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Increased circulating serpinB1 levels in children with overweight/obesity are associated with obesity-related parameters: a cross‑sectional study

BMC Pediatrics volume 24, Article number: 762 (2024) Cite this article

Abstract

Background

Circulating serpinB1 levels are increased in obese mice and have been shown to promote β-cell proliferation in several species. However, the data on serum serpinB1 levels in children with obesity are scarce. This study aimed to determine serum serpinB1 levels in children with overweight/obesity, and to study its association with obesity-related parameters.

Methods

A total of 54 children with overweight/obesity and 36 normal-weight healthy controls aged 6–14 were recruited in this study. Anthropometric parameters, glucolipid metabolic biochemical parameters, sex hormones, and serum serpinB1 levels were measured in all subjects. The association of serum serpinB1 levels with obesity-related parameters and the risk of overweight/obesity were analyzed using correlation analysis and binary regression analysis, respectively.

Results

The serum serpinB1 level in overweight/obese children was notably greater than in normal-weight controls (2.03 ± 0.70 vs. 1.41 ± 0.58 ng/mL, p < 0.001). SerpinB1 levels were positively correlated with body mass index (BMI), BMI Z-score, triglyceride (TG), uric acid, fasting insulin, C-peptide, and homeostasis model assessment of insulin resistance (HOMA-IR) levels. Additionally, we found that elevated circulating serpinB1 levels were associated with the increased risk of childhood overweight/obesity even after adjustment for age, gender, and HOMA-IR (odds ratio, 4.132; 95% confidence interval, 1.315–12.983; p = 0.015).

Conclusions

Circulating serpinB1 level was significantly increased in children with overweight/obesity and positively associated with obesity-related glucolipid metabolic parameters. These results indicate a close association between serum serpinB1 concentrations and childhood overweight/obesity.

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Introduction

Overweight and obesity in children have emerged as significant global health challenges in recent years [1]. The implications of overweight and obesity during childhood are profound, as these conditions are associated with a higher risk of various health issues, including type 2 diabetes (T2DM), cardiovascular diseases, and psychological disorders [2]. Additionally, obese individuals adapt to insulin resistance (IR) by increasing β-cell proliferation, and dysfunction of the compensatory proliferation is a key determinant of the development of T2DM in these patients [3, 4]. Recently, it has been reported that serpinB1 is a novelly confirmed liver-derived secretory protein enriched in liver and serum, and facilitates pancreatic β-cell proliferation by modulating proteins involved in growth/survival pathways [5]. Several studies have shown that serum serpinB1 is increased in obese mice and associated with insulin resistance in adults with T2DM [5,6,7,8]. However, serum serpinB1 concentrations in children with overweight/obesity remain to be thoroughly elucidated.

Nowadays, the interference between circulating cytokines from various tissues and pancreatic β-cells is increasingly recognized. For example, leptin and adiponectin derived from adipose tissue; osteocalcin derived from bone; and kisspeptin1 and betatrophin derived from the liver play crucial roles in β-cell function and/or mass [9,10,11]. SerpinB1, as a member of the serine proteinase inhibitors (Serpins) family, is profusely expressed in the cytoplasm of polymorphonuclear neutrophils and protects host cells from proteases (neutrophil elastase, cathepsin G, chymase, etc.) during stress or infection [12, 13]. High-fat diet (HFD) induced obese mice displayed enhanced β-cell proliferation and mass compared with controls, while serpinB1 deficient mice fed the same HFD exhibited markedly reduced β-cell proliferation [5]. Consistently, Talukdar et al. also revealed that the deletion of neutrophil protease decreased chronic inflammation in adipose tissue and improved obesity-related glucose metabolism disorders in HFD-induced obese mice [14].

