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Gastric Pacing Promising for Morbid Obesity

Laurie Barclay, MD

Dec. 30, 2003 — Gastric pacing is a promising therapy for morbid obesity,

according to the results of a small trial published in the December issue of

Obesity Research. Patients lost a mean of 10.4 kg over six months.

" A gastric pacemaker has been developed to treat morbid obesity, " write

Valerio Cigaina from Venice Hospital in Italy and L. Hirschberg from

Karolinska Hospital in Stockholm, Sweden. " Patients experience increased

satiety,

the ability to reduce food intake, and a resultant weight loss. However, the

mechanism behind the changed eating behavior in paced patients is still under

investigation. "

This study enrolled 11 morbidly obese patients with mean body mass index

(BMI) of 46.0 kg/m2. Subjects had blood samples drawn 12 hours after fasting and

in response to a hypocaloric meal of 270 kcal one month before gastric pacer

implantation, one month after implantation, and six months after activation of

electrical stimulation. These samples were analyzed for levels of satiety

signals of cholecystokinin (CCK), somatostatin, glucagon-like peptide-1 (GLP-1),

and leptin, and monthly vital signs and weight were recorded.

Mean weight loss was 10.4 kg (4.4 BMI units), which correlated significantly

with decreased leptin levels (R = .79; P < .01). No negative adverse effects

or complications were reported. Compared with levels before pacing,

meal-related response of CCK and somatostatin levels and basal levels of GLP-1

and leptin

were reduced (P < .05) after pacemaker activation.

The authors suggest that possible mechanisms for gastric pacing may include

increased satiety or altered gastrointestinal motility.

" Gastric pacing is a novel and promising therapy for morbid obesity, " they

write. " Activation of the gastric pacer was associated with a decrease in plasma

levels of CCK, somatostatin, GLP-1, and leptin. More studies are necessary to

elucidate the correlations between satiety, weight loss, and digestive

neuro-hormone changes. "

Transneuronix Inc., the Swedish Medical Research Council, and the Karolinska

Institute supported this study.

Obes Res. 2003;11:1456-1462

Reviewed by D. Vogin, MD

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