Emerging Roles of Asprosin and Nesfatin-1 in Uncontrolled Type 2 Diabetes

• Al-Khazraji

  College of Science, Diyala University

  Author

  https://orcid.org/0000-0003-3453-9031 (unauthenticated)

• Rihab Mansoor

  College of Science, Diyala University

  Author

  https://orcid.org/0009-0003-7210-3447 (unauthenticated)

• Shahad Alwan

  College of Science, Diyala University

  Author

  https://orcid.org/0000-0003-0988-997X (unauthenticated)

• Anfal Abed

  College of Science, Diyala University

  Author

  https://orcid.org/0000-0001-9866-8356 (unauthenticated)

• Alaa Mahmoud

  Department of Medical Laboratory Technologies, Al-Amarah University College, Iraq

  Author

  https://orcid.org/0000-0003-2014-5795 (unauthenticated)

• Safaa Ahmed

  College of Science, Diyala University

  Author

  https://orcid.org/0009-0009-3343-4124 (unauthenticated)

The global surge in diabetes and obesity underscores the role of adipokines. Asprosin disrupts glucose homeostasis, while nesfatin-1 may offer protective effects. This study investigated their serum levels in poorly controlled T2DM and associations with hyperglycemia and obesity. The study included 110 type 2 diabetes patients and 70 healthy controls, aged 40–70 years. Fasting plasma glucose (FPG) and glycated hemoglobin (HbA1c) were measured using the Roche Cobas Integra 400 Plus. Serum asprosin and nesfatin-1 levels were quantified by ELISA, and body mass index (BMI) was calculated as weight/height². T2DM patients exhibited significantly higher serum levels of asprosin and nesfatin-1 compared to controls (p < 0.001). A significant positive correlation was observed between asprosin and nesfatin-1, as well as between nesfatin-1 and disease duration (p = 0.01). Serum asprosin was strongly associated with glucose levels, whereas neither biomarker showed a significant correlation with BMI. Elevated asprosin and nesfatin-1 levels in poorly controlled T2DM patients contribute to disease mechanisms. Increased nesfatin-1 represents a compensatory mechanism to mitigate insulin deficiency, highlighting its potential as a predictive biomarker.

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