Human AHSG ELISA Matched Antibody Pair

Insulin resistance and beta-cell function impairment play a role in the pathogenesis of type 2 diabetes (T2DM). Insulin signaling is inhibited by fetuin-A, an abundant plasma protein. Fetuin-A is also a candidate marker of the T2DM risk. This case-control study aimed to determine whether fetuin-A serum level is related to insulin resistance, beta-cell function impairment, and total and ionized Ca and Mg serum levels in Erbil patients with T2DM. A total of 60 patients with T2DM were recruited, and 30 healthy persons were included in the control group. Fetuin-A and insulin concentrations were measured through ELISA. Other biochemical parameters were determined spectrophotometrically. Insulin resistance (HOMA2IR), insulin sensitivity (HOMA2%S), and beta-cell function were examined by using a homeostatic model assessment 2 (HOMA2). Fasting serum insulin, fetuin-A serum levels, and HOMA2IR were significantly increased. HOMA2%S of the patients with diabetes was significantly lower than that of the control group. The total serum and ionized Ca and Mg contents and the Ca/Mg ratio were reduced in the patients. Therefore, fetuin-A is related to T2DM pathogenesis and is strongly associated with insulin resistance and glycemic control in T2DM patients. Future large-scale studies are necessary to validate fetuin-A as an indicator of IR in T2DM patients.

Acute pancreatitis (AP) is acute inflammation of the pancreas, mainly caused by gallstones and alcohol, driven by changes in communication between cells. Heparin-binding proteins (HBPs) play a central role in health and diseases. Therefore, we used heparin affinity proteomics to identify extracellular HBPs in pancreas and plasma of normal mice and in a caerulein mouse model of AP. Many new extracellular HBPs (360) were discovered in the pancreas, taking the total number of HBPs known to 786. Extracellular pancreas HBPs form highly interconnected protein-protein interaction networks in both normal pancreas (NP) and AP. Thus, HBPs represent an important set of extracellular proteins with significant regulatory potential in the pancreas. HBPs in NP are associated with biological functions such as molecular transport and cellular movement that underlie pancreatic homeostasis. However, in AP HBPs are associated with additional inflammatory processes such as acute phase response signalling, complement activation and mitochondrial dysfunction, which has a central role in the development of AP. Plasma HBPs in AP included known AP biomarkers such as serum amyloid A, as well as emerging targets such as histone H2A. Other HBPs such as alpha 2-HS glycoprotein (AHSG) and histidine-rich glycoprotein (HRG) need further investigation for potential applications in the management of AP. Pancreas HBPs are extracellular and so easily accessible and are potential drug targets in AP, whereas plasma HBPs represent potential biomarkers for AP. Thus, their identification paves the way to determine which HBPs may have potential applications in the management of AP.