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1 Research Department of Human
Nutrition,
An impaired fat
oxidation has been implicated to play a role in the etiology of
obesity, but it is unclear to what extent impaired fat mobilization
from adipose tissue or oxidation of fat is responsible. The present
study aimed to examine fat mobilization from adipose tissue and whole
body fat oxidation stimulated by exercise in seven formerly obese women
(FO) and eight matched controls (C). Lipolysis in the periumbilical
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
assessed by glycerol release using microdialysis and blood flow
measurement by 133Xe 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 responded 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 µmol · 100 g
1 · min
1,
P < 0.05) but increased similarly in
FO and C in response to exercise. Despite higher plasma nonesterified
fatty acids (NEFA) in FO (P < 0.001), fat oxidation rates during rest and recovery were lower in FO
than in C (1.32 ± 0.84 vs. 3.70 ± 0.57 kJ/min, P < 0.02) and fat oxidation for a
given plasma NEFA concentration was lower at rest
(P < 0.001) and during exercise
(P = 0.01) in the formerly obese
group. In conclusion, fat mobilization both at rest and during exercise
is intact in FO, whereas fat oxidation is subnormal despite higher
circulation NEFA levels. The lower resting EE and the failure to use
fat as fuel contribute to a positive fat balance and weight gain in FO
subjects.
adipose tissue; catecholamines; energy expenditure; lipolysis; obesity; respiratory quotient; substrate oxidations
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