eISSN: 1896-9151
ISSN: 1734-1922
Archives of Medical Science
Current issue Archive Manuscripts accepted About the journal Special issues Editorial board Abstracting and indexing Subscription Contact Instructions for authors
SCImago Journal & Country Rank
Clinical research

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

Teresa Grzelak, Anna Wedrychowicz, Joanna Grupinska, Marta Pelczynska, Marcelina Sperling, Aniceta A. Mikulska, Violetta Naughton, Krystyna Czyzewska

Arch Med Sci
Online publish date: 2018/05/16
View full text
Get citation
JabRef, Mendeley
Papers, Reference Manager, RefWorks, Zotero
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 B (free sRANKL) were conducted.

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.

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.


insulin, biochemistry, type 1 diabetes mellitus

Ferron M, Wei J, Yoshizawa T, et al. Insulin signaling in osteoblasts integrates bone remodeling and energy metabolism. Cell 2010; 23: 296-308.
Wedrychowicz A, Stec M, Sztefko K, Starzyk JB. Associations between bone, fat tissue and metabolic control in children and adolescents with type 1 diabetes mellitus. Exp Clin Endocrinol Diabetes 2014; 122: 491-5.
Takenoya F, Wang L, Kageyama H, et al. Neuropeptide W-induced hypophagia is mediated through corticotropin-releasing hormone-containing neurons. J Mol Neurosci 2015; 56: 789-98.
Rucinski M, Nowak KW, Chmielewska J, Ziolkowska A, Malendowicz LK. Neuropeptide W exerts a potent suppressive effect on blood leptin and insulin concentrations in the rat. Int J Mol Med 2007; 19: 401-5.
Harris RBS. Direct and indirect effects of leptin on adipocyte metabolism. Biochim Biophys Acta 2014; 1842: 414-23.
Matsuda M, Shimomura I. Roles of adiponectin and oxidative stress in obesity-associated metabolic and cardiovascular diseases. Rev Endocr Metab Disord 2014; 15: 1-10.
Chen PC, Kryukova YN, Shyng SL. Leptin regulates KATP Channel trafficking in pancreatic beta-cells by a signaling mechanism involving AMP-activated protein kinase (AMPK) and cAMP-dependent protein kinase (PKA).
J Biol Chem 2013; 288: 34098-109.
Soedling H, Hodson DJ, Adrianssens AE, et al. Limited impact on glucose homeostasis of leptin receptor deletion from insulin- or proglucagon-expressing cells. Mol Metab 2015; 25: 619-30.
Bernotiene E, Palmer G, Gabay C. The role of leptin in innate and adaptive immune responses. Arthritis Res Ther 2006; 8: 217.
Combs TP, Marliss EB. Adiponectin signaling in the liver. Rev Endocr Metab Disord 2014; 15: 137-47.
Khalil RB, Hachem C. Adiponectin in eating disorders. Eat Weight Disord 2014; 19: 3-10.
Pereira RI, Snell-Bergeon JK, Erickson C, et al. Adiponectin dysregulation and insulin resistance in type 1 diabetes. J Clin Endocrinol Metab 2012; 97: 642-7.
Neve A, Corrado A, Cantatore FP. Osteoblast physiology in normal and pathological conditions. Cell Tissue Res 2011; 343: 289-302.
Ferron M, Hinoi E, Karsenty G, Ducy P. Osteocalcin differentially regulates beta cell and adipocyte gene expression and affects the development of metabolic diseases in wild-type mice. Proc Natl Acad Sci USA 2008; 105: 5266-70.
Goldstone AP, Howard JK, Lord GM, et al. Leptin prevents the fall in plasma osteocalcin during starvation in male mice. Biochem Biophys Res Commun 2002; 295: 475-81.
Ferron M, McKee MD, Levine RL, Ducy P, Karsenty G. Intermittent injections of osteocalcin improve glucose metabolism and prevent type 2 diabetes in mice. Bone 2012; 50: 568-75.
