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Nesfatin-1 influences the excitability of glucosensing neurons in the dorsal vagal complex and inhibits food intake.

Dong J, Guan HZ, Jiang ZY, Chen X - PLoS ONE (2014)

Bottom Line: Additional micro-injection studies will improve the understanding of how nesfatin-1 acts on the brain and define specific nuclei responsive to nesfatin-1, which will provide insight on its effects on food intake.Chronic administration of nesfatin-1 into the DVC reduced body weight gain over a 10-day period.Nesfatin-1 inhibited 88.9% (16/18) of gastric distension inhibitory (GD-INH) neurons and excited 76.2% (32/42) of gastric distension excitatory (GD-EXC) neurons.

View Article: PubMed Central - PubMed

Affiliation: Department of Special Medicine, Medical College of Qingdao University, Qingdao, China; Department of Physiology, Medical College of Qingdao University, Qingdao, China.

ABSTRACT
Nesfatin-1 is a recently discovered metabolic peptide hormone that decreases food intake after lateral, third, or fourth brain ventricle; cisterna magna; or paraventricular nucleus (PVN) injection in ad libitum fed rats. Additional micro-injection studies will improve the understanding of how nesfatin-1 acts on the brain and define specific nuclei responsive to nesfatin-1, which will provide insight on its effects on food intake. We evaluated how nesfatin-1 injection into the dorsal vagal complex (DVC) modulates food intake response in rats during the dark phase. Consistent with previous observations, nesfatin-1-injected rats significantly reduced cumulative food intake over a 5-h period in rats. Chronic administration of nesfatin-1 into the DVC reduced body weight gain over a 10-day period. Because glucosensing neurons in the DVC are involved in glucoprivic feeding and homeostatic control of blood glucose, we examined the effect of nesfatin-1 on the excitability of DVC glucosensing neurons. Nesfatin-1 inhibited most of the glucose-inhibitory (GI) neurons and excited most of the glucose-excitatory (GE) neurons in the DVC. Current-clamp electrophysiology recordings from DVC glucosensing neurons in slice preparation showed that bath applied nesfatin-1(10 nM) increased the firing frequency of GE neurons and inhibited the firing rate of GI-neurons. Nesfatin-1 inhibited 88.9% (16/18) of gastric distension inhibitory (GD-INH) neurons and excited 76.2% (32/42) of gastric distension excitatory (GD-EXC) neurons. Thus, nesfatin-1 may control food intake by modulating the excitability of glucosensing neurons in the DVC.

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Change in body weight gain after continuous injection of nesfatin-1 for 10 days.Body weight gain (increment from day 0) in rats after nesfatin-1 injection (15, 25, or 50 pmol daily). Data are mean ± SEM *, P<0.01 compared with vehicle.
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pone-0098967-g002: Change in body weight gain after continuous injection of nesfatin-1 for 10 days.Body weight gain (increment from day 0) in rats after nesfatin-1 injection (15, 25, or 50 pmol daily). Data are mean ± SEM *, P<0.01 compared with vehicle.

Mentions: To determine whether chronically administered nesfatin-1 caused any changes in body weight gain, 67 rats received an injection of either nesfatin-1 or saline into the DVC in the early dark phase once daily for 10 days. Among them, 14 rats were excluded due to misplacement of the cannula. Compared with saline-treated group, 15, 25, and 50 pmol nesfatin-1 injections reduced body weight gain in a dose-dependent manner (Fig. 2). Compared with the saline-treated group (n = 14), body weight gain was reduced by 34.0% (nesfatin-1-treated 25.6±0.9 g vs. saline-treated 38.8±1.0 g; P<0.01), 50.7% (nesfatin-1-treated 19.1±0.9 g vs. saline-treated 38.8±1.0 g, P<0.01) and 58.5% (nesfatin-1-treated 16.1±0.8 g vs. saline-treated 38.8±1.0 g, P<0.01) in the 15 pmol (n = 14), 25 pmol (n = 15) and 50 pmol (n = 10) nesfatin-1 treated groups, respectively, at the end of treatment. Fig. 3 showed the maps of injection sites in DVC for the feeding and body weight experiments.


