Influence of acute hyperglycemia in human sepsis on inflammatory cytokine and counterregulatory hormone concentrations

Yu, Wenkui; Li, Weiqin; Li, Ning; Li, Jieshou

doi:10.3748/wjg.v9.i8.1824

Cited by 86 publications

(62 citation statements)

References 34 publications

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“…Hyperglycemia has been previously linked in animal and human studies to alterations in the immune response owing to modulation of both pro-and anti-inflammatory cytokines, [21][22][23][24][25] impairment of the neutrophil response 26 and depression of cell-mediated immunity. 27 Clinically, elevated glucose levels have been associated with increased risk of infectious complications, particularly after surgery, 8,28 and improved glycemic control has been associated with a reduction in surgical site 8 and bloodstream infections.…”

Section: Discussionmentioning

confidence: 99%

Hyperglycemia and morbidity and mortality in extremely low birth weight infants

Kao

Morris²,

Lally³

et al. 2006

J Perinatol

168

110

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Objective: The purpose of this study was to determine the association between hyperglycemia and mortality and late-onset infections (>72 h) in extremely low birth weight (ELBW) infants.Study design: Retrospective analysis of a prospective cohort study of 201 ELBW infants who survived greater than 3 days after birth. Mean morning glucose levels were categorized as normoglycemia (<120 mg/dl), mildmoderate hyperglycemia (120 to 179 mg/dl) and severe hyperglycemia (X180 mg/dl). Hyperglycemia was further divided into early (first 3 days of age) and persistent (first week of age). Logistic regression was performed to assess whether hyperglycemia was associated with either mortality or late-onset culture-proven infection, measured after 3 and 7 days of age.Results: Adjusting for age, the odds ratio (OR) for either dying or developing a late infection was 5.07 (95% confidence interval (CI): 1.06 to 24.3) for infants with early severe hyperglycemia and 6.26 (95% CI: 0.73 to 54.0) for infants with persistent severe hyperglycemia. Adjusting for age, both severe early and persistent hyperglycemia were associated with increased mortality. Among survivors, there was no significant association between hyperglycemia and length of mechanical ventilation or length of hospital stay. Persistent severe hyperglycemia was associated with the development of Stage II/III necrotizing enterocolitis, after adjusting for age and male gender (OR: 9.49, 95% CI: 1.52 to 59.3). Conclusion:Severe hyperglycemia in the first few days after birth is associated with increased odds of death and sepsis in ELBW infants.

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Section: Discussionmentioning

confidence: 99%

Hyperglycemia and morbidity and mortality in extremely low birth weight infants

Kao

Morris²,

Lally³

et al. 2006

J Perinatol

168

110

View full text Add to dashboard Cite

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“…In situations such as the early phase after surgical trauma and in the metabolic response to severe acute phase sepsis, circulating pro-inflammatory cytokines are highly upregulated (30,31). The dosedependent acute metabolic responses to IL6 have been well analyzed in healthy subjects by administering recombinant IL6 to mimic the acute inflammatory state of sepsis (2,21).…”

Section: Discussionmentioning

confidence: 99%

Circulating glucagon is associated with inflammatory mediators in metabolically compromised subjects

Ortega¹,

Moreno-Navarrete²,

Sabater³

et al. 2011

European Journal of Endocrinology

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Background: Acute phase mediators promote metabolic changes by modifying circulating hormones. However, there is virtually no data about the link between glucagon and inflammatory parameters in obesity-related chronic low-grade inflammation. Study design: We performed both cross-sectional and longitudinal (diet-induced weight loss) studies. Methods: Circulating glucagon concentrations (ELISA), parameters of glucose and lipid metabolism, interleukin 6 (IL6), and complement factor B (CFB) were analyzed in 316 subjects (250 men and 66 women). The effects of weight loss were investigated in an independent cohort of 20 subjects. Results: Circulating glucagon significantly correlated with glucose (rZ0.407, P!0.0001), HbAlc (rZ0.426, P!0.0001), fasting triglycerides (rZ0.356, PZ0.001), and parameters of innate immune response system such as IL6 (rZ0.342, PZ0.050) and CFB (rZ0.404, PZ0.002) in obese subjects with altered glucose tolerance, but not in individuals with normal glucose tolerance (NGT). In obese and NGT subjects, glucagon was associated with fasting triglycerides (rZ0.475, PZ0.003) and CFB (rZ0.624, PZ0.001). In obese subjects, glucagon (PZ0.019) and CFB (PZ0.002) independently contributed to 26% of fasting triglyceride variance (P!0.0001) after controlling for the effects of age and fasting serum glucose concentration in multiple lineal regression models. Moreover, concomitant with fat mass, fasting triglycerides, and CFB, weight loss led to significantly decreased circulating glucagon (K23.1%, PZ0.004). Conclusions: According to the current results, acute phase reactants such as IL6 and CFB are associated with fasting glucagon in metabolically compromised subjects. This suggests that glucagon may be behind the association between inflammatory and metabolic parameters in obesity-associated chronic low-grade inflammation.

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“…From previous studies on sepsis it is known that bacterial endotoxins interfere significantly with the action of insulin at the cellular level and may cause hyperglycaemia as well as hypoglycaemia in septic patients (Das, 2003;Yu et al, 2003).…”

Section: Discussionmentioning

confidence: 99%

Model of septic shock induced by live E. coli (O18) in a laboratory rat

Dembovska¹,

Svoboda²,

Scheer³

et al. 2008

Vet. Med. - Czech

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ABSTRACT:This study was concerned with the development of induced septic shock in a laboratory rat using a series of measurements including body temperature, heart and respiratory rates, haematocrit value, red and white blood cell counts, differential leukocyte count, haemoglobin value, glycaemia, analysis of arterial blood gases, and serum levels of interleukin 6 (IL-6) during the first five hours. A total of 12 specific pathogen free (SPF) laboratory rats were used for the study. Septic shock was induced under general anaesthesia by introducing live E. coli (O18) into the jugular vein in the dose of 1 × 10 9 per 100 g of body weight (group SESH). Clinical measurements and blood collection from a. carotis were performed just prior to, and then 1.5 and 5 h after the administration of E. coli. The control group (C) contained 9 SPF laboratory rats which received physiological saline only, at the same volume into the jugular vein, and blood collection followed according to the same scheme as above described for group SESH. The results of the experiment showed that changes in clinical, haematological and biochemical parameters could be detected as early as 1.5 hours after induction. These changes correspond with the activation of an inflammatory reaction and the development of metabolic acidosis. They are accompanied by a considerable rise in IL-6 already 1.5 h after the application of live E. coli and after 5 h the levels exceeded 2 000 pg/ml in all experimental animals. Our results clearly document the importance of IL-6 for the early detection of developing septic shock and of some less specific but routinely determined parameters such as white blood cell count and base excess.

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Influence of acute hyperglycemia in human sepsis on inflammatory cytokine and counterregulatory hormone concentrations

Abstract: Acute hyperglycemia pricks up hyperinsulinemia and increases circulating cytokine concentrations and these effects are more pronounced in sepsis with IGT. This suggests a potential modulation of immunoinflammatory responses in human sepsis by hyperglycemia.

Cited by 86 publications

References 34 publications

Hyperglycemia and morbidity and mortality in extremely low birth weight infants

Hyperglycemia and morbidity and mortality in extremely low birth weight infants

Circulating glucagon is associated with inflammatory mediators in metabolically compromised subjects

Model of septic shock induced by live E. coli (O18) in a laboratory rat

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