Beta-cell function and insulin resistance among First-Degree relatives of persons with type 2 diabetes in a Northwestern Nigerian Population

Background and Aims: Pancreatic beta-cell deficit and insulin resistance (IR) form two major factors in the etiopathogenesis of type 2 diabetes. The aim of this study is to assess beta-cell function and IR among first-degree relatives (FDRs) of persons with type 2 diabetes in a Northwestern Nigerian population. Other objectives include assessing the relationships among HOMA-%B, HOMA-IR, plasma glucose levels, and some obesity indices and to determine whether beta cell function, IR, and some obesity indices are independent determinants of glucose intolerance in the studied population. Materials and Methods: A total of 200 individuals and 200 controls were recruited through cluster sampling from their respective communities after due consent. The relevant biodata was documented and appropriate examinations including anthropometric measurements were carried out. Oral glucose tolerance test was carried out and fasting plasma insulin levels were also measured. IR and beta-cell function were calculated using homeostasis model assessment (HOMA) method. Results: Mean HOMA-IR was higher while HOMA-% B lower among FDRs compared to controls. Significant independent determinants of glucose intolerance with odds ratio (OR) and confidence interval (CI) included age (OR = 1.9, CI 1.9–2.0, P = 0.002), body mass index (OR = 1.9, CI 1.8–2.0, P = 0.032), waist circumference (OR = 2.0, CI 1.9–2.0, P = 0.043), waist-to-hip ratio (OR = 1.1, CI 1.0–15.7, P = 0.022), HOMA-IR (OR = 3.0, CI 2.3–3.3, P < 0.001), and HOMA-B (OR = 0.43, CI 0.24–0.65, P < 0.001) which means HOMA-%B is protective against glucose intolerance with inverse OR of 1/0.43 = 2.3. Conclusions: IR was higher and beta cell functions lower among FDRs compared to controls. IR (HOMA-IR) and some obesity indices were significant determinants of glucose intolerance while HOMA-%B was protective against glucose intolerance in this study.