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Original Studies |
Metabolism Unit of the CNR Institute of Clinical Physiology and the Department of Internal Medicine, University of Pisa, Pisa, Italy
Address all correspondence and requests for reprints to: Dr. E. Ferrannini, CNR Institute of Clinical Physiology, Via Savi 8, 56126 Pisa, Italy.
Metabolic and hemodynamic abnormalities have been separately described
in obesity, and weight reduction is known to lead to some improvement
in each. Our aim was to simultaneously assess metabolic and
cardiovascular function in normotensive, normotolerant patients with
moderate obesity (body mass index = 32.6 ± 1.1
kg/m2) before and after weight loss. The obese were insulin
resistant [37.4 ± 4.8 µmol/min·kg FFM; P
< 0.02 vs. 12 lean controls (50.6 ± 2.6), on a
euglycemic insulin clamp], secreted more insulin both in the fasting
state and after oral glucose (70 ± 10 vs. 48
± 6 nmol/mmol·L plasma glucose; P < 0.05), and
had higher resting energy expenditure (4.62 ± 0.18
vs. 4.00 ± 0.23 kJ/min), systolic and mean blood
pressure, stroke volume (87 ± 8 vs. 67 ± 4
mL/min; P = 0.05), and cardiac output. There was,
however, no relationship between the metabolic and hemodynamic
abnormalities. After a weight loss of 11 ± 1 kg (
15%),
insulin sensitivity improved in proportion to the weight reduction,
whereas insulin hypersecretion and high energy expenditure persisted.
In contrast, all hemodynamic changes reverted to normal. We conclude
that in moderate obesity, the metabolic and cardiovascular
abnormalities are largely independent of one another; accordingly,
weight loss affects them differentially. Partial weight normalization
may provide sufficient cardiovascular protection.
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