Implantable Gastric Stimulation (IGS™) as Therapy for Human Morbid Obesity: Report from the 2001 IFSO Symposium in Crete

Greenstein, Robert J.; Belachew, M

doi:10.1007/bf03342139

Cited by 18 publications

(13 citation statements)

References 19 publications

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“…20 During every visits, values were analytically determined of plasma calcium and phosphorus, calcium in the urine, total alkaline phosphate and tartrate resistant acid phosphate (TRAP) by self-analyzer Hitachi 717 (Roche Diagnostics, Switzerland). The urinary pyrodinolines were studied by EIA using a kit (DPC, Dipesa).…”

Section: Methodsmentioning

confidence: 99%

Phosphocalcic Metabolism after Biliopancreatic Diversion

et al. 2007

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Morbid obesity is accompanied by a high percentage of hyperparathyroidism. BPD produces malabsorption of vitamin D during the first years, favoring the persistence or appearance of hyperparathyroidism. It is important to recognize and treat the secondary hyperparathyroidism. The postoperative period could necessitate more energetic interventions to get more efficient control of the phosphocalcic metabolism.

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Section: Methodsmentioning

confidence: 99%

Phosphocalcic Metabolism after Biliopancreatic Diversion

et al. 2007

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“…Basic and clinical investigations show that gastric electrical stimulation (GES) may be a suitable treatment for some gastric motility disorders and morbid obesity (Abell and Minocha 2002;D'Argent et al 2002;Greenstein and Belachew 2002;Lin and Chen 2002;Liu et al 2006). However, the neural and hormonal mechanisms underlying the effects of GES on gastric sensory and motor functions are little known.…”

Section: Introductionmentioning

confidence: 99%

Modulatory effects and afferent pathways of gastric electrical stimulation on rat thoracic spinal neurons receiving input from the stomach

Qin

Chen

Zhang

et al. 2007

Neuroscience Research

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Gastric electrical stimulation (GES) has been suggested as a potential therapy for patients with obesity or gastric motility disorders. The aim of this study was to investigate the spinal mechanism of GES effects on gastric functions. Extracellular potentials of single spinal (T9-T10) neurons were recorded in pentobarbital anesthetized, paralyzed, ventilated male rats (n=19). Gastric distension (GD) was produced by air inflation of a balloon. One pair of platinum electrodes (1.0-1.5 cm apart) was sutured onto the serosal surface of the lesser curvature of the stomach. GES with four sets of parameters was applied for one minute: GES-A (6 mA, 0.3 ms, 40 Hz, 2s on, 3s off), GES-B (6 mA, 0.3 ms, 14 Hz, 0.1s on, 5s off), GES-C (6 mA, 3 ms, 40 Hz, 2s on, 3s off), GES-D (6 mA, 200 ms, 12 pulses/min). 62/158 (39%) spinal neurons responded to GD (20, 40, 60 mmHg, 20s. Most GD-responsive neurons (n=43) had excitatory responses; the remainder had inhibitory (n=12) or biphasic responses (n=7). GES-A, -B, -C and -D affected activity of 12/33 (36%), 4/31 (13%), 22/29 (76%) and 13/30 (43%) GD-responsive neurons, respectively. Bilateral cervical vagotomy did not significantly alter mean excitatory neuronal responses to GD (n=5) or GES (n=6). Resiniferatoxin (2.0 μg/kg, i.v.), an ultrapotent agonist of vanilloid receptor-1, abolished excitatory responses to GD and GES in 4/4 neurons recorded in vagotomized rats. The results suggested that GES mainly had an excitatory effect on T9-T10 spinal neurons with gastric inputs; neuronal responses to GES were strengthened with stimulation at an increased pulse width and/or number of pulses. The modulatory effect of GES involved thoracic spinal (sympathetic) afferent fibers containing vanilloid receptor-1.

