Early suppression of adipocyte lipid turnover induces immunometabolic modulation in cancer cachexia syndrome [Research]

Cancer cachexia is a multifactorial syndrome characterized by body weight loss, atrophy of adipose tissue (AT) and systemic inflammation. However, there is restrict information regarding the mechanisms of immunometabolic response in AT from cancer cachexia. Male Wistar rats were inoculated with 2 x 10⁷ of Walker 256 tumor cells [tumor bearing (TB)]. The mesenteric AT (MeAT) was collected on d 0, 4, 7 (early stage), and 14 (cachexia stage) after tumor cell injection. Surgical biopsies for MeAT were obtained from patients who had gastrointestinal cancer with cachexia. Lipolysis showed an early decrease in glycerol release in TB d 4 (TB4) rats in relation to the control, followed by a 6-fold increase in TB d 14 (TB14), whereas de novo lipogenesis was markedly lower in the incorporation of glucose into fatty acids in TB14 during the development of cachexia. CD11b and CD68 were positive in TB rats (d 7 and 14, respectively). In addition, we found cachexia stage results similar to those of animals in MeAT from patients: an increased presence of CD68⁺, iNOS2⁺, TNFα⁺, and HSL⁺ cells. In summary, translational analysis of MeAT from patients and animal model of cancer cachexia enabled us to identify early disruption in Adl turnover and subsequent inflammatory response during the development of cancer cachexia.—Henriques, F. S., Sertié, R. A. L., Franco, F. O., Knobl, P., Neves, R. X., Andreotti, S., Lima, F. B., Guilherme, A., Seelaender, M., Batista, M. L., Jr. Early suppression of adipocyte lipid turnover induces immunometabolic modulation in cancer cachexia syndrome.

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