Altered insulin sensitivity and immune function in patients with colorectal cancer.


Journal

Clinical nutrition ESPEN
ISSN: 2405-4577
Titre abrégé: Clin Nutr ESPEN
Pays: England
ID NLM: 101654592

Informations de publication

Date de publication:
Dec 2023
Historique:
received: 24 08 2023
revised: 01 09 2023
accepted: 19 09 2023
medline: 11 12 2023
pubmed: 7 12 2023
entrez: 6 12 2023
Statut: ppublish

Résumé

Insulin resistance and chronic inflammation have been reported in patients with cancer. However, many of the underlying mechanisms and associations are yet to be unveiled. We examined both the level of insulin sensitivity and markers of inflammation in patients with colorectal cancer for comparison to controls. Clinical exploratory study of patients with colorectal cancer (n = 20) and matched controls (n = 10). Insulin sensitivity was quantified using the hyperinsulinemic normoglycemic clamp and blood samples were taken for quantification of several key, both intra- and extracellular, inflammatory markers. We analysed the differences in these parameters between the two groups. Patients exhibited both insulin resistance (M-value, patients median (Mdn) 4.57 interquartile range (IQR) 3.49-5.75; controls Mdn 5.79 (IQR 5.20-6.81), p = 0.049), as well as increased plasma levels of the pro-inflammatory cytokines IL-1β (patients Mdn 0.48 (IQR 0.33-0.58); controls Mdn 0.36 (IQR 0.29-0.42), p = 0.02) and IL-6 (patients Mdn 3.21 (IQR 2.31-4.93); controls Mdn 2.16 (IQR 1.50-2.65), p = 0.02). The latter is present despite an almost two to three fold decrease (p < 0.01) in caspase-1 activity, a facilitating enzyme of IL-1β production, within circulating immune cells. Patients with colorectal cancer displayed insulin resistance and higher levels of plasma IL-1β and IL-6, in comparison to matched healthy controls. The finding of a seemingly disconnect between inflammasome (caspase-1) activity and plasma levels of key pro-inflammatory cytokines in cancer patients may suggest that, in parallel to dysregulated immune cells, tumour-driven inflammatory pathways also are in effect.

Sections du résumé

BACKGROUND & AIMS OBJECTIVE
Insulin resistance and chronic inflammation have been reported in patients with cancer. However, many of the underlying mechanisms and associations are yet to be unveiled. We examined both the level of insulin sensitivity and markers of inflammation in patients with colorectal cancer for comparison to controls.
METHODS METHODS
Clinical exploratory study of patients with colorectal cancer (n = 20) and matched controls (n = 10). Insulin sensitivity was quantified using the hyperinsulinemic normoglycemic clamp and blood samples were taken for quantification of several key, both intra- and extracellular, inflammatory markers. We analysed the differences in these parameters between the two groups.
RESULTS RESULTS
Patients exhibited both insulin resistance (M-value, patients median (Mdn) 4.57 interquartile range (IQR) 3.49-5.75; controls Mdn 5.79 (IQR 5.20-6.81), p = 0.049), as well as increased plasma levels of the pro-inflammatory cytokines IL-1β (patients Mdn 0.48 (IQR 0.33-0.58); controls Mdn 0.36 (IQR 0.29-0.42), p = 0.02) and IL-6 (patients Mdn 3.21 (IQR 2.31-4.93); controls Mdn 2.16 (IQR 1.50-2.65), p = 0.02). The latter is present despite an almost two to three fold decrease (p < 0.01) in caspase-1 activity, a facilitating enzyme of IL-1β production, within circulating immune cells.
CONCLUSION CONCLUSIONS
Patients with colorectal cancer displayed insulin resistance and higher levels of plasma IL-1β and IL-6, in comparison to matched healthy controls. The finding of a seemingly disconnect between inflammasome (caspase-1) activity and plasma levels of key pro-inflammatory cytokines in cancer patients may suggest that, in parallel to dysregulated immune cells, tumour-driven inflammatory pathways also are in effect.

Identifiants

pubmed: 38057005
pii: S2405-4577(23)02147-2
doi: 10.1016/j.clnesp.2023.09.917
pii:
doi:

Substances chimiques

NLR Family, Pyrin Domain-Containing 3 Protein 0
Interleukin-6 0
Cytokines 0
Interleukin-1beta 0
Caspases EC 3.4.22.-

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

193-200

Informations de copyright

Copyright © 2023 The Authors. Published by Elsevier Ltd.. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of competing interest Authors declare that they have no competing interests.

Auteurs

Bayar Baban (B)

Department of Surgery, School of Medical Sciences, Faculty of Medicine and Health, Örebro University, SE-701 82 Örebro, Sweden. Electronic address: bayar.baban@regionorebrolan.se.

Daniel Eklund (D)

School of Medical Sciences, Faculty of Medicine and Health, Örebro University, SE-701 82 Örebro, Sweden; Inflammatory Response and Infection Susceptibility Centre (iRiSC), Faculty of Medicine and Health, Örebro University, SE-701 82 Örebro, Sweden.

Kedeye Tuerxun (K)

School of Medical Sciences, Faculty of Medicine and Health, Örebro University, SE-701 82 Örebro, Sweden; Inflammatory Response and Infection Susceptibility Centre (iRiSC), Faculty of Medicine and Health, Örebro University, SE-701 82 Örebro, Sweden.

Muhammed Alshamari (M)

School of Medical Sciences, Department of Radiology, Örebro University & Örebro University Hospital, SE-701 85 Örebro, Sweden.

Alessandro Laviano (A)

Department of Translational and Precision Medicine, Sapienza University, Rome, Italy.

Olle Ljungqvist (O)

Department of Surgery, School of Medical Sciences, Faculty of Medicine and Health, Örebro University, SE-701 82 Örebro, Sweden.

Eva Särndahl (E)

School of Medical Sciences, Faculty of Medicine and Health, Örebro University, SE-701 82 Örebro, Sweden; Inflammatory Response and Infection Susceptibility Centre (iRiSC), Faculty of Medicine and Health, Örebro University, SE-701 82 Örebro, Sweden.

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Classifications MeSH