Some researchers have investigated the associations of circulating serpinB1 levels with IR and T2DM in adults [6,7,8]. However, they drew inconsistent conclusions regarding the association between serpinB1 levels and T2DM, but all of those studies suggested that serpinB1 levels were positively correlated with BMI. This controversial conclusion is likely due to the weight bias in individuals with T2DM, as the β-cell mass increases adaptively in nondiabetic obese individuals, whereas it gradually declines over the course of T2DM progression [15,16,17,18]. Obesity is a key driving factor of IR and one of the influencing factors on the dynamics of β-cell mass in patients with T2DM [16, 19]. We speculate that serpinB1 may participate in the progression of IR and T2DM through its interaction with obesity. Understanding the relationship between serum serpinB1 levels and obesity in children can help in developing targeted interventions and treatments to mitigate the health risks associated with childhood obesity. Therefore, this study aims to investigate the serum concentrations of serpinB1 in overweight/obese children and to assess their relationship with obesity-related anthropometric and metabolic parameters.

Methods

Study participants

This cross-sectional study was approved by the ethics committee of Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology (TJ-IRB20201016) and written informed consent was obtained from the guardians of all minor participants. This study recruited 90 children aged 7 to 14 years between June 2019 and December 2021 at the Pediatric Endocrinology Clinic of Tongji Hospital in Wuhan, China, including 54 children with overweight/obesity and 36 healthy normal-weight controls. Overweight and obesity were defined as ≥ 85th and ≥ 95th percentiles of sex-specific body mass index, respectively, according to the BMI growth curves of Chinese children [20]. Subjects were excluded if they were diagnosed with diabetes or specific genetic or endocrine obesity (e.g., Prader–Willi syndrome, Cushing’s disease, hypothyroidism, or polycystic ovary syndrome) or if they used medications affecting glucose or lipid metabolism (e.g., metformin, dexamethasone, or thyroid medications). All methods were performed in accordance with the ethical standards as laid down in the Declaration of Helsinki.

Anthropometric and biochemical measurements

Anthropometric assessments, including height (cm) and weight (kg), were conducted by trained physicians using standardized procedures [10]. BMI was calculated using the measured weight and height, and the BMI Z-score was converted from BMI values as described previously [10, 20]. The levels of fasting blood glucose, glycated haemoglobin A1c (HbA1c), C-peptide, fasting insulin, TG, total cholesterol (TC), high-density lipoprotein-cholesterol (HDL-C), uric acid, low-density lipoprotein cholesterol (LDL-C), and sex hormones were tested by standard autoanalyzer techniques in the Pediatric Metabolic and Endocrine Laboratory. The values of fasting insulin and fasting blood glucose were multiplied and divided by 22.5 to determine the value of HOMA-IR with a cut-off value ≥ 2.93 for both sexes [21]. Blood samples from all subjects were obtained after a 12-h overnight fast, and the supernatants were separated after centrifugation at room temperature at 2400 × g for 10 min and stored in a − 80 °C refrigerator for further assays. The serum serpinB1 level of each sample was measured twice utilizing a commercially available ELISA according to the manufacturer’s recommendations (CUSABIO, Wuhan, China; Catalogue No. CSB-EL0121065HU), with intra-assay precision and inter-assay precision < 8% and < 10%, respectively.

Statistical analysis

Results are displayed as mean ± standard deviation (SD) or median (interquartile range) according to data distribution. The assessments of various data distributions were done with the Shapiro‒Wilk test. For the analysis of variables in two groups, the unpaired two-tailed Student’s t-test was done for the comparison of normally distributed variables, whereas the Mann‒Whitney U test was applied to compare variables with nonnormal distribution. Differences in categorical variable were tested utilizing Chi-square test. Multiple groups of normally distributed data were analyzed by analysis of variance (ANOVA), followed by Bonferroni’s post hoc test. Simple linear correlations between variables were assessed by Pearson’s correlation analysis or Spearman’s rank correlation analysis according to data distribution. Binary logistic regression models with odds ratio (OR) and 95% confidence interval (CI) were employed to assess the likelihood of using serum serpinB1 levels to predict the risk of overweight and obesity in children and further adjusting for possible confounding effects of age, sex, and HOMA-IR. IBM SPSS version 25.0 was applied for all the statistical analyses, and a p-value (two-tailed) < 0.05 was considered statistically significant.

