Mouse GIP, Active form (high sensitivity) Assay Kit used for measurement of active glucose-dependent insulinotropic peptide (GIP) (1-42) in new publication.

Meng, Q, Chepurny, OG, Leech, CA, et al. The alpha-7 nicotinic acetylcholine receptor agonist GTS-21 engages the glucagon-like peptide-1 incretin hormone axis to lower levels of blood glucose in db/db mice. Diabetes Obes Metab. 2022; 1- 12. doi:10.1111/dom.14693

Abstract

Background: Oxygen therapy, using supraphysiological concentrations of oxygen (hyperoxia), is routinely administered to patients who require respiratory support including mechanical ventilation (MV). However, prolonged exposure to hyperoxia results in acute lung injury (ALI) and accumulation of high mobility group box 1 (HMGB1) in the airways. We previously showed that airway HMGB1 mediates hyperoxia-induced lung injury in a mouse model of ALI. Cholinergic signaling through the α7 nicotinic acetylcholine receptor (α7nAChR) attenuates several inflammatory conditions. The aim of this study was to determine whether 3-(2,4 dimethoxy-benzylidene)-anabaseine dihydrochloride, GTS-21, an α7nAChR partial agonist, inhibits hyperoxia-induced HMGB1 accumulation in the airways and circulation, and consequently attenuates inflammatory lung injury.

Methods: Mice were exposed to hyperoxia (≥99% O2) for 3 days and treated concurrently with GTS-21 (0.04, 0.4 and 4 mg/kg, i.p.) or the control vehicle, saline.

Results: The systemic administration of GTS-21 (4 mg/kg) significantly decreased levels of HMGB1 in the airways and the serum. Moreover, GTS-21 (4 mg/kg) significantly reduced hyperoxia-induced acute inflammatory lung injury, as indicated by the decreased total protein content in the airways, reduced infiltration of inflammatory monocytes/macrophages and neutrophils into the lung tissue and airways, and improved lung injury histopathology.

Conclusions: Our results indicate that GTS-21 can attenuate hyperoxia-induced ALI by inhibiting extracellular HMGB1-mediated inflammatory responses. This suggests that the α7nAChR represents a potential pharmacological target for the treatment regimen of oxidative inflammatory lung injury in patients receiving oxygen therapy.

Incretins are a group of gastrointestinal hormones that cause an increase in the amount of insulin released from the beta cells of the islets of Langerhans after eating and they also inhibit glucagon release from the alpha cells of the Islets of Langerhans. 

GIP, typical incretin like GLP-1, was isolated and sequenced from intestinal mucosa as “gastric inhibitory peptide” in 1970, and then it was renamed as “glucose-dependent insulinotropic peptide”. 

It has been reported that GIP receptor is expressed in cells such as beta cell of pancreas, adipocyte or osteoblastic cell, and it plays essential roles in reserving of ingested nutrients within the body in each cell, and the control of GIP signal can lead to improvement of metabolic syndrome. 

It is rapidly inactivated to GIP (3-42) from active form of GIP (1-42) by DPP-IV in blood. The IBL-America ELISA kit (27702) can measure only active form of Human GIP (1-42).  The control set is available for sale on request.  For Reference Use Only.  Learn More