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“…It has been shown to be effective in normalizing gastric dysrhythmia, accelerating gastric emptying, decreasing nausea and vomiting, and treating gastroparesis as well as obesity (see review, Zhang and Chen 2006). However, previous basic and clinical studies have only investigated the effects of GES on gastric functions and diseases (Abell and Minocha 2002;D'Argent et al 2002;Greenstein and Belachew 2002;Lin and Chen 2002;Liu et al 2006;Zhang and Chen 2006). We hypothesize that GES not only modulates gastric motility but also affects the functions of other segments of the gastrointestinal tract, such as the intestine.…”

Section: Introductionmentioning

confidence: 88%

Characterization of T9–T10 spinal neurons with duodenal input and modulation by gastric electrical stimulation in rats

et al. 2007

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Gastric electrical stimulation (GES) has been suggested as a therapy for patients with gastric motility disorders or morbid obesity. However, it is unclear whether GES also affects intestinal sensory and motor functions. Furthermore, little is known about intraspinal visceroreceptive transmission and processing for duodenal afferent information. The aims of this study were to characterize responses of thoracic spinal neurons to duodenal distension, to determine the afferent pathway, and to examine the effects of GES on activity of these neurons. Extracellular potentials of single T9-T10 spinal neurons were recorded in pentobarbital anesthetized, paralyzed, ventilated male rats (n=19). Graded duodenal distension (DD, 0.2-0.6 ml, 20 s) was produced by water inflation of a latex balloon surgically placed into the duodenum. One pair of platinum electrodes (1.0-1.5 cm apart) was sutured onto the serosal surface of the lesser curvature of the stomach. GES with four sets of parameters was applied for one minute: GES-A (6 mA, 0.3 ms, 40 Hz, 2s on, 3s off), GES-B (6 mA, 0.3 ms, 14 Hz, 0.1s on, 5s off), GES-C (6 mA, 3 ms, 40 Hz, 2s on, 3s off), GES-D (6 mA, 200 ms, 12 pulses/min). Results showed that 33/117 (28%) spinal neurons responded to noxious DD (0.4 ml, 20s). Of these, 7 (6%) neurons had low-threshold responses to DD (≤0.2 ml) and 26 (22%) had high-threshold responses to DD (≥0.4 ml). DD-responsive spinal neurons were encountered more frequently in deeper (depth: 0.3-1.2 mm) than in superficial laminae (depth: <0.3 mm) of the dorsal horn (24/67 vs 9/50, P<0.05). DD excited all 9 superficial neurons. In contrast, 20 deeper neurons were excited and 4 neurons were inhibited by DD. Activity of DD-responsive neurons was affected more frequently with GES-C (13/15, 87%) than GES-A (6/16, 38%), -B (3/15, 20%), -D (5/14, 36%), (P<0.01). Bilateral cervical vagotomy did not significantly alter the effects of DD and GES on 5/5 neurons. Resiniferatoxin (2.0 μg/kg, i.v.), an ultrapotent agonist of transient receptor potential vanilloid receptor-1 (TRPV1), abolished DD responses and GES effects on all neurons examined in vagotomized rats. Additionally, 29/33 (88%) DD-responsive neurons received inputs from somatic receptive fields on the back, flank, and medial/lateral abdominal areas. It was concluded that GES mainly exerted an excitatory effect on T9-T10 spinal neurons with duodenal input transmitted by sympathetic afferent fibers expressing TRPV1; spinal neuronal responses to GES were strengthened with an increased pulse width and/or frequency of stimulation; T9-T10 spinal neurons processed input from the duodenum and might mediate effects of GES on duodenal sensation and motility.

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Implantable Gastric Stimulation (IGS™) as Therapy for Human Morbid Obesity: Report from the 2001 IFSO Symposium in Crete

Cited by 18 publications

References 19 publications

Phosphocalcic Metabolism after Biliopancreatic Diversion

Phosphocalcic Metabolism after Biliopancreatic Diversion

Modulatory effects and afferent pathways of gastric electrical stimulation on rat thoracic spinal neurons receiving input from the stomach

Characterization of T9–T10 spinal neurons with duodenal input and modulation by gastric electrical stimulation in rats

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