Results

Comparison of group characteristics

The clinical characteristics and biochemical data of the participating children are presented in Table 1. In the overweight/obese group, the characteristic parameters of obesity such as BMI Z-score, TG, TC, LDL-C, uric acid, as well as the ratios of TC/HDL-C and LDL-C/HDL-C were significantly higher than those in the normal-weight group. In addition, there were also remarkable differences in the levels of fasting insulin, C-peptide, HbA1c, HOMA-IR, luteinizing hormone (LH), and follicle-stimulating hormone (FSH) between the two groups.

Table 1 Clinical and laboratory characteristics of children with normal weight and overweight/obesity
Full size table

Circulating serpinB1 levels were increased in children with overweight/obesity

Strikingly, serum serpinB1 levels were notably greater in overweight/obese children than in normal-weight healthy controls (2.03 ± 0.70 vs. 1.41 ± 0.58 ng/mL, p < 0.001; Fig. 1-a). Afterward, all subjects were classified into three groups according to BMI (parameters comparisons among the three subgroups are shown in Table S1), and serpinB1 levels in both groups were markedly different from those in the obese group (normal weight vs. obese: 1.41 ± 0.58 vs. 2.29 ± 0.75 ng/mL, p < 0.001; overweight vs. obese: 1.71 ± 0.45 vs. 2.29 ± 0.75 ng/mL, p = 0.002; Fig. 1-b), while normal weight group did not show any difference from the overweight group. In adults, serum serpinB1 levels have been reported to be associated with insulin sensitivity [8, 22]. Hence, we classified overweight/obese subjects into insulin-resistant (IR) (n = 13) and non-insulin-resistant (non-IR) (n = 41) subgroups to explore whether there were variations in serpinB1 levels between the two groups. However, serpinB1 levels in IR subjects showed no remarkable difference compared to those in non-IR subjects (1.90 ± 0.72 vs. 2.07 ± 0.69 ng/mL, p > 0.05, Fig. 1-c). Furthermore, we studied the effect of gender on serpinB1 levels. No significant variation was seen between boys and girls within either the normal weight or the overweight/obese groups, as shown in Fig. 1-d.

Fig. 1
figure 1

Circulating serpinB1 levels in each subgroup. (a) SerpinB1 levels in overweight/obese children (n = 54) compared to those in normal-weight controls (n = 36). (b) Comparison of serpinB1 levels in the normal weight (n = 36), overweight (n = 25), and obese (n = 29) groups. (c) SerpinB1 levels in the non-IR overweight/obese (n = 41) and IR-overweight/obese groups (n = 13). (d) Comparison of serpinB1 levels between boys and girls in the normal-weight control and overweight/obese groups. The data were shown as the mean ± SD. *p < 0.05, **p < 0.01, ***p < 0.001, NS, nonsignificant

Full size image

Correlations between circulating serpinB1 levels and various parameters

Moreover, we performed simple linear correlation analyses to study the relationships of serpinB1 with age, BMI, BMI Z-score, plasma lipid profiles, uric acid, glucose metabolism parameters, and sex hormones in all subjects (Table S2). Notably, we observed that serpinB1 levels had significant moderate correlations with BMI (r = 0.456, p < 0.001; Fig. 2-a) and BMI Z-score (r = 0.465, p < 0.001; Fig. 2-b). Additionally, it also showed relatively weak positive correlation correlations between the levels of serpinB1 and TG (r = 0.280, p = 0.007; Fig. 2-c), uric acid (r = 0.257, p = 0.015; Fig. 2-d), fasting insulin (r = 0.339, p = 0.001; Fig. 2-e), C-peptide (r = 0.362, p < 0.001; Fig. 2-f), and HOMA-IR (r = 0.327, p = 0.002; Fig. 2-g). Nevertheless, no correlations were found between serpinB1 and age, fasting glucose, TC, LDL-C, HDL-C, HbA1c, the ratios of TC/HDL-C or LDL-C/HDL-C, or sex hormones. The above results further suggested that serum serpinB1 levels were associated with obesity-related lipid metabolic and insulin sensitivity parameters in recruited children.

