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The direct effects of exercise on white adipose tissue morphology and metabolic function remain unclear, due in large part to confounding effects of the reduction in fat mass that often accompanies exercise training. The purpose of this study was to determine if a session of endurance exercise could impact the rate of adipogenesis. Eight lean, healthy human subjects performed a single session of exercise (1 hour of endurance exercise at 65% of their maximal aerobic capacity; VO2max). Blood samples were collected without prior exercise (No-EX) and immediately after exercise (EX). Serum was extracted, and human adipocyte precursor cells were incubated for 72 hours in vitro in either the No-EX or EX serum. This serum preincubation was immediately followed by a standard 14-day differentiation protocol. On both days 3 and 9 of differentiation, mRNA expression levels of differentiation markers, PPARG and FABP4, were significantly greater (P In summary, factors released into the circulation during and/or immediately after a session of endurance exercise can accelerate the rate of differentiation in human adipocyte precursor cells. Enhanced adipogenic signaling in response to exercise may have metabolic health benefits by priming adipose tissue for a more effective energy storage during periods of weight gain. Disclosure P. Varshney: None. L.M. Guth: None. C.M. Anderson: None. A. Raajendiran: None. M.J. Watt: None. J.F. Horowitz: Research Support; Self; American Diabetes Association. Funding National Institutes of Health (R01DK077966, T32DK101357)

High body iron stores are positively related to insulin resistance in humans, but the underlying mechanisms remain unresolved. Iron stimulates lipolysis in murine adipocytes in vitro, but the influence of iron stores on lipolytic rate in vivo is unknown. Our aim was to determine if body iron stores are associated with lipolytic rate and whole-body insulin sensitivity in obese, pre-menopausal women. We studied 20 subjects with clinically-normal (20-200 ng/mL) plasma [ferritin], an index of body iron stores. Fatty acid rate of appearance into systemic circulation (FA Ra) was assessed by 13C-palmitate isotope dilution, insulin resistance was assessed by hyperinsulinemic-euglycemic clamp, and abdominal subcutaneous adipose tissue protein expression was assessed via immunoblot. [Ferritin] was significantly (p < 0.01), positively correlated with FA Ra (r2 = 0.42), adipose hormone sensitive lipaseser660 phosphorylation (p-HSLser660, a marker of lipolytic activation in adipose tissue; r2 = 0.41), and whole-body insulin resistance (r2 = 0.33). Importantly, [ferritin] remained a significant, independent predictor for these parameters in multiple regression models including body mass index, plasma [adiponectin], and plasma [CRP] as covariates. We stratified subjects into tertiles based on [ferritin] to compare high-normal and low-normal [ferritin] groups (138 ± 30 vs. 40 ± 15 ng/mL). Compared with the low-normal [ferritin] group, the high-normal [ferritin] group had significantly (p < 0.02) higher FA Ra (15.6 ± 5.5 vs. 8.8 ± 2.4 µmol/kg fat mass/min), adipose p-HSLser660 (1.3 ± 0.4 vs. 0.6 ± 0.2 AU) and whole-body insulin resistance (glucose infusion rate 9.2 ± 2.3 vs. 14.3 ± 3.5 mg/kg fat free mass/min). There were no between-group differences in anthropometric characteristics, plasma [adiponectin], or plasma [CRP]. Our findings suggest that iron-mediated activation of adipose lipolysis may be a mechanism linking body iron stores and insulin resistance in obese humans. Disclosure B.J. Ryan: None. D.W. Van Pelt: None. L.M. Guth: None. A. Ludzki: None. R.A. Gioscia-Ryan: None. C. Ahn: None. J.F. Horowitz: None.