The DOI matches its Crossref record; 114 of the 114 references it cites were found in a registry or an index.
Glucose metabolism in lymphoid and inflammatory cells and tissues
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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“This is relevant for leukocytes that, importantly, cannot become insulin-resistant but upregulate GLUT1, GLUT3, and GLUT4 transporters upon activation [14].”
From Interaction of the endocrine system with inflammation: a function of energy and volume regulation (2014) · cites this paper as [14]
In the citing paper
“It is proposed that insulin resistance is the critical determinant of the pro- or anti-inflammatory effect of insulin, because only liver, muscle, and fat tissue, but not leukocytes, become insulin-resistant [14].”
From Interaction of the endocrine system with inflammation: a function of energy and volume regulation (2014) · cites this paper as [14]
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Metadata
- Authors
- Calder, P. C., Dimitriadis, G., & Newsholme, P.
- Affiliations
- University of Southampton (GB)
- University General Hospital Attikon (GR)
- University College Dublin (IE)
- Corresponding author
- Calder, Philip C
- Venue
- Current Opinion in Clinical Nutrition and Metabolic Care
- Published
- 2007-07
- Volume
- 10
- Issue
- 4
- Pages
- 531-540
- ISSN
- 1363-1950 (ISSN-L)
- OpenAlex
- W2042827948
- Cited by
- 143
- References
- 113
- Citations by year
- 2026: 1 · 2025: 6 · 2024: 6 · 2023: 8 · 2022: 9 · 2021: 11 · 2020: 18 · 2019: 8 · 2018: 10 · 2017: 7 · 2016: 7 · 2015: 9 · 2014: 11 · 2013: 8 · 2012: 5
- FWCI
- 0.66
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Current Opinion in Clinical Nutrition & Metabolic Care (publishedVersion)
- PubMed (publishedVersion)
- ePrints Soton (University of Southampton) (submittedVersion)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Hyperglycemia and glycemic control in critically ill and hospitalized patients
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Management and Research
- Keywords
- glucose metabolism, immune cells, glucose transporters, insulin receptor, insulin, hyperglycemia, hypoglycemia, inflammation, lymphocytes, energy metabolism, insulin therapy, immune function
- MeSH terms
- Gene Expression Regulation, Glucose, Humans, Hypoglycemic Agents, Immune System, Insulin, Lymphocyte Activation, Lymphocytes, Macrophages, Monocytes, Glucose Transport Proteins, Facilitative
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