Fig. 2
figure 2

Simple linear correlation analysis between serpinB1 levels and clinical and biochemical parameters. SerpinB1 levels were positively associated with body mass index (BMI), BMI Z-score, triglyceride (TG), uric acid, fasting insulin, C-peptide, and homeostasis model assessment of insulin resistance (HOMA-IR) in all subjects. (a) BMI, r = 0.456, p < 0.001; (b) BMI Z-score, r = 0.465, p < 0.001; (c) TG, r = 0.280, p = 0.007; (d) uric acid, r = 0.257, p = 0.015; (e) fasting insulin, r = 0.339, p = 0.001; (f) C-peptide, r = 0.350, p = 0.001; and (g) HOMA-IR, r = 0.327, p = 0.002

Full size image

Association between serum serpinB1 levels and the risk of overweight/obesity in children

Binary logistic regression models were established to further explore the association between serum serpinB1 concentration and the risk of overweight/obesity in children. As shown in Table 2, serum serpinB1 concentration was significantly associated with overweight/obesity (OR, 5.181; 95% CI, 2.162–12.419; p < 0.001). This positive correlation persisted after adjusting for potential confounding factors such as age and sex (OR, 4.791; 95% CI, 2.004–11.452; p < 0.001). Furthermore, after additionally adjusting for the confounding factors of age, sex and HOMA-IR, serum serpinB1 levels remained independently associated with overweight/obesity (OR, 4.132; 95% CI, 1.315–12.983; p = 0.015).

Table 2 Association between serum serpinB1 concentrations and the risk of overweight/obesity
Full size table

Discussion

In this cross-sectional study, we revealed that circulating serpinB1 levels were notably greater in children with overweight/obesity than in normal-weight controls. We further studied the correlations of serpinB1 levels with obesity-related parameters in all participants, and it showed that serpinBl had moderate positive correlations with BMI and BMI Z-score and relatively weak positive correlations with TG, uric acid, fasting insulin, C-peptide, and HOMA-IR levels. This suggests that circulating serpinB1 concentrations are related to childhood overweight/obesity.

Childhood obesity not only persists into adulthood but also contributes to a series of chronic diseases, such as diabetes, cardiac-cerebral vascular diseases, fatty liver disease, and psychological and social comorbidities [23, 24]. Obesity-related abnormal lipid metabolism can cause insulin resistance and compensatory β-cell proliferation, and the failure of compensatory beta-cell responses eventually leads to T2DM [25]. The precise mechanisms that trigger compensatory β-cell expansion and subsequent decompensation of β-cell are still unknown. SepinB1, as a newly discovered hepatocyte-derived circulating protein, has been recently shown to stimulate β-cell proliferation and augment pancreatic islet mass [5, 6]. Therefore, exploring the level of serpinB1 in obese individuals and its correlation with metabolic parameters may provide new directions for the intervention of childhood obesity and T2DM.

Previously, Takebayashi et al. [6] revealed that the circulating serpinB1 level was significantly elevated in adult patients with T2DM, while Kamal et al. [7] and Kyohara et al. [8] reported that the serpinB1 level was significantly reduced in adults with T2DM. Moreover, the associations between serum serpinB1 levels and glycemic and lipid profile parameters in adults have been inconsistent in previous studies [5,6,7,8]. Kamal et al. [7] suggested that these opposite or inconsistent findings can be explained by differences in patient characteristics, treatment regimens, and ethnicity. However, we considered that overweight/obesity may be a significant factor contributing to the discrepancies in the conclusions of these studies. This is particularly relevant as the degree of overweight or obesity among T2DM patients varied across studies; for instance, Takebayashi et al. reported a significant difference in BMI between their control group and T2DM group (21.2 ± 2.5 vs. 25.5 ± 5.0, p < 0.05), whereas Kamal et al. found no significant difference in BMI (29.5 ± 0.81 vs. 30.98 ± 0.57, p > 0.05). In our study, we observed that circulating serpinB1 levels were significantly elevated in overweight/obese children without diabetes, and these levels were positively correlated with BMI and obesity-related metabolic parameters. In light of the established role of serpinB1 in promoting beta-cell proliferation, along with findings suggesting enhanced β-cell mass in obese individuals, we considered that serpinB1 may be associated with the compensatory β-cell proliferation process in overweight/obese individuals.

