Nesfatin-1 and pancreatic β-cells in hypertension with abdominal obesity: implications for dysglycemia

Hypertension and obesity are often accompanied with insulin resistance, predisposing individuals to carbohydrate metabolism disorders, and emphasizing the critical role of pancreatic β‑cells in glucose regulation. The escalating incidence of diabetes worldwide underscores the urgency for innovative preventive and treatment strategies. Nesfatin‑1, detected in pancreatic islets and associated with glucose metabolism, emerges as a promising focus of research, with studies suggesting its potential influence on β‑cell function and insulin secretion. However, variations in findings warrant further investigation into its mechanisms and clinical implications. Objective — to investigate the relationship between plasma nesfatin‑1 levels and pancreatic β‑cell functionality in patients with concomitant hypertension and abdominal obesity. Materials and methods. The study included 43 hospitalized hypertension patients, divided into three groups by hypertension and abdominal obesity status. Diagnosis of hypertension followed European Society of Cardiology guidelines; abdominal obesity criteria were defined by WHO recommendations according to the waist‑to‑hip ratio calculated. Glucometabolic profile assessment included fasting and postprandial glucose levels, insulin levels, HOMA‑IR index, and HOMA‑β index calculation. Plasma nesfatin‑1 levels were determined via ELISA. Inclusion criteria involved the absence of prediabetes and type 2 diabetes. Statistical analysis was performed using non‑parametric methods, with significance set at p <0.05. Results. The occurrence of hypertension demonstrated a twofold increase in nesfatinemia levels (p <0.001). However, a subsequent reduction in nesfatinemia may be attributed to the presence of concurrent abdominal obesity (p=0.04), likely owing to the anorexigenic characteristics of the peptide. Our study reveals a positive correlation between nesfatin‑1 levels and key carbohydrate metabolism indicators, including fasting glucose (p=0.04), insulin (p=0.003), and HOMA‑IR index (p=0.002), particularly pronounced in patients with comorbid pathology. In contrast, hypertensive patients with normal body constitution showed a tendency towards an inverse association. Furthermore, a significant correlation between nesfatin‑1 levels and the HOMA‑β index across the entire patient cohort (p=0.001) underscores the peptide’s potential involvement in glucose homeostasis regulation. Conclusions. Nesfatin‑1 displays diverse effects including prohypertensive action and glucose‑dependent insulinotropic activity mediated through pancreatic β‑cells. However, its capacity to modulate pancreatic function in cases of dysfunction is constrained due to multifactorial influences on nesfatinemia levels and its predominantly localized impact on carbohydrate metabolism regulation. While its potential as a pharmacological agent is limited, nesfatin‑1 emerges as a promising marker for diagnosing and preventing dysglycemic disorders, necessitating further extensive clinical investigation.