BACKGROUND: Gastric electrical stimulation (GES) has recently been proposed for the treatment of obesity. The aim of this study was to explore the possible central mechanisms involved in GES by investigating the expression of orexigenic and anorexigenic peptides in the rodent hypothalamus and hippocampus. METHODS: The experiment was designed in two parts: an acute experiment with 2 h GES and a chronic experiment with 14-day continuous GES. After stimulation, the expressions of an orexigenic hormone, ghrelin, in the hypothalamus and an anorexigenic hormone, cholecystokinin (CCK), in the hippocampus were detected by the immunohistochemical method. GES was performed using parameters similar to those used in clinical studies for treating obesity. RESULTS: Compared with the control group, 2 h GES resulted in a decrease in the number of ghrelin-immunoreactive (ghrelin-IR) neurons in the hypothalamic paraventricular nucleus (PVN, 34.8 +/- 1.86 vs 57.2 +/- 2.95, P = 0.02) and the supraoptic nucleus (SON, 51.2 +/- 3.21 vs 82.8 +/- 3.08, P = 0.01); the CCK-immunoreactive (CCK-IR) neurons in the hippocampus were of no changes (7.4 +/- 0.87 vs 6.2 +/- 0.58, P = 0.29). After the 14-day GES, the number of CCK-IR neurons in the hippocampus was increased compared with that of the control group (4.0 +/- 0.32 vs 2.4 +/- 0.51, P = 0.03). However, there were no changes in the number of ghrelin-IR neurons either in the PVN or in the SON. CONCLUSIONS: These results indicate that the expression of ghrelin and CCK can be altered by GES. GES may be able to alter energy homeostasis by modulating the expressions of food intake-related hormones in the central nervous system: reducing the level of orexigenic ghrelin acutely and increasing the level of anorexigenic CCK chronically.
BACKGROUND: Gastric electrical stimulation (GES) has recently been proposed for the treatment of obesity. The aim of this study was to explore the possible central mechanisms involved in GES by investigating the expression of orexigenic and anorexigenic peptides in the rodent hypothalamus and hippocampus. METHODS: The experiment was designed in two parts: an acute experiment with 2 h GES and a chronic experiment with 14-day continuous GES. After stimulation, the expressions of an orexigenic hormone, ghrelin, in the hypothalamus and an anorexigenic hormone, cholecystokinin (CCK), in the hippocampus were detected by the immunohistochemical method. GES was performed using parameters similar to those used in clinical studies for treating obesity. RESULTS: Compared with the control group, 2 h GES resulted in a decrease in the number of ghrelin-immunoreactive (ghrelin-IR) neurons in the hypothalamic paraventricular nucleus (PVN, 34.8 +/- 1.86 vs 57.2 +/- 2.95, P = 0.02) and the supraoptic nucleus (SON, 51.2 +/- 3.21 vs 82.8 +/- 3.08, P = 0.01); the CCK-immunoreactive (CCK-IR) neurons in the hippocampus were of no changes (7.4 +/- 0.87 vs 6.2 +/- 0.58, P = 0.29). After the 14-day GES, the number of CCK-IR neurons in the hippocampus was increased compared with that of the control group (4.0 +/- 0.32 vs 2.4 +/- 0.51, P = 0.03). However, there were no changes in the number of ghrelin-IR neurons either in the PVN or in the SON. CONCLUSIONS: These results indicate that the expression of ghrelin and CCK can be altered by GES. GES may be able to alter energy homeostasis by modulating the expressions of food intake-related hormones in the central nervous system: reducing the level of orexigenic ghrelin acutely and increasing the level of anorexigenic CCK chronically.
Authors: Zhenjun T Tan; Matthew Ward; Robert J Phillips; Xueguo Zhang; Deborah M Jaffey; Logan Chesney; Bartek Rajwa; Elizabeth A Baronowsky; Jennifer McAdams; Terry L Powley Journal: Am J Physiol Regul Integr Comp Physiol Date: 2021-01-20 Impact factor: 3.619