Circulating Concentrations of Cathelicidin Anti-Microbial Peptide (CAMP) Are Increased during Oral Glucose Tolerance Test

Abstract

Recent investigation has revealed the significant role of Cathelicidin antimicrobial peptide (CAMP) in infection defense and innate immunity processes in adipose tissue. Meanwhile, knowledge of its regulation and functions in metabolic contexts as an adipokine remains sparce. The present study investigated the postprandial regulation of circulating CAMP levels during oral glucose tolerance tests (OGTTs). Eighty-six metabolically healthy volunteers participated in a standardized 75 g-2 h-OGTT setting. The effects of exogenous glucose, insulin, and incretins on CAMP expression in human adipocyte culture (cell-line SGBS) were studied in vitro. CAMP concentrations in blood serum samples were measured by ELISA techniques and adipocyte gene expression levels were quantified by real-time PCR. Of note, base-line CAMP serum quantities were negatively correlated with HDL cholesterol levels as well as with the anti-inflammatory adipokine adiponectin. During the 2 h following glucose ingestion, a significant rise in circulating CAMP concentrations was observed in considerable contrast to reduced quantities of fatty acid binding proteins (FABP) 2 and 4 and dipeptidyl peptidase 4 (DPP4). In SGBS adipocytes, neither differing glucose levels nor insulin or incretin treatment significantly induced CAMP mRNA levels. According to our data, glucose represents a positive postprandial regulator of systemic CAMP. This effect apparently is not mediated by the regulatory impact of glucose metabolism on adipocyte CAMP expression.

Cathelicidin Antimicrobial Peptide Levels in Atherosclerosis and Myocardial Infarction in Mice and Human

“…In obesity, adipocytes and adipose tissue produce predominant proinflammatory adipokines [ 4 ]. The state of local and systemic low-grade inflammation is aggravated by an increased amount and activation/polarization of macrophages in adipose tissue [ 23 , 24 ]. As we described previously, nutritional carbohydrates and lipids can regulate postprandial CAMP serum levels in humans [ 24 , 25 ].…”

“…The state of local and systemic low-grade inflammation is aggravated by an increased amount and activation/polarization of macrophages in adipose tissue [ 23 , 24 ]. As we described previously, nutritional carbohydrates and lipids can regulate postprandial CAMP serum levels in humans [ 24 , 25 ]. Ldlr −/− mice are well established as a model for nutritional-induced atherosclerosis.…”

Targeting β Cells with Cathelicidin Nanomedicines Improves Insulin Function and Pancreas Regeneration in Type 1 Diabetic Rats

“…Pertinent in the case of T1D, cathelicidin expression has been detected in the islets of mice, rats, and human pancreas in insulin-producing cells, with decreased expression in animals susceptible to T1D relative to healthy individuals. , Cathelicidin serum levels have been shown to be influenced by glucose levels, being increased after oral glucose challenge in humans .…”

“…11,12 Cathelicidin serum levels have been shown to be influenced by glucose levels, being increased after oral glucose challenge in humans. 15 In vitro cathelicidin supplementation improved β cell function, increasing the glucose-mediated insulin release, while in vivo administration in rats contributed to the regeneration of β cells from ductal precursors. 11 Also, cathelicidin was observed to modify the gut microbiome, favoring the presence of beneficial bacteria in detriment of others that cause dysbiosis, 11 with its expression being under the influence of short-chain fatty acids produced by gut microbiota.…”