Glucose metabolism in lymphoid and inflammatory cells and tissues
Glucose metabolism in lymphoid and inflammatory cells and tissues
PURPOSE OF REVIEW: To examine the role of glucose as a fuel for immune cells and the influence of glucose supply on immune-cell functional responses. RECENT FINDINGS: Immune cells express the insulin receptor and a range of glucose-transporter isoforms. Glucose transporters are responsive to both immune stimulation and insulin. The pattern of glucose-transporter upregulation differs among different types of immune cell. In-vitro studies reveal that both hypo- and hyperglycaemia impair immune-cell functions and promote inflammatory responses. Clamp studies have revealed proinflammatory effects of hyperglycaemia and antiinflammatory and immune-promoting effects of insulin. SUMMARY: Glucose is readily utilized by cells of the immune system and is used to generate energy and biosynthetic precursors. Activation of immune cells is associated with increased glucose utilization and this is facilitated, in part, by increased expression of glucose transporters. Immune cells express the insulin receptor and respond to insulin. Both hypo- and hyperglycaemia impair immune-cell functions and promote inflammatory responses. Insulin therapy in hyperglycaemic subjects may be of benefit through effects of both insulin itself and lowered glucose concentration. Excessive lowering of blood glucose concentration may also be harmful to the immune response
lymphocyte activation, monocytes, blood glucose, lymphocytes, cytology, protein, human, immune system, therapy, humans, metabolism, glucose transport proteins, pharmacology, glucose, proteins, blood, gene expression regulation, drug effects, immunology, nutrition, facilitative, macrophages, review, insulin, utilization, hypoglycemic agents
531-540
Calder, P.C.
1797e54f-378e-4dcb-80a4-3e30018f07a6
Dimitriadis, G.
35cd6cb5-d42b-41ae-949f-81bfdb94e5ed
Newsholme, P.
c9ecc215-995e-4a2f-ba08-0cab7dc66883
2007
Calder, P.C.
1797e54f-378e-4dcb-80a4-3e30018f07a6
Dimitriadis, G.
35cd6cb5-d42b-41ae-949f-81bfdb94e5ed
Newsholme, P.
c9ecc215-995e-4a2f-ba08-0cab7dc66883
Calder, P.C., Dimitriadis, G. and Newsholme, P.
(2007)
Glucose metabolism in lymphoid and inflammatory cells and tissues.
Current Opinion in Clinical Nutrition and Metabolic Care, 10 (4), .
Abstract
PURPOSE OF REVIEW: To examine the role of glucose as a fuel for immune cells and the influence of glucose supply on immune-cell functional responses. RECENT FINDINGS: Immune cells express the insulin receptor and a range of glucose-transporter isoforms. Glucose transporters are responsive to both immune stimulation and insulin. The pattern of glucose-transporter upregulation differs among different types of immune cell. In-vitro studies reveal that both hypo- and hyperglycaemia impair immune-cell functions and promote inflammatory responses. Clamp studies have revealed proinflammatory effects of hyperglycaemia and antiinflammatory and immune-promoting effects of insulin. SUMMARY: Glucose is readily utilized by cells of the immune system and is used to generate energy and biosynthetic precursors. Activation of immune cells is associated with increased glucose utilization and this is facilitated, in part, by increased expression of glucose transporters. Immune cells express the insulin receptor and respond to insulin. Both hypo- and hyperglycaemia impair immune-cell functions and promote inflammatory responses. Insulin therapy in hyperglycaemic subjects may be of benefit through effects of both insulin itself and lowered glucose concentration. Excessive lowering of blood glucose concentration may also be harmful to the immune response
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Published date: 2007
Keywords:
lymphocyte activation, monocytes, blood glucose, lymphocytes, cytology, protein, human, immune system, therapy, humans, metabolism, glucose transport proteins, pharmacology, glucose, proteins, blood, gene expression regulation, drug effects, immunology, nutrition, facilitative, macrophages, review, insulin, utilization, hypoglycemic agents
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Local EPrints ID: 60967
URI: http://eprints.soton.ac.uk/id/eprint/60967
ISSN: 1363-1950
PURE UUID: c1882cce-5118-4738-91a6-7014f6c7622a
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Date deposited: 09 Sep 2008
Last modified: 31 May 2023 01:33
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Author:
G. Dimitriadis
Author:
P. Newsholme
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