Secreted human adipose leptin decreases mitochondrial respiration in HCT116 colon cancer cells.

ABSTRACT: Obesity is a key risk factor for the development of colon cancer; however, the endocrine/paracrine/metabolic networks mediating this connection are poorly understood. Here we hypothesize that obesity results in secreted products from adipose tissue that induce malignancy-related metabolic alterations in colon cancer cells. Human HCT116 colon cancer cells, were exposed to conditioned media from cultured human adipose tissue fragments of obese vs. non-obese subjects. Oxygen consumption rate (OCR, mostly mitochondrial respiration) and extracellular acidification rate (ECAR, mostly lactate production via glycolysis) were examined vis-à-vis cell viability and expression of related genes and proteins. Our results show that conditioned media from obese (vs. non-obese) subjects decreased basal (40

SUBMITTER: Yehuda-Shnaidman E 

PROVIDER: S-EPMC3779244 | biostudies-literature | 2013

REPOSITORIES: biostudies-literature