Oury F, Ferron M, Huizhen W, et al. Osteocalcin regulates murine and human fertility through a pancreas-bone-testis axis. J Clin Invest 2013; 123: 2421-33.
Ikeda T, Kasai M, Suzuki J, et al. Multimerization of the receptor activator of nuclear factor-kappaB ligand (RANKL) isoforms and regulation of osteoclastogenesis. J Biol Chem 2003; 278: 47217-22.
Motiur RM, Takeshita S, Matsuoka K, et al. Proliferation-coupled osteoclast differentiation by RANKL: cell density as a determinant of osteoclast formation. Bone 2015; 81: 392-9.
Starup-Linde J. Diabetes, biochemical markers of bone turnover, diabetes control, and bone. Front Endocrinol (Lausanne) 2013; 8: 21.
Tsentidis C, Gourgiotis D, Kossiva L, et al. Higher levels of s-RANKL and osteoprotegerin in children and adolescents with type 1 diabetes mellitus may indicate increased osteoclast signaling and predisposition to lower bone mass: a multivariate cross-sectional analysis. Osteoporos Int 2016; 27: 1631-43.
Gehrmann W, Elsner M, Lenzen S. Role of metabolically generated reactive oxygen species for lipotoxicity in pancreatic beta-cells. Diabetes Obes Metab 2010; 12: 149-58.
Drews G, Krippeit-Drews P, Düfer M. Oxidative stress and beta-cell dysfunction. Pflugers Arch 2010; 460: 703-18.
World Medical Association Declaration of Helsinki: ethical principles for medical research involving human subjects. JAMA 2013; 310: 2191-4.
Roberts C. Tanner’s Puberty Scale: exploring the historical entanglements of children, scientific photography and sex. Sexualities 2016; 19: 328-46.
Palczewska I, Niedźwiecka Z. Somatic development indices in children and youth of Warsaw. Med Wieku Rozwoj 2001; 5 (Suppl 1): 18-118.
Desmons A, Jaisson S, Leroy N, Gillery P, Guillard E. Labile glycated haemoglobin and carbamylated haemoglobin are still critical points for HbA1c measurement. Biochem Med (Zagreb) 2017; 27: 378-86.
Li Y, Browne RW, Bonner MR, et al. Positive relationship between total antioxidant status and chemokines observed in adults. Oxid Med Cell Longev 2014; 2014: 693680.
Dezakia K, Kageyamab H, Sekib M, Shiodab S, Yadaa T. Neuropeptide W in the rat pancreas: potentiation of glucose-induced insulin release and Ca2+ influx through L-type Ca2+ channels in beta-cells and localization in islets. Regul Pept 2008; 145: 153-8.
Samson WK, Baker JR, Samson CK, Samson HW, Taylor MM. Central neuropeptide B administration activates stress hormone secretion and stimulates feeding in male rats. J Neuroendocrinol 2004; 16: 842-9.
Baker JR, Cardinal K, Bober C, Taylor MM, Samson WK. Neuropeptide W acts in brain to control prolactin, corticosterone, and growth hormone release. Endocrinology 2003; 144: 2816-21.
Levine AS, Winsky-Sommerer R, Huitron-Resendiz S, Grace MK, de Lecea L. Injection of neuropeptide W into paraventricular nucleus of hypothalamus increases food intake. Am J Physiol 2005; 288: 1727-32.
Mondal MS, Yamaguchi H, Date Y, et al. A role for neuropeptide W in the regulation of feeding behavior. Endocrinology 2003; 144: 4729-33.
Li H, Feinle-Bisset C, Frisby C, Kentish S, Wittert GA, Page AJ. Gastric neuropeptide W is regulated by meal-related nutrients. Peptides 2014; 28: 6-14.
Li H, Kentish SJ, Kritas S, et al. Modulation of murine gastric vagal afferent mechanosensitivity by neuropeptide W. Acta Physiol Scand 2013; 209: 179-91.
Motoike T, Long JM, Tanaka H, et al. Mesolimbic neuropeptide W coordinates stress responses under novel environments. Proc Natl Acad Sci USA 2016; 113: 6023-8.
