Immune responses are highly energy dependent processes. Activated T cells increase glucose uptake and aerobic glycolysis to survive and function. Malnutrition and starvation limit nutrients and are associated with immune deficiency and increased susceptibility to infection. While it is clear that immunity is suppressed in times of nutrient stress, mechanisms that link systemic nutrition to T cell function are poorly understood. We show here that fasting leads to persistent defects in T cell activation and metabolism, as T cells from fasted animals had low glucose uptake and decreased ability to produce inflammatory cytokines, even when stimulated in nutrient-rich media. To explore the mechanism of this long-lasting T cell metabolic defect, we examined leptin, an adipokine reduced in fasting that regulates systemic metabolism and promotes effector T cell function. We show leptin is essential for activated T cells to upregulate glucose uptake and metabolism. This effect was cell-intrinsic and specific to activated effector T cells, as naïve T cells and Treg did not require leptin for metabolic regulation. Importantly, either leptin addition to cultured T cells from fasted animals or leptin injections to fasting animals was sufficient to rescue both T cell metabolic and functional defects. Leptin-mediated metabolic regulation was critical, as transgenic expression of the glucose transporter Glut1 rescued cytokine production of T cells from fasted mice. Together, these data demonstrate that induction of T cell metabolism upon activation is dependent on systemic nutritional status, and leptin links adipocytes to metabolically license activated T cells in states of nutritional sufficiency.

Prostate cancer most commonly metastasizes to bone, lung and liver. Omental metastasis of prostate cancer is extremely rare, with only a few cases reported in the literature, many of which have associated ascites. We present a case of non-ascitic omental metastasis of prostate cancer without any bone metastases. Furthermore, this patient has had two negative measurements of circulating tumor cells (CTCs) in the blood, suggesting a non-hematogenous route of metastasis to the omentum.

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RESULTS: Length of time on console was 267 minutes. Estimated blood loss was 50cc. Total warm ischemia time was 12 minutes and 46 seconds. There were no postoperative complications and the patient was discharged on postoperative day 2. Final pathology was T1a clear cell, renal cell carcinoma.CONCLUSIONS: RALPN in a pelvic kidney is safe and feasible. A CT angiogram obtained prior to surgery may be beneficial to delineate the altered anatomy. A technique of hitching the lateral peritoneal flap to the anterior abdominal wall may assist with bowel retraction and widen the surgical field.