Glutamine and glucose metabolism in rat splenocytes and mesenteric lymph node lymphocytes

1991 ◽  
Vol 260 (1) ◽  
pp. E141-E147 ◽  
Author(s):  
G. Y. Wu ◽  
C. J. Field ◽  
E. B. Marliss

The metabolism of glutamine (2 mM) and glucose (5 mM) was studied in splenocytes and mesenteric lymph node lymphocytes of Wistar-Furth rats to assess their relative importance as energy substrates. The major products from glutamine were ammonia, glutamate, aspartate, and CO2, whereas those from glucose were lactate, pyruvate, and CO2 in cells from both lymphoid organs. The individual rates of glutamine and glucose metabolism were decreased in the presence of both substrates, compared with the rates when present separately. The rates of glucose and some (but not all) aspects of glutamine metabolism were higher (P less than 0.01) in splenocytes than in mesenteric lymphocytes. In cells from both lymphoid organs, glutamine and glucose could potentially contribute almost equal amounts of ATP in the presence of both substrates. Glutamine and glucose individually were able to provide sufficient amounts of ATP to maintain its concentrations in the cells throughout a 2-h incubation period at the same levels as with both substrates present. We also found that splenocyte concentration (3.3-100 x 10(6) cells/ml) in the incubations is an important determinant of rates of metabolite formation from glutamine when expressed per 10(6) cells. We conclude that glucose is not the only quantitatively significant energy substrate or even the major one for lymphocytes, because glutamine at near-physiological concentration can be readily utilized by these cells.

1994 ◽  
Vol 72 (7) ◽  
pp. 827-832 ◽  
Author(s):  
Catherine J. Field ◽  
Guoyao Wu ◽  
Errol B. Marliss

Increased energy substrate metabolism accompanies the functional activation of extrathymic immunocytes in the autoimmune BB diabetic rat, but the specific cells responsible have not been identified. To determine the possible contribution of lymphocytes to the elevated metabolism of glucose and glutamine, mesenteric lymph node cells were selected because they contain few macrophages or natural killer (NK) cells. Results from diabetic (BBd, n = 7) and non-diabetes-prone (BBn, n = 7) rats were compared with those from streptozotocin-induced diabetic (STZ-BBn, n = 6) rats. In BBd cells, all measured metabolites of glutamine (CO2, glutamate, aspartate, and NH3) in the presence of 5 mM glucose were elevated (1.5- to 2.5-fold) compared with BBn. In contrast, the only product of glucose metabolism (in the presence of 2 mM glutamine) that was increased was pyruvate (1.6-fold). All measured products of glucose metabolism were significantly lower in cells from STZ-BBn than from BBn rats. Products from glutamine did not differ. Calculated potential ATP production was greater (p < 0.05) in BBd than in BBn and STZ-BBn cells (86 ± 5 vs. 65 ± 2 and 53 ± 5 nmol∙2 h−1∙10−6 cells, respectively). However, in BBn and STZ-BBn rats, about three quarters of the cells were T (CD5+) cells and one quarter were B (MARK-1+) cells, whereas in BBd three quarters of the cells were MARK-1+. Therefore, to distinguish the role of T- versus B-cells, enriched T-lymphocyte (CD5+) preparations were studied: glutamate (5.3-fold) and NH3 (4.2-fold) production from glutamine and lactate (1.7-fold) production from glucose were greater (p < 0.05) in cells from BBd rats. This establishes that in BBd cells (i) lymphocytes (especially CD4+) contribute to the increased metabolism, (ii) T-lymphocytes are especially active in glutamine metabolism, but because of their reduced numbers, this cannot fully account for the increase in the unfractionated population, and therefore (iii) B-lymphocytes probably also contribute, and (iv) the altered metabolism of these cells is not a result of the diabetic state. These findings are consistent with activation of immunocytes of multiple lineages in this autoimmune syndrome.Key words: glutamine, glucose, lymphocytes, BB rat.


1997 ◽  
Vol 56 ◽  
pp. 16
Author(s):  
M.B. Alimzhanov ◽  
M.H. Kosco-Vilbois ◽  
D.V. Kuprash ◽  
R.L. Turetskaya ◽  
A. Tarakhovsky ◽  
...  

1999 ◽  
Author(s):  
D. Damman ◽  
P. B. Bahnson ◽  
R. M. Weigel ◽  
R. E. Isaacson ◽  
H. F. Troutt ◽  
...  

Author(s):  
Joy Nakawesi ◽  
Konjit Getachew Muleta ◽  
Dragos‐Christian Dasoveanu ◽  
Bengt Johansson‐Lindbom ◽  
Katharina Lahl

Lipids ◽  
1980 ◽  
Vol 15 (6) ◽  
pp. 475-478 ◽  
Author(s):  
Takayuki Sugiura ◽  
Yasuo Masuzawa ◽  
Keizo Waku

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