Phytochemical reports demonstrate that conifer wood has high lignan content in wood knots. The great common occurrence of conifers in Europe as well as their use in the wood industry makes both plant material and industrial waste material easily accessible and inexpensive. This is a promising prognosis for both discovery of new active compounds as well as for finding new applications for wood and its industry waste products. Polyphenols may reduce the risk of many chronic diseases including type 2 diabetes mellitus. In this context, lignans are likely good candidates to potentially regulate factors implicated in T2D pathophysiology notably insulin secretion defect and inflammation. The aim of this study was to isolate lignans from the conifer wood and to assess their effects on insulin secretion and inflammation modulation. Material and methods: Plant material was collected from the Polish Academy of Sciences Botanical Garden, Powsin, Poland, from which lignans were isolated. The effects of lignans on insulin secretion were assessed on the INS-1 β-cell line. Anti-inflammatory effects of lignans were studied on activated THP-1 cells and macrophages isolated from human peripheral blood by assessing IL-6, TNF-α, and IL-1β concentrations. Results: Eight lignans were isolated from conifer wood and chemically characterized: nortrachelogenin, pinoresinol, and matairesinolfrom Scots pine; secoisolariciresinol, lariciresinol, 7-hydroxylariciresinol, 7-hydroxymatairesinol andcyclolariciresinol from silver fir. These compounds did not modulate basal (1.4mM glucose) nor 8.3mM glucose-induced insulin secretion in the pancreatic beta cells. On the other hand, these compounds reduced the secretion of LPS-induced pro-inflammatory cytokines secretion in macrophages. Discussion/Conclusion: The isolated compounds did not modulate insulin secretion, suggesting that lignans are not able to activate pharmacological targets involved in insulin secretion. On the other hand, lignans present anti-inflammatory properties suggesting that they may modulate inflammation-induced beta cell dysfunction; a hypothesis that should be tested later.