LAUSR

Introduction The prevalence for childhood overweight and obesity increased steadily in the past decades. Childhood obesity was defined as a disease by the World Health Organization [25] and by the American Medical Association (2013) [7] and is listed in the International Statistical Classification of Diseases and Related Health Problems in (ICD). In 2016 over 340 million children and adolescents, aged 5–19 were overweight or obese and current estimates suggest approximately 38 million children under the age of 5 as overweight or obese [25]. Amongst genetic factors and environmental influences, a variety of perinatal risk factors individually or in combination contributes to the development of infant obesity. Especially maternal pre-pregnancy obesity, excessive gestational weight gain and gestational diabetes result in pathological pregnancy conditions. Insulin resistance (IR), elevated blood glucose levels and hormonal disturbance provoke the malprogramming of infant’s energy metabolism [11]. In 2016, Romere et al. discovered asprosin as a new adipokine exerting decisive metabolic functions. Asprosin is the C-terminal peptide of the extracellular matrix protein fibrillin-1 that is cleaved off by the propeptide convertase furin during the secretory pathway [17]. According to the current paradigm, asprosin is released from white adipose tissue (WAT) into the blood stream to target metabolically relevant organs. Following a circadian oscillation, asprosin triggers hepatic glucose release via the OLFR734 receptor [14, 19] and impairs insulin secretion from pancreatic beta-cells [13]. Furthermore, asprosin crosses the blood–brain barrier, activates hunger-stimulating AgRP (Agouti-related peptide) hypothalamic neurons thereby evoking appetite stimulation in mice [6]. Also, insulin sensitivity in muscle cells is impaired by asprosin via the PKCδ/ SERCA-2 pathway by increasing inflammation and ER stress [12]. Serum asprosin levels are elevated in obese humans and mice, and neutralisation of asprosin via antibody treatment reduces food intake and body weight as well as improves insulin sensitivity in mice [6]. Further studies revealed that asprosin levels were significantly higher in patients with impaired glucose regulation and correlated with a variety of clinical parameters of glucose and lipid metabolic disorders [24]. Furthermore, asprosin levels were significantly higher in women with type 2 diabetes mellitus (T2DM), and positively correlated with IR in women with polycystic ovary syndrome (PCOS) [1, 15]. These observations suggest asprosin as a potential biomarker of early diagnosis in metabolic-related diseases and a new therapeutic target not only for T2DM and other metabolic disorders but also for counteracting the perinatal programming of childhood obesity (overview see Fig. 1). Currently, only little data regarding asprosin levels in pregnant women or children are available. So far, two clinical studies addressed maternal and newborn asprosin levels [3, 26] whereas three studies examined serum asprosin in overweight and obese children [16, 21, 23]. Zhong et al. examined 80 pregnant, non-obese women; 40 with gestational diabetes mellitus (GDM), and 40 with normal glucose tolerance (NGT), aged 18–40. All participants were without pre-existing diabetes mellitus (DM), history of macrosomia, nor stillbirth, polycystic ovary syndrome, nor medications of corticosteroids or antipsychotics. The authors performed asprosin measurements at three different time points, 18–20 gestational weeks (gws), 24–28 gws, as well as before delivery. Neonate asprosin protein concentrations were determined in umbilical cord plasma by ELISA, and additional asprosin protein expression analysis via western blots and immunohistochemistry were performed in placenta. Asprosin levels were elevated in plasma of