3-MG influx rate constant and permeability-surface area product by 20-30% in nearly all brain structures. The 3-MG results fit a model in which both the half-saturation constant and the maximal velocity of the glucose carrier are decreased by pentobarbital. After pentobarbital treatment, the ratio of local cerebral plasma flow (LCPF) to LCGU was the same as in controls for brain areas in which LCGU was less than 35 mumol.100 g-1.min-1 but was higher in brain areas where LCGU exceeded 35 mumol.100 g-1.min-1. Pentobarbital produced dissimilar changes in LCGU, 3-MG influx, and LCPF; these processes may thus not be closely linked during pentobarbital anesthesia.


Microbiology ◽  
2011 ◽  
Vol 157 (5) ◽  
pp. 1509-1518 ◽  
Author(s):  
Samantha Cialfi ◽  
Daniela Uccelletti ◽  
Augusto Carducci ◽  
Micheline Wésolowski-Louvel ◽  
Patrizia Mancini ◽  
...  

In Saccharomyces cerevisiae, HSL1 (NIK1) encodes a serine-threonine protein kinase involved in cell cycle control and morphogenesis. Deletion of its putative orthologue in Kluyveromyces lactis, KlHSL1, gives rise to sensitivity to the respiratory inhibitor antimycin A (AA). Resistance to AA on glucose (Rag+ phenotype) is associated with genes (RAG) required for glucose metabolism/glycolysis. To understand the relationship between RAG and KlHSL1, rag and Klhsl1Δ mutant strains were investigated. The analysis showed that all the mutants contained a phosphorylated form of Hog1 and displayed an inability to synthesize/accumulate glycerol as a compatible solute. In addition, rag mutants also showed alterations in both cell wall and membrane fatty acids. The pleiotropic defects of these strains indicate that a common pathway regulates glucose utilization and stress response mechanisms, suggesting impaired adaptation of the plasma membrane/cell wall during the respiratory–fermentative transition. KlHsl1 could be the link between these adaptive pathways and the morphogenetic checkpoint.


2021 ◽  
Vol 15 (4) ◽  
pp. 87-104
Author(s):  
A. O. Maslakova ◽  
◽  
M. Ya. Liuta ◽  
N. O. Sybirna ◽  
◽  
...  

For most cells, including lymphocytes, glucose is a primary energy source, and, therefore, it is vital to understand the regulatory mechanisms that control the work of glucose transporters. Lymphocytes are pivotal for mediation of immune and inflammatory responses. A feature of lymphocytes is increasing glucose utilization during activation of the immune function, which is strongly dependent on glucose uptake. Some studies show that elevated glucose concentration in diabetes mellitus affects lymphocytes’ glucose transporters expression, whichcorrelates with impaired immune functions and may become one of the predisposing factors of contracting infectious diseases. Recent studies have focused on glucose transporters as therapeutic targets for a variety of diseases, including diabetes mellitus. This review demonstrates the effect of photobiomodulationtherapy on glucose uptake by Na+-coupled glucose carrier SGLT1 and facilitated diffusion glucose carriers of the GLUT family (GLUT1, GLUT3, GLUT4) in normal and diabetic lymphocytes.


2014 ◽  
Author(s):  
Magdalena Sendrakowska ◽  
Tomasz Milewicz ◽  
Jozef Krzysiek ◽  
Pawel Zagrodzki
Keyword(s):  

Reproduction ◽  
2000 ◽  
pp. 127-135 ◽  
Author(s):  
W Bone ◽  
NG Jones ◽  
G Kamp ◽  
CH Yeung ◽  
TG Cooper

The effects of the male antifertility agent ornidazole on glycolysis as a prerequisite for fertilization were investigated in rats. Antifertility doses of ornidazole inhibited glycolysis within mature spermatozoa as determined from the lack of glucose utilization, reduced acidosis under anaerobic conditions and reduced glycolytic enzyme activity. As a consequence, cauda epididymidal spermatozoa from ornidazole-fed rats were unable to fertilize rat oocytes in vitro, with or without cumulus cells, which was not due to transfer of an inhibitor in epididymal fluid with the spermatozoa. Under IVF conditions, binding to the zona pellucida was reduced in spermatozoa from ornidazole-fed males and the spermatozoa did not undergo a change in swimming pattern, which was observed in controls. The block to fertilization could be explained by the disruption of glycolysis-dependent events, since reduced binding to the zona pellucida and a lack of kinematic changes were demonstrated by control spermatozoa in glucose-free media in the presence of respiratory substrates. The importance of glycolysis for binding to, and penetration of, the zona pellucida, and hyperactivation in rats is discussed in relation to the glycolytic production of ATP in the principal piece in which local deprivation of energy may explain the reduced force of spermatozoa from ornidazole-fed males.


Diabetes ◽  
1983 ◽  
Vol 32 (5) ◽  
pp. 408-411 ◽  
Author(s):  
M. Rosenthal ◽  
W. L. Haskell ◽  
R. Solomon ◽  
A. Widstrom ◽  
G. M. Reaven

Diabetes ◽  
1987 ◽  
Vol 36 (9) ◽  
pp. 1041-1046 ◽  
Author(s):  
S. Sasson ◽  
D. Edelson ◽  
E. Cerasi

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