To our knowledge, studies investigating the association between serpinB1 and obesity are scarce, and the exact molecular mechanisms underlying the interplay between serpinB1 and obesity need to be further studied. Chronic low-grade adipose tissue inflammation is the main cause of systemic insulin resistance and obesity-related metabolic disorders [26]. Some studies have shown that neutrophils can promote inflammatory responses by secreting neutrophil elastase, and the deletion of neutrophil elastase in obese mice can reduce tissue inflammation and improve glucose tolerance [14, 27]. As serpinB1 is a neutrophil elastase inhibitor, serpinB1 may decrease systemic inflammation and insulin resistance in subjects with obesity by inhibiting neutrophil elastase rather than merely by directly promoting β-cell proliferation. As serpinB1 is also abundantly present in the cytoplasm of neutrophils [12, 28], the increased serpinB1 serum levels may be a sign of enhanced lytic neutrophil death or inflammation associated with metabolic disease. Future related studies may need to trace the source of serum serpinB1 and consider the relationship between inflammatory markers and circulating levels of serpinB1. Moreover, current studies on serum serpinB1 concentrations utilizing ELISA or proteomic mass spectrometry analysis are unknown whether the detected serpinB1 is native or other forms of serpinB1 (in a covalent complex with a target protease, or in post complex form). Further studies detecting different forms of serpinB1 might help understand the functional roles of serpinB1 and its association with various physiological and pathological states.

Our study has several limitations. First, the sample size was relatively small, and the age range of children involved in the study was narrow, which may not represent the broader population of children and adolescents. Second, we identified overweight and obesity based on BMI; due to technical constraints, we did not obtain data on fat distribution closely related to obesity complications through CT or MRI measurements [29, 30]. Furthermore, this study was a cross-sectional study and could not determine the causal relationship between serpinB1 and overweight/obesity.

Conclusions

This study revealed that the circulating serpinB1 levels were significantly increased in children with overweight/obesity and were positively correlated to obesity-related traits (BMI, BMI Z-score, TG, and uric acid) and glycemic control parameters (fasting insulin, C-peptide, and HOMA-IR). Although this study provides preliminary evidence for the correlation between serum serpinB1 levels and the risk of overweight/obesity in children, the interaction mechanisms between serpinB1 and obesity require further investigation.

Data availability

No datasets were generated or analysed during the current study.

Abbreviations

BMI:

Body Mass Index

TG:

Triglyceride

HOMA-IR:

Homeostasis Model Assessment of Insulin Resistance

T2DM:

Type 2 Diabetes Mellitus

HFD:

High-Fat Diet

LDL-C:

Low-Density Lipoprotein Cholesterol

TC:

Total Cholesterol

HbA1c:

Glycated Haemoglobin A1c

HDL-C:

High-Density Lipoprotein Cholesterol

FSH:

Follicle-Stimulating Hormone

LH:

Luteinizing Hormone

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Funding

This work was supported by the National Key Research and Development Program of China (2023YFC2706300).

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Authors and Affiliations

  1. Department of Pediatrics, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China

    Qing Li, Zhuxi Li, Shusen Guo, Sujuan Li, Minglan Yao, Yingying Li & Xiaoping Luo

  2. Hubei Key Laboratory of Pediatric Genetic Metabolic and Endocrine Rare Diseases, Wuhan, China

    Xiaoping Luo

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Contributions

Q.L. collected sample data and drafted the manuscript. Z.X.L. and S.S.G. concepted the study and conducted data analysis S.J.L., M.L.Y. and Y.Y.L. reviewed and discussed the results. X.P.L. revised the paper. All authors reviewed the manuscript.

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Correspondence to Xiaoping Luo.

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Ethics approval and consent to participate

The ethics committee of Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology (TJ-IRB20201016) approved this cross-sectional study. Written informed consent was obtained from parents/guardians for all minor participants.

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Not applicable.

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The authors declare no competing interests.

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Li, Q., Li, Z., Guo, S. et al. Increased circulating serpinB1 levels in children with overweight/obesity are associated with obesity-related parameters: a cross‑sectional study. BMC Pediatr 24, 762 (2024). https://doiorg.publicaciones.saludcastillayleon.es/10.1186/s12887-024-05251-7

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BMC Pediatrics

ISSN: 1471-2431

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