Nesfatin-1 influences the excitability of glucosensing neurons in the dorsal vagal complex and inhibits food intake.

Dong J, Guan HZ, Jiang ZY, Chen X - PLoS ONE (2014)

Change in body weight gain after continuous injection of nesfatin-1 for 10 days.Body weight gain (increment from day 0) in rats after nesfatin-1 injection (15, 25, or 50 pmol daily). Data are mean ± SEM *, P<0.01 compared with vehicle.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4048226&req=5

pone-0098967-g002: Change in body weight gain after continuous injection of nesfatin-1 for 10 days.Body weight gain (increment from day 0) in rats after nesfatin-1 injection (15, 25, or 50 pmol daily). Data are mean ± SEM *, P<0.01 compared with vehicle.
Mentions: To determine whether chronically administered nesfatin-1 caused any changes in body weight gain, 67 rats received an injection of either nesfatin-1 or saline into the DVC in the early dark phase once daily for 10 days. Among them, 14 rats were excluded due to misplacement of the cannula. Compared with saline-treated group, 15, 25, and 50 pmol nesfatin-1 injections reduced body weight gain in a dose-dependent manner (Fig. 2). Compared with the saline-treated group (n = 14), body weight gain was reduced by 34.0% (nesfatin-1-treated 25.6±0.9 g vs. saline-treated 38.8±1.0 g; P<0.01), 50.7% (nesfatin-1-treated 19.1±0.9 g vs. saline-treated 38.8±1.0 g, P<0.01) and 58.5% (nesfatin-1-treated 16.1±0.8 g vs. saline-treated 38.8±1.0 g, P<0.01) in the 15 pmol (n = 14), 25 pmol (n = 15) and 50 pmol (n = 10) nesfatin-1 treated groups, respectively, at the end of treatment. Fig. 3 showed the maps of injection sites in DVC for the feeding and body weight experiments.

Bottom Line: Additional micro-injection studies will improve the understanding of how nesfatin-1 acts on the brain and define specific nuclei responsive to nesfatin-1, which will provide insight on its effects on food intake.Chronic administration of nesfatin-1 into the DVC reduced body weight gain over a 10-day period.Nesfatin-1 inhibited 88.9% (16/18) of gastric distension inhibitory (GD-INH) neurons and excited 76.2% (32/42) of gastric distension excitatory (GD-EXC) neurons.

View Article: PubMed Central - PubMed

Affiliation: Department of Special Medicine, Medical College of Qingdao University, Qingdao, China; Department of Physiology, Medical College of Qingdao University, Qingdao, China.

ABSTRACT
Nesfatin-1 is a recently discovered metabolic peptide hormone that decreases food intake after lateral, third, or fourth brain ventricle; cisterna magna; or paraventricular nucleus (PVN) injection in ad libitum fed rats. Additional micro-injection studies will improve the understanding of how nesfatin-1 acts on the brain and define specific nuclei responsive to nesfatin-1, which will provide insight on its effects on food intake. We evaluated how nesfatin-1 injection into the dorsal vagal complex (DVC) modulates food intake response in rats during the dark phase. Consistent with previous observations, nesfatin-1-injected rats significantly reduced cumulative food intake over a 5-h period in rats. Chronic administration of nesfatin-1 into the DVC reduced body weight gain over a 10-day period. Because glucosensing neurons in the DVC are involved in glucoprivic feeding and homeostatic control of blood glucose, we examined the effect of nesfatin-1 on the excitability of DVC glucosensing neurons. Nesfatin-1 inhibited most of the glucose-inhibitory (GI) neurons and excited most of the glucose-excitatory (GE) neurons in the DVC. Current-clamp electrophysiology recordings from DVC glucosensing neurons in slice preparation showed that bath applied nesfatin-1(10 nM) increased the firing frequency of GE neurons and inhibited the firing rate of GI-neurons. Nesfatin-1 inhibited 88.9% (16/18) of gastric distension inhibitory (GD-INH) neurons and excited 76.2% (32/42) of gastric distension excitatory (GD-EXC) neurons. Thus, nesfatin-1 may control food intake by modulating the excitability of glucosensing neurons in the DVC.

Show MeSH
Related in: MedlinePlus