An impaired fat oxidation has been implicated to play a role in the et
iology of obesity, but it is unclear to what extent impaired fat mobil
ization from adipose tissue or oxidation of fat is responsible. The pr
esent study aimed to examine fat mobilization from adipose tissue and
whole body fat oxidation stimulated by exercise in seven formerly obes
e women (FO) and eight matched controls (C). Lipolysis in the periumbi
lical subcutaneous adipose tissue, whole body energy expenditure (EE),
and substrate oxidation rates were measured before, during, and after
a 60-min bicycle exercise bout of moderate intensity. Lipolysis was a
ssessed by glycerol release using microdialysis and blood flow measure
ment by Xe-133 clearance technique. The FO women had lower resting EE
than C (3.77 +/- 1.01 vs. 4.88 +/- 0.74 kJ/min, P < 0.05) but responde
d similarly to exercise. Adipose tissue glycerol release was twice as
high in FO than in C at rest (0.455 +/- 0.299 vs. 0.206 +/- 0.102 mu m
ol . 100 g(-1) . min(-1), P < 0.05) but increased similarly in FO and
C in response to exercise. Despite higher plasma nonesterified fatty a
cids (NEFA) in FO (P < 0.001), fat oxidation rates during rest and rec
overy were lower in FO than in C (1.32 +/- 0.84 vs. 3.70 /- 0.57 kJ/mi
n, P < 0.02) and fat oxidation for a given plasma NEFA concentration w
as lower at rest (P < 0.001) and during exercise (P = 0.01) in the for
merly obese group. In conclusion, fat mobilization both at rest and du
ring exercise is intact in FO, whereas fat oxidation is subnormal desp
ite higher circulation NEFA levels. The lower resting EE and the failu
re to use fat as fuel contribute to a positive fat balance and weight
gain in FO subjects.