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Introduction: The goals of this experiment were to study therapeutic potential of intestinal electrical stimulation (IES) for obesity, its mechanisms involving gastrointestinal motility and hormones, and role of pulse width in diet-induced obese rats. Methods: In a 4-week study, rats equipped with one pair of electrodes at the duodenum were assigned to receive either a sham or IES of varied pulse widths in a sequential way. Food intake was measured daily and body weight measured weekly. Blood samples were collected for the measurement of glucagon-like peptide-1 (GLP-1). Solid gastric emptying (GE) and small bowel transit (SIT) tests were performed at the end of the experiment. Results: The results of the study were as follows: (1) Daily food intake, not affected by IES of 0.3 ms, was pulse width-dependently reduced by 1.9 g with 1 ms and by 5.7 g with 3 ms. Accordingly, body weight was pulse width-dependently reduced by 2.4 g with 1 ms and by 12.8 g with 3 ms compared to a gain of 5.6 g in sham. (2) GLP-1 level was elevated by both 0.3 and 3 ms at 15 min, but was elevated only with 3 ms at 60 min. (3) GE was delayed to 52.3 % by IES of 3 ms but not 0.3 ms, compared to that at 64.4 % with sham IES. (4) Compared to the geometric center of 7.0 with sham IES, SIT was accelerated by 3 ms to 7.8 but not by 0.3 ms. Conclusion: IES pulse width-dependently reduces food intake and body weight, attributed to the delay of gastric emptying and the acceleration of small bowel transit, as well as the enhancement of GLP-1 secretion. [ABSTRACT FROM AUTHOR]

Background: The aim of this study was to investigate effects and mechanisms of chronic electrical stimulation at acupoints (CEA) using surgically implanted electrodes on food intake, body weight, and metabolisms in diet-induced obese (DIO) rats. Methods: Thirty-six DIO rats were chronically implanted with electrodes at acupoints ST-36 (Zusanli). Three sets of parameters were tested: electrical acupuncture (EA) 1 (2-s on, 3-s off, 0.5 ms, 15 Hz, 6 mA), EA2 (same as EA1 but continuous pulses), and EA3 (same as EA2 but 10 mA). A chronic study was then performed to investigate the effects of CEA on body weight and mechanisms involving gastrointestinal hormones and autonomic functions. Results: EA2 significantly reduced food intake without uncomfortable behaviors. CEA at EA2 reduced body weight and epididymal fat pad weight ( P < 0.05). CEA reduced both postprandial blood glucose and HbA1c ( P < 0.05). CEA delayed gastric emptying ( P < 0.03) and increased small intestinal transit ( P < 0.02). CEA increased fasting plasma level of glucagon-like peptide-1 (GLP-1) and peptide YY ( P < 0.05); the increase of GLP-1 was inversely correlated with postprandial blood glucose ( R = 0.89, P < 0.05); and the plasma ghrelin level remained unchanged. EA increased sympathetic activity ( P < 0.01) and reduced vagal activity ( P < 0.01). Conclusions: CEA at ST-36 reduces body weight and improves blood glucose possibly attributed to multiple mechanisms involving gastrointestinal motility and hormones via the autonomic pathway. [ABSTRACT FROM AUTHOR]

Background: Gastric electrical stimulation (GES) has recently been introduced as a potential therapy for the treatment of obesity. The main challenge for the new generation of devices is to achieve desired clinical outcomes at a suitably low level of energy consumption. The aim of this study is to compare the effectiveness of GES with continuous and intermittent duty cycles in reducing food intake and body weight in diet-induced obesity-prone rats. Methods: In macro duty cycle experiment, 40 rats were divided into groups to receive a sham GES, continuous GES, or intermittent GES (15 min On-45 min Off or 15 min On-15 min Off) for 28 days. In micro duty cycle experiment, 18 rats received cross-over treatment of continuous stimulation, 60 % time cycle or 40 % time cycle. Food intake, body weight, gastric emptying and ghrelin level were measured to evaluate the effect of different GES. Results: GES with macro duty cycle intensity-dependently reduced mean daily food intake increase by 18.6, 10.2 and -6.0 % compared to 42.7 % with sham GES and body weight gain by 6.1 %, 3.4 and -0.8 % compared to 5 % with sham GES. Daily food intake decreased with increasing micro duty cycle intensity, averaging 16.5, 15.6 and 13.7 g/day under 40 % cycle, 60 % cycle and continuous stimulation respectively. Gastric emptying was intensity-dependently delayed by GES. GES has no effect in modulating plasma ghrelin level. Conclusions: GES energy-dependently reduces food intake, body weight and gastric emptying. Peripheral modulation of plasma ghrelin level is not related to the GES effects. [ABSTRACT FROM AUTHOR]

Introduction: The goals of this experiment were to study therapeutic potential of intestinal electrical stimulation (IES) for obesity, its mechanisms involving gastrointestinal motility and hormones, and role of pulse width in diet-induced obese rats., Methods: In a 4-week study, rats equipped with one pair of electrodes at the duodenum were assigned to receive either a sham or IES of varied pulse widths in a sequential way. Food intake was measured daily and body weight measured weekly. Blood samples were collected for the measurement of glucagon-like peptide-1 (GLP-1). Solid gastric emptying (GE) and small bowel transit (SIT) tests were performed at the end of the experiment., Results: The results of the study were as follows: (1) Daily food intake, not affected by IES of 0.3 ms, was pulse width-dependently reduced by 1.9 g with 1 ms and by 5.7 g with 3 ms. Accordingly, body weight was pulse width-dependently reduced by 2.4 g with 1 ms and by 12.8 g with 3 ms compared to a gain of 5.6 g in sham. (2) GLP-1 level was elevated by both 0.3 and 3 ms at 15 min, but was elevated only with 3 ms at 60 min. (3) GE was delayed to 52.3 % by IES of 3 ms but not 0.3 ms, compared to that at 64.4 % with sham IES. (4) Compared to the geometric center of 7.0 with sham IES, SIT was accelerated by 3 ms to 7.8 but not by 0.3 ms., Conclusion: IES pulse width-dependently reduces food intake and body weight, attributed to the delay of gastric emptying and the acceleration of small bowel transit, as well as the enhancement of GLP-1 secretion.