The association between biological aging and type 2 diabetes mellitus (T2DM) incidence in individuals with and without metabolic dysfunction-associated steatotic liver disease (MASLD) remains unclear.We assessed biological age by calculating phenotypic age (PhenoAge), Klemera-Doubal method (KDMAge), and homeostatic dysregulation (HDAge). To examine the association of biological ageing with the risk of T2DM, cox regression models were conducted. Furthermore, we applied survival analysis, restricted cubic spline models and population attributable fraction (PAF) to further evaluate the association between biological ageing and T2DM incidence.
Abdominal ultrasound data available in annual health check-up records
Age <20 or >90 years
Other causes of hepatic steatosis (e.g., alcoholic liver disease or hepatitis B infection)
Type 2 diabetes mellitus at baseline
Missing baseline data for any of the following variables: systolic blood pressure, albumin, alkaline phosphatase, blood urea nitrogen, creatinine, glycated hemoglobin (HbA1c), total cholesterol, lymphocyte percentage, white blood cell count, mean corpuscular volume, uric acid, fasting plasma glucose, and red cell distribution width (RDW)
This retrospective cohort study is based on physical examination at the Physical Examination Center of The First Affiliated Hospital of Ningbo University and included participants aged 20 to 90 years. Individuals included had available abdominal ultrasound data and at least one recorded metabolic indicator per year. Participants with type 2 diabetes at baseline or with other causes of hepatic steatosis were excluded. The study population was categorized into MASLD and non-MASLD groups for comparative analysis.
Cohort
Retrospective
Observational
Other interventionObservational
Incidence of onset T2DM
Click on the lead sponsor to view all of their trials.
