Nesfatin-1
Nesfatin-1 is a neuropeptide produced in the hypothalamus of mammals. It participates in the regulation of hunger and fat storage.[1] Increased nesfatin-1 in the hypothalamus contributes to diminished hunger, a 'sense of fullness', and a potential loss of body fat and weight.
A study of metabolic effects of nesfatin-1 in rats was done in which subjects administered nesfatin-1 ate less, used more stored fat and became more active. Nesfatin-1-induced inhibition of feeding may be mediated through the inhibition of orexigenic neurons.[2] In addition, the protein stimulated insulin secretion from the pancreatic beta cells of both rats and mice.[3] Nesfatin-1 can cross the blood–brain barrier without saturation.[4]
See also
References
- ^ Oh-i, Shinsuke; Shimizu, Hiroyuki; Satoh, Tetsurou; Okada, Shuichi; Adachi, Sachika; Inoue, Kinji; Eguchi, Hiroshi; Yamamoto, Masanori; et al. (2006). "Identification of nesfatin-1 as a satiety molecule in the hypothalamus". Nature. 443 (7112): 709–12. Bibcode:2006Natur.443..709O. doi:10.1038/nature05162. PMID 17036007. S2CID 4366701.
- ^ Price, Christopher J.; Samson, Willis K.; Ferguson, Alastair V. (2008). "Nesfatin-1 inhibits NPY neurons in the arcuate nucleus". Brain Research. 1230: 99–106. doi:10.1016/j.brainres.2008.06.084. PMC 2590930. PMID 18625211.
- ^ Gonzalez, R.; Reingold, B. K.; Gao, X.; Gaidhu, M. P.; Tsushima, R.; Unniappan, S. (2011). "Nesfatin-1 Exerts a Direct, Glucose-Dependent Insulinotropic Action on Mouse Islet Beta and MIN6 Cells". Journal of Endocrinology. 208 (3): R9–R16. doi:10.1530/JOE-10-0492. PMID 21224288.
- ^ Pan, Weihong; Hsuchou, Hung; Kastin, Abba J. (2007). "Nesfatin-1 crosses the blood–brain barrier without saturation". Peptides. 28 (11): 2223–8. doi:10.1016/j.peptides.2007.09.005. PMID 17950952. S2CID 17973594.
- ^ ProSci inc. "Nesfatin-1 Recombinant Protein". Retrieved 21 March 2013.
{{cite web}}: CS1 maint: deprecated archival service (link) - ^ Stengel, A.; Tache, Y. (2011). "Minireview: Nesfatin-1--An Emerging New Player in the Brain-Gut, Endocrine, and Metabolic Axis". Endocrinology. 152 (11): 4033–8. doi:10.1210/en.2011-1500. PMC 3199002. PMID 21862618.
- ^ Maejima, Yuko; Sedbazar, Udval; Suyama, Shigetomo; Kohno, Daisuke; Onaka, Tatsushi; Takano, Eisuke; Yoshida, Natsu; Koike, Masato; et al. (2009). "Nesfatin-1-Regulated Oxytocinergic Signaling in the Paraventricular Nucleus Causes Anorexia through a Leptin-Independent Melanocortin Pathway". Cell Metabolism. 10 (5): 355–65. doi:10.1016/j.cmet.2009.09.002. PMID 19883614.
- ^ Shimizu, H; Ohsaki, A; Oh-I, S; Okada, S; Mori, M (May 2009). "A new anorexigenic protein, nesfatin-1". Peptides. 30 (5): 995–8. doi:10.1016/j.peptides.2009.01.