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Open access

Esben S Lauritzen, Nikolaj Rittig, Ermina Bach, Niels Møller and Mette Bjerre

Context

During the inflammatory acute phase response, plasma glucose and serum triglycerides are increased in humans. Fibroblast growth factor (FGF) 21 has plasma glucose and lipid-reducing actions, but its role in the acute inflammatory response in human is unknown.

Objective

To investigate circulating levels of FGF21 after lipopolysaccharide (LPS) infusion.

Design

Two randomized, single-blinded, placebo-controlled crossover trials were used.

Setting

The studies were performed at a university hospital clinical research center.

Patients and interventions

Study 1 (LPS bolus): Eight young, healthy, lean males were investigated two times: (1) after isotonic saline injection and (2) after LPS injection (bolus of 1 ng/kg). Each study day lasted 4 h. Study 2 (continuous LPS infusion): Eight, healthy males were investigated two times: (1) during continuously isotonic saline infusion and (2) during continuous LPS infusion (0.06 ng/kg/h). Each study day lasted 4 h. Circulating FGF21 levels were quantified every second hour by an immunoassay.

Results

A LPS bolus resulted in a late suppression (t = 240 min) of serum FGF21 (P = 0.035). Continuous LPS infusion revealed no significant effects on FGF21 levels (P = 0.82).

Conclusions

Our studies show that a bolus of LPS results in decreased FGF21 levels 4 h from exposure.

Open access

Ermina Bach, Niels Møller, Jens Otto Lunde Jørgensen, Mads Buhl and Holger Jon Møller

Aims/hypothesis: The macrophage-specific glycoprotein sCD163 has emerged as a biomarker of low grade inflammation in the metabolic syndrome and related disorders. High sCD163 levels are seen in acute sepsis as result of direct lipopolysaccharide-mediated shedding of the protein from macrophage surfaces including Kupffer cells. The aims of this study were to investigate if low grade endotoxinemia in human subjects results in increasing levels of sCD163 in a cortisol-dependent manner.

Methods: We studied eight male hypopituitary patients and eight age and gender matched healthy controls during intravenous low dose LPS or placebo infusion administered continuously over 360 min. Furthermore, we studied eight healthy volunteers with bilateral femoral vein and artery catheters during a 360 minutes infusion with saline and low dose LPS in each leg respectively.

Results: Systemic low grade endotoxinemia resulted in a gradual increase in sCD163 from 1.65±0.51 mg/L (placebo) to 1.92±0.46 mg/L (LPS) at 220 min, p=0.005; and from 1.66±0.42 mg/L (placebo) to 2.19±0.56 mg/L (LPS) at 340 min, p=0.006. A very similar response was observed in hypopituitary patients: from 1.59±0.53 mg/L (placebo) to 1.83±0.45 mg/L (LPS) at 220 min, p=0.021; and from 1.52±0.53 mg/L (placebo) to 2.03±0.44 mg/L (LPS) at 340 min, p<0.001. As opposed to systemic treatment, continuous femoral artery infusion did not result in increased sCD163.

Conclusion: Systemic low grade endotoxinemia resulted in increased sCD163 to levels seen in the metabolic syndrome in both controls and hypopituitary patients. This suggests a direct and cortisol-independent effect of LPS on the shedding of sCD163. We observed no effect of local endotoxinemia on levels of serum sCD163.

Open access

Ermina Bach, Niels Møller, Jens Otto L Jørgensen, Mads Buhl and Holger Jon Møller

Aims/hypothesis

The macrophage-specific glycoprotein sCD163 has emerged as a biomarker of low-grade inflammation in the metabolic syndrome and related disorders. High sCD163 levels are seen in acute sepsis as a result of direct lipopolysaccharide-mediated shedding of the protein from macrophage surfaces including Kupffer cells. The aim of this study was to investigate if low-grade endotoxinemia in human subjects results in increasing levels of sCD163 in a cortisol-dependent manner.

Methods

We studied eight male hypopituitary patients and eight age- and gender-matched healthy controls during intravenous low-dose LPS or placebo infusion administered continuously over 360 min. Furthermore, we studied eight healthy volunteers with bilateral femoral vein and artery catheters during a 360-min infusion with saline and low-dose LPS in each leg respectively.

Results:

Systemic low-grade endotoxinemia resulted in a gradual increase in sCD163 from 1.65 ± 0.51 mg/L (placebo) to 1.92 ± 0.46 mg/L (LPS) at 220 min, P = 0.005 and from 1.66 ± 0.42 mg/L (placebo) to 2.19 ± 0.56 mg/L (LPS) at 340 min, P = 0.006. A very similar response was observed in hypopituitary patients: from 1.59 ± 0.53 mg/L (placebo) to 1.83 ± 0.45 mg/L (LPS) at 220 min, P = 0.021 and from 1.52 ± 0.53 mg/L (placebo) to 2.03 ± 0.44 mg/L (LPS) at 340 min, P < 0.001. As opposed to systemic treatment, continuous femoral artery infusion did not result in increased sCD163.

Conclusion:

Systemic low-grade endotoxinemia resulted in increased sCD163 to levels seen in the metabolic syndrome in both controls and hypopituitary patients. This suggests a direct and cortisol-independent effect of LPS on the shedding of sCD163. We observed no effect of local endotoxinemia on levels of serum sCD163.