Objective: Upper body obese (UBO) subjects have greater cardiovascular disease (CVD) risk than lower body obese (LBO) or lean. Obesity is also associated with hypertriglyceridemia that may involve greater production and impaired removal of Very-Low-Density-Lipoprotein-Triglycerides (VLDL-TG). In these studies we assessed the impact of body composition on basal VLDL-TG production, VLDL-TG oxidation, and VLDL-TG storage. Research design and methods: VLDL-TG kinetics were assessed in 10 UBO, 10 LBO, and 10 lean women using a bolus injection of [1-14C]VLDL-TG. VLDL-TG oxidation was measured by 14CO2 production (hyamine trapping) and VLDL-TG adipose tissue storage by fat biopsies. Insulin sensititvity was assessed by the hyperinsulinemic-euglycemic clamp technique and body composition by dual X-ray absorptiometry in combination with computed tomography. Results: Hepatic VLDL-TG production was significantly greater in UBO than in lean women [(µmol/min) UBO: 64.8 (SD 40.0) vs. LBO: 42.5 (SD 25.6) vs. lean: 31.8 (SD 13.3), p=0.04], whereas VLDL-TG oxidation was similar in the three groups and averaged 20% of resting energy expenditure [(µmol/min) UBO: 38.3 (SD 26.5) vs. LBO: 23.5 (SD 13.5) vs. lean: 21.1 (SD 9.7), p=0.09]. In UBO women more VLDL-TG was deposited in upper body subcutaneous fat (UBSC) [VLDL-TG redeposition in abdominal adipose tissue (µmol/min): UBO: 5.0 (SD 2.9) vs. LBO: 4.0 (SD 3.2) vs. Lean: 1.3 (SD 1.0), ANOVA p = 0.01]; in LBO women more VLDL-TG was deposited in femoral fat [VLDL-TG redeposition in femoral adipose tissue (µmol/min): UBO: 5.1 (SD 3.1) vs. LBO: 5.8 (SD 4.3) vs. Lean: 2.3 (SD 1.5), ANOVA p = 0.04]. Only a small proportion of VLDL-TG (8-16 %) was partitioned into redeposition in either group. Conclusion: Elevated VLDL-TG production without concomitant increased clearance via oxidation and adipose tissue redeposition contribute to hypertriglyceridemia in UBO women.