Influences on lipid metabolism and multi-generational obesogenic effects raised new concerns on lipophilic pollutants (e.g., lindane). Yet, the mechanisms remained unanswered. The present study exposed Caenorhabditis elegans to lindane for 4 consecutive generations (F0 to F3) at 1.0 ng/L, and measured effects in the directly exposed generations (F0 to F3), indirectly exposed ones (T1 and T1′) and un-exposed ones (T3 and T3′). Lindane stimulated fat storages in all generations. At the biochemical level, lindane stimulated both acetyl-CoA carboxylase (ACC) and carnitine palmitoyl-transferases (CPT) in F0, T1 and T2, while inhibited them in F3, T1′ and T3′, demonstrating the balance between fatty acid synthesis and its depletion toward fat accumulation over generations. Moreover, lindane caused different effects on insulin among generations. It inhibited insulin in F0 and F3 and exhibited consistent effects on the expression changes of daf-2, sgk-1 and daf-16 genes in insulin-like signal pathway. Lindane also inhibited insulin in T1 and T3 but exhibited consistent effects on the expression changes of daf-2, akt-1 and daf-16. Different roles of sgk-1 and akt-1 indicated the response strategies from tolerance (F0 and F3) to avoidance (T1 and T3). Lindane stimulated insulin in T1′ and T3′ and exhibited consistent effects on expression changes of daf-2, sgk-1 and daf-16 genes that were similar in F0 and F3.

对脂质代谢和多代致肥胖作用的影响引起了对亲脂性污染物（如林丹）的新关注。但是，这些机制仍未得到答复。本研究暴露了秀丽隐杆线虫在1.0 ng / L下连续4代（F0至F3）转化为林丹，并测量了直接暴露的代（F0至F3），间接暴露的代（T1和T1'）和未暴露的代（T3和T3' ）。林丹世代相传刺激了脂肪的储存。在生化水平上，林丹刺激F0，T1和T2中的乙酰辅酶A羧化酶（ACC）和肉碱棕榈酰转移酶（CPT），同时在F3，T1'和T3'中抑制它们，证明了脂肪酸合成与它消耗了几代人的脂肪。而且，林丹世代之间对胰岛素造成了不同的影响。它抑制F0和F3中的胰岛素，并且对daf-2，sgk-1和daf-16的表达变化具有一致的作用。基因在胰岛素样信号通路中。林丹也抑制T1和T3中的胰岛素，但对daf-2，akt-1和daf-16的表达变化表现出一致的作用。sgk-1和akt-1的不同作用表明了从耐受性（F0和F3）到回避（T1和T3）的响应策略。林丹刺激T1'和T3'中的胰岛素，并且对daf-2，sgk-1和daf-16基因在F0和F3中相似的表达变化表现出一致的影响。