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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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Nesfatin-1(15, 25, or 50 pmol) injected into the dorsal vagal complex (DVC) decreased dark phase food intake in rats.Cumulative food intake was monitored for 12±SEM. *P<0.05; **P<0.01 vs. vehicle.
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pone-0098967-g001: Nesfatin-1(15, 25, or 50 pmol) injected into the dorsal vagal complex (DVC) decreased dark phase food intake in rats.Cumulative food intake was monitored for 12±SEM. *P<0.05; **P<0.01 vs. vehicle.

Mentions: Feeding response was tested in 65 rats, among which 9 were excluded due to misplacement of the cannula. All three doses (15, 25, and 50 pmol) of nesfatin-1 significantly decreased cumulative food intake (Fig.1). Rats administered 25 or 50 pmol nesfatin-1 consumed less food throughout the first 5 h of testing than their vehicle-treated counterparts. Rats administered 15 pmol nesfatin-1 ate less food at all time points compared to control, but this difference only reached significance 3 h and 5 h after injection. The 15, 25 and 50 pmol doses of nesfatin-1 induced 20.8%, 56.8% and 68.8% decreases in food intake, respectively, compared with their respective controls 1 h after injection. The 25 pmol nesfatin-1 injection into the DVC decreased cumulative food intake by 56.8%, 37.8%, 31.3%, 20.0% and 18.2%, respectively, compared with vehicle-injected controls at the 1, 2, 3, 4 and 5 h time points. Rats administered the highest dose tested (50 pmol nesfatin-1) consumed less food throughout the first 6 h of testing (vehicle vs. nesfatin-1, 1 h: 1.6±0.2 vs. 0.5±0.1 g/300 g body weight, P<0.01; 6 h: 6.7±0.3 vs. 5.5±0.3 g/300 g body weight, P<0.01) but no significant difference was observed between the 25 and 50 pmol nesfatin-1 groups.


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)

Nesfatin-1(15, 25, or 50 pmol) injected into the dorsal vagal complex (DVC) decreased dark phase food intake in rats.Cumulative food intake was monitored for 12±SEM. *P<0.05; **P<0.01 vs. vehicle.
© Copyright Policy
Related In: Results  -  Collection

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

pone-0098967-g001: Nesfatin-1(15, 25, or 50 pmol) injected into the dorsal vagal complex (DVC) decreased dark phase food intake in rats.Cumulative food intake was monitored for 12±SEM. *P<0.05; **P<0.01 vs. vehicle.
Mentions: Feeding response was tested in 65 rats, among which 9 were excluded due to misplacement of the cannula. All three doses (15, 25, and 50 pmol) of nesfatin-1 significantly decreased cumulative food intake (Fig.1). Rats administered 25 or 50 pmol nesfatin-1 consumed less food throughout the first 5 h of testing than their vehicle-treated counterparts. Rats administered 15 pmol nesfatin-1 ate less food at all time points compared to control, but this difference only reached significance 3 h and 5 h after injection. The 15, 25 and 50 pmol doses of nesfatin-1 induced 20.8%, 56.8% and 68.8% decreases in food intake, respectively, compared with their respective controls 1 h after injection. The 25 pmol nesfatin-1 injection into the DVC decreased cumulative food intake by 56.8%, 37.8%, 31.3%, 20.0% and 18.2%, respectively, compared with vehicle-injected controls at the 1, 2, 3, 4 and 5 h time points. Rats administered the highest dose tested (50 pmol nesfatin-1) consumed less food throughout the first 6 h of testing (vehicle vs. nesfatin-1, 1 h: 1.6±0.2 vs. 0.5±0.1 g/300 g body weight, P<0.01; 6 h: 6.7±0.3 vs. 5.5±0.3 g/300 g body weight, P<0.01) but no significant difference was observed between the 25 and 50 pmol nesfatin-1 groups.

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