Abstract
Secretogranin III (SCG3) plays a crucial role in the biogenesis of secretory granules in endocrine cells, and thus affects glucose homeostasis by regulating insulin secretion by pancreatic beta cells. Insulin resistance and compensatory hyperinsulinemia are hallmarks of metabolic syndrome (MetS). However, the role of SCG3 in MetS remains unclear. Therefore, we investigated the relationship between serum SCG3 levels and metabolic parameters in subjects with and without MetS. This was a case control study, and 295 subjects were recruited. Serum SCG3 concentrations were compared between groups. Associations between SCG3 levels and clinico-metabolic parameters were also examined. We found serum SCG3 levels were higher in the MetS group than non-MetS group (122.6 ± 79.2 vs. 90.6 ± 58.5 nmol/L, p = 0.009). Specifically, elevated SCG3 levels were found in subjects with high fasting plasma glucose (FPG) levels, central obesity, or hypertriglyceridemia. Additionally, MetS was an independent factor of serum SCG3 levels in multivariate linear regression analyses. Moreover, FPG, free fatty acids, and waist circumference were positively associated with serum SCG3 concentrations after adjusting for insulin levels, high-sensitivity C-reactive protein, and cardiovascular risk factors. In conclusion, serum SCG3 concentrations were higher in subjects with MetS and were independently associated with FPG levels.
Highlights
Metabolic syndrome (MetS) is a cluster of interrelated risk factors which include an elevated waist circumference (WC), hypertriglyceridemia, reduced high-density lipoprotein cholesterol (HDL-C), high blood pressure, and dysglycemia [1]
90, 165, and 40 subjects were diagnosed with normal glucose tolerance, prediabetes, and diabetes, respectively, according to the results of fasting plasma glucose (FPG) and the oral glucose tolerance test (OGTT)
Of note, when we assessed SCG3 levels in patients with and those without each respective single component of MetS, higher serum SCG3 levels were only found in subjects with high FPG (120.7 ± 75.5 vs. 84.9 ± 54.7 nmol/L, p < 0.001), elevated WC (111.3 ± 69.8 vs. 90.6 ± 60.4 nmol/L, p = 0.012), or hypertriglyceridemia (115.1 ± 73.6 vs. 92.4 ± 60.4 nmol/L, p = 0.025), but not elevated blood pressure (100.0 ± 66.0 vs. 94.3 ± 62.3 nmol/L, p = 0.53) or reduced HDL-C levels (105.6 ± 66.0 vs. 94.3 ± 62.3 nmol/L, p = 0.47) (Figure 2)
Summary
Metabolic syndrome (MetS) is a cluster of interrelated risk factors which include an elevated waist circumference (WC), hypertriglyceridemia, reduced high-density lipoprotein cholesterol (HDL-C), high blood pressure, and dysglycemia [1]. It has been shown that significantly increased SCG3 levels were detected in serum-free media conditioned with non-responsive high-passage MIN-6 cells, a model of dysfunctional beta cells These data implied that secretory granules can no longer form properly, decreasing the insulin-secreting ability of beta cells, when SCG3 was massively released from, but did not remain inside, those cells [18]. Proinsulin was found to be insufficiently converted into the mature form, insulin, in islet cells, leading to hyperglycemia, in SCG3-knockout mice fed a high-fat/high-sucrose diet [19] This finding suggests the role of SCG3 in proteolytic conversion of the inactive prohormone to the active hormone [19]. We conducted a case control study to investigate the relationship between serum SCG3 levels and metabolic parameters in subjects with and those without MetS
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