Ishii M, Fei H, Friedman JM. Targeted disruption of GPR7, the endogenous receptor for neuropeptides B and W, leads to metabolic defects and adult-onset obesity. Proc Natl Acad Sci USA 2003; 100: 10540-5.
Loureiro MB, Ururahy MA, Freire-Neto FP, et al. Low bone mineral density is associated to poor glycemic control and increased OPG expression in children and adolescents with type 1 diabetes. Diabetes Res Clin Pract 2014; 103: 452-7.
Galler A, Gelbrich G, Kratzsch J, Noack N, Kapellen T, Kiess W. Elevated serum levels of adiponectin in children, adolescents and young adults with type 1 diabetes and the impact of age, gender, body mass index and metabolic control: a longitudinal study. Eur J Endocrinol 2007; 157: 481-9.
Al Saeed M. The utility of adiponectin and nitric oxide metabolites as biomarkers for prediction and follow up of vascular complications in children with type 1 diabetes mellitus. Saudi J Health Sci 2013; 2: 156-60.
Frystyk J, Tarnow L, Hansen TK, Parving HH, Flyvbjerg A. Increased serum adiponectin levels in type 1 diabetic patients with microvascular complications. Diabetologia 2005; 48: 1911-8.
Kanazawa I, Yamaguchi T, Yamauchi M, et al. Serum undercarboxylated osteocalcin was inversely associated with plasma glucose level and fat mass in type 2 diabetes mellitus. Osteoporos Int 2011; 22: 187-94.
Salmonowicz B, Krzystek-Korpacka M, Noczynska A. Trace elements, magnesium, and the efficacy of antioxidant systems in children with type 1 diabetes mellitus and in their siblings. Adv Clin Exp Med 2014; 23:
Sainz N, Rodríguez A, Catalán V, et al. Leptin administration downregulates the increased expression levels of genes related to oxidative stress and inflammation in the skeletal muscle of ob/ob mice. Mediators Inflamm 2010; 2010: 784343.
DuBose SN, Hermann JM, Tamborlane WV, et al. Obesity in youth with type 1 diabetes in Germany, Austria, and the United States. J Pediatr 2015; 167: 627-32.
Wedrychowicz A, Stelmach M, Wyka K, Starzyk J. Like-triple diabetes as first manifestation of MODY2 in an overweight teenager with transient multiple antibodies. Diabetes Care 2014; 37: 66-7.
McDonald TJ, Colclough K, Brown R, et al. Islet autoantibodies can discriminate maturity-onset diabetes of the young (MODY) from type 1 diabetes. Diabet Med 2011; 28: 1028-33.
Urrutia I, Martínez R, López-Euba T, et al. Lower frequency of HLA-DRB1 type 1 diabetes risk alleles in pediatric patients with MODY. PLoS One 2017; 4: e0169389.
Olsen B, Johannesen J, Fredheim S, Svensson J. The Danish Society for Childhood and Adolescent Diabetes. Insulin pump treatment; increasing prevalence, and predictors for better metabolic outcome in Danish children and adolescents with type 1 diabetes. Pediatric Diab 2015; 16: 256-62.
Cameron FJ, Amin R, de Beaufort C, Codner E, Acerini CL. International Society for Pediatric and Adolescent Diabetes. ISPAD Clinical Practice Guidelines 2014: diabetes in adolescence. Pediatr Diabetes 2014; 15: 245-56.
American Diabetes Association. Standards of medical care in diabetes – 2016. Diabetes Care 2016; 39: 1-108.
Ramírez-Vélez R, Correa-Bautista JE, Martínez-Torres J, et al. Performance of two bioelectrical impedance analyses in the diagnosis of overweight and obesity in children and adolescents: the FUPRECOL Study. Nutrients 2016; 8: 575.
Quick links
© 2018 Termedia Sp. z o.o. All rights reserved.
Developed by Bentus.
PayU - płatności internetowe