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Pro-inflammatory cytokines after an episode of acute pancreatitis: associations with fasting gut hormone profile
PENDHARKAR, Sayali A. - Personal Name
Introduction Pro-inflammatory cytokines, such as interleukin (IL)-6, tumour necrosis factor (TNF)α, and monocyte chemoattractant protein (MCP)-1, are often elevated in individuals after acute pancreatitis but what determines their levels is
poorly understood. Gut hormones have emerged as possible modulators of inflammatory response. The aim was to investigate
the associations between pro-inflammatory cytokines and a comprehensive panel of gut hormones after an episode of acute
pancreatitis.
Materials and methods Fasting blood samples were collected to measure cytokines (IL-6, TNFα, and MCP-1) and gut hormones (cholecystokinin, gastric inhibitory peptide (GIP), ghrelin, glicentin, glucagon-like peptide-1, oxyntomodulin, peptide
YY, secretin, and vasoactive intestinal peptide). A series of linear regression analyses was conducted and four statistical
models were used to adjust for patient- and pancreatitis-related covariates.
Results A total of 83 individuals were recruited. GIP and peptide YY were significantly (p < 0.001) associated with IL-6,
TNFα, MCP-1, consistently in all the four models. Every 1 ng/mL change in GIP resulted in a 16.2, 3.2, and 50.8% increase
in IL-6, TNFα, and MCP-1, respectively, in the most adjusted model. Every 1 ng/mL change in peptide YY resulted in a 7.0,
2.4, and 32.1% increase in IL-6, TNFα, and MCP-1, respectively, in the most adjusted model. GIP independently contributed
29.0–36.5% and peptide YY − 17.4–48.9% to circulating levels of the studied pro-inflammatory cytokines. The other seven
studied gut hormones did not show consistently significant associations with pro-inflammatory cytokines.
Conclusions GIP and peptide YY appear to be involved in perpetuation of subclinical inflammation following an episode
of acute pancreatitis, which is known to play an important role in the pathogenesis of blood glucose derangements. These
findings advance the understanding of mechanisms underlying diabetes of the exocrine pancreas and have translational
implications.
poorly understood. Gut hormones have emerged as possible modulators of inflammatory response. The aim was to investigate
the associations between pro-inflammatory cytokines and a comprehensive panel of gut hormones after an episode of acute
pancreatitis.
Materials and methods Fasting blood samples were collected to measure cytokines (IL-6, TNFα, and MCP-1) and gut hormones (cholecystokinin, gastric inhibitory peptide (GIP), ghrelin, glicentin, glucagon-like peptide-1, oxyntomodulin, peptide
YY, secretin, and vasoactive intestinal peptide). A series of linear regression analyses was conducted and four statistical
models were used to adjust for patient- and pancreatitis-related covariates.
Results A total of 83 individuals were recruited. GIP and peptide YY were significantly (p < 0.001) associated with IL-6,
TNFα, MCP-1, consistently in all the four models. Every 1 ng/mL change in GIP resulted in a 16.2, 3.2, and 50.8% increase
in IL-6, TNFα, and MCP-1, respectively, in the most adjusted model. Every 1 ng/mL change in peptide YY resulted in a 7.0,
2.4, and 32.1% increase in IL-6, TNFα, and MCP-1, respectively, in the most adjusted model. GIP independently contributed
29.0–36.5% and peptide YY − 17.4–48.9% to circulating levels of the studied pro-inflammatory cytokines. The other seven
studied gut hormones did not show consistently significant associations with pro-inflammatory cytokines.
Conclusions GIP and peptide YY appear to be involved in perpetuation of subclinical inflammation following an episode
of acute pancreatitis, which is known to play an important role in the pathogenesis of blood glucose derangements. These
findings advance the understanding of mechanisms underlying diabetes of the exocrine pancreas and have translational
implications.
Availability
| EB00000003208K | Available |
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Content Type
E-Jurnal
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Subject(s)
Acute pancreatitis
Chronic hyperglycaemia
Gastric inhibitory peptide
Interleukin-6
Monocyte chemoattractant protein-1
Peptide YY
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Statement of Responsibility
Sayali A. Pendharkar...[et al.]
No other version available
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