Visceral Adiposity Index in prediabetes and diabetes: The Polish Norwegian Study (PONS)

Prediabetes (preDM) is associated with an increased risk for progression to diabetes (DM). Visceral adiposity has been associated with diabetes and atherosclerosis, yet controversy exists about its measurement at population level. The Visceral Adiposity Index (VAI) has been proposed as a surrogate marker of visceral adiposity dysfunction. Purpose to compare VAI score between individuals with normal, impaired and abnormal glucose levels. Methods Cross‐sectional data of 12636 participants, age 45 to 64 years, in an ongoing cohort study, with structured questionnaires and fasting blood samples. We classified glucose control in three categories: normal (no DM and fasting glucose <100 mg/dL), impaired fasting glucose (IFG, no DM and fasting glucose between 100–125.9 mg/dL) and diabetes (history of diabetes or antidiabetic medication or fasting glucose >= 126 mg/dL). VAI score was based on the Amato sex‐specific formulae. Multivariable regression analysis was conducted using general linear and logistic models. Results The prevalence of IFG and or/DM was 34.60% and 11.24% respectively in men, and 21.04% and 6.83% in women. Across the optimal‐IFG‐DM spectrum, we found a statistically significant gradual increase in age, poor education, smoking, alcohol intake, prevalent cardiovascular disease, dyslipidemia, statin use, systolic and diastolic blood pressure, BMI and waist circumference. For the optimal‐IFG‐DM categories, VAI score averages (95% CI), adjusted for age, education, smoking, alcohol, prevalent cardiovascular disease, statin use and blood pressure were 3.36 (3.30–3.42), 4.18 (4.08–4.28) and 5.36 (5.18–5.52) respectively. Among those without diabetes, each one‐unit increase in the VAI index increased the odds of IFG by 1.13 (95% CI 1.12–1.15). Conclusion VAI is independently associated with IFG/prediabetes and diabetes status. Potential implications: identification of prediabetes and IFG individuals with increased VAI may guide targeted aggressive prevention interventions. Support or Funding Information The data collection was supported by a grant from the Polish‐Norwegian Research Fund (PNRF‐228‐AI‐1/07