Neuropeptide B and neuropeptide W as new serum predictors of nutritional status and of clinical outcomes in pediatric patients with type 1 diabetes mellitus treated with the use of pens or insulin pumps

Abstract

Introduction The aim of our study was to determine the relationship between neuropeptide B (NPB), neuropeptide W (NPW), nutritional and antioxidant status and selected fat- and bone-derived factors in type 1 diabetes mellitus (T1DM) treated using pens (T1DM pen group) or insulin pumps (T1DM pump group) in order to investigate the potential role of NPB and NPW in the clinical outcomes of T1DM. Material and methods Fifty-eight patients with T1DM and twenty-five healthy controls (CONTR) participated in the study. Assessments of NPB, NPW, total antioxidant status (TAS), leptin, adiponectin, osteocalcin, and free soluble receptor activator for nuclear factor κB (free sRANKL) were conducted. Results NPB, NPW, leptin, and TAS were lower (by 33%, p < 0.013; 34%, p < 0.008; 290%, p < 0.00004; 21%, p < 0.05; respectively), while adiponectin was by 51% higher ( p < 0.006) in T1DM vs. CONTR, while osteocalcin and free sRANKL levels were similar in both groups. NPW was lower in the T1DM pen group both vs. the T1DM pump group (36% lower, p < 0.0009) and vs. the CONTR group (35% lower, p < 0.002). In the T1DM pen group, but not in the T1DM pump group or the CONTR group, the Cole index and TAS levels explain (besides NPB) the variation in NPW values. ROC curves showed that serum levels of leptin, adiponectin, NPB and NPW (but not osteocalcin or free sRANKL) were predictive indicators for T1DM. Conclusions Measurements of NPB and NPW, besides leptin and adiponectin, are worth considering in the detailed prognosis of nutritional status in T1DM, primarily in the T1DM pen-treated population.

Neuropeptide�B stimulates insulin secretion and expression but not proliferation in rat insulin‑producing INS‑1E cells

“…We found that nPB and its receptor are present in rat adipocytes (11) where nPB stimulates lipolysis and suppresses leptin expression, and secretion (11). others have reported that nPB serum level is upregulated in humans who suffer from anorexia nervosa (12), while it is reduced in type 1 diabetic patients (13). overall, these results collectively indicate that the nPB/nPBW1 system is involved in controlling body weight and energy homeostasis and its alternation may contribute to obesity.…”

Transcriptome Signatures Reveal Candidate Key Genes in the Peripheral Blood Mononuclear Cells of Patients With Coronary Artery Disease

“…Enriched genes such as CCR2 [56], CCL19 [57], CX3CL1 [58], CXCL12 [59], IL20 [60], epidermal growth factor receptor (EGFR) [61], ERBB3 [62], adrenomedullin (ADM) [63], SCUBE1 [64], LMAN1L [65] and EGFL7 [66] were responsible for pathogenesis of CAD. Enriched genes such as CXCL6 [67], BMP7 [68], RXFP2 [69], BRS3 [70], FFAR3 [71], neuropeptide B (NPB) [72], SPON2 [73], FCN3 [74], REG3A [75] and ornithine carbamoyltransferase (OTC) [76] were culpable for pathogenesis of diabetes, but these genes may be involved in development of CAD. Enriched genes such as COL18A1 [77], cortistatin (CORT) [78], guanine nucleotide binding protein (G protein) [79] and MUC2 [80] were involved in development of obesity, but these genes may be associated with pathogenesis of CAD.…”

Transcriptome signatures reveal candidate key genes in the peripheral blood mononuclear cells of patients with coronary artery disease and prediction of small drug molecules

“…Genes such as CCR2 [61], CCL19 [62], CX3CL1 [63], CXCL12 [64], IL20 [65], epidermal growth factor receptor (EGFR) [66], ERBB3 [67], adrenomedullin (ADM) [68], SCUBE1 [69], LMAN1L [70] and EGFL7 [71] were responsible for pathogenesis of CAD. Genes such as CXCL6 [72], BMP7 [73], RXFP2 [74], BRS3 [75], FFAR3 [76], neuropeptide B (NPB) [77], SPON2 [78], FCN3 [79], REG3A [80] and ornithine carbamoyltransferase (OTC) [81] were culpable for pathogenesis of diabetes, but these genes might be involved in development of CAD. Genes such as COL18A1 [82], cortistatin (CORT) [83], guanine nucleotide binding protein (G protein) [84] and MUC2 [85] were involved in development of obesity, but these genes might be associated with pathogenesis of CAD.…”