The increased adipose tissue mass of obese individuals enhances the risk of metabolic syndrome, type 2 diabetes and cardiovascular diseases. During pathological expansion of adipose tissue, multiple molecular controls of lipid storage, adipocyte turn-over and endocrine secretion are perturbed and abnormal lipid metabolism results in a distinct lipid profile. There is a role for ceramides and sphingosine 1-phosphate (S1P) in inducing adipose dysfunction. For instance, the alteration of ceramide biosynthesis, through the de-regulation of key enzymes, results in aberrant formation of ceramides (e.g. C_16:0 and C_18:0) which block insulin signaling and promote adipose inflammation. Furthermore, S1P can induce defective adipose tissue phenotypes by promoting chronic inflammation and inhibiting adipogenesis. These abnormal changes are discussed in the context of possible therapeutic approaches to re-establish normal adipose function and to, thereby, increase insulin sensitivity in type 2 diabetes. Such novel approaches include blockade of ceramide biosynthesis using inhibitors of sphingomyelinase or dihydroceramide desaturase and by antagonism of S1P receptors, such as S1P₂.

肥胖个体脂肪组织量的增加增加了代谢综合症，2型糖尿病和心血管疾病的风险。在脂肪组织的病理学扩展过程中，脂质存储，脂肪细胞周转和内分泌分泌的多种分子控制受到干扰，异常的脂质代谢导致不同的脂质分布。神经酰胺和鞘氨醇1-磷酸（S1P）在诱导脂肪功能异常中起作用。例如，通过关键酶的失调，改变神经酰胺的生物合成，会导致神经酰胺的异常形成（例如C _16：0和C _18：0），可阻断胰岛素信号传导并促进脂肪炎症。此外，S1P可通过促进慢性炎症和抑制脂肪形成而诱导脂肪组织表型缺陷。在可能的治疗方法中讨论这些异常变化，以重建正常的脂肪功能，从而增加2型糖尿病的胰岛素敏感性。这样的新方法包括使用鞘磷脂酶或二氢神经酰胺去饱和酶的抑制剂以及对S1P受体（例如S1P _2）的拮抗作用来阻断神经酰胺的生物合成。