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Obesity, leptin resistance, and the effects of insulin reduction

By October 10, 2004September 24th, 2020No Comments


International journal of obesity and related metabolic disorders

R H Lustig 1 ,
S Sen,
J E Soberman,
P A Velasquez-Mieyer

Leptin resistance is a hallmark of obesity, but its etiology is unknown,
and its clinical measurement is elusive. Leptin-sensitive subjects have
normal resting energy expenditure (REE) at a low leptin concentration,
while leptin-resistant subjects have a normal REE at a higher leptin
concentration; thus, the ratio of REE:Leptin may provide a surrogate index
of leptin sensitivity. We examined changes in REE and leptin in a cohort of
17 obese subjects during experimental weight loss therapy with the
insulin-suppressive agent octreotide-LAR, 40 mg i.m. q28d for 6 months. Six
subjects lost significant weight (>10%) and BMI (>-3 kg/m(2)) with a 34%
decline in leptin and a 46% decrease in insulin area under the curve (IAUC)
to oral glucose tolerance testing. These subjects maintained their
pretreatment REE, and thus exhibited a rise in REE:Leptin, while the other
11 showed minimal changes in each of these parameters. For the entire
cohort, the change in IAUC correlated negatively with the change in
REE:Leptin. These results suggest that the REE:Leptin ratio, while
derivative, may serve as a useful clinical indicator of changes in leptin
sensitivity within obese subjects. They also support the possibilities that
hyperinsulinemia may be a proximate cause of leptin resistance, and that
reduction of insulinemia may promote weight loss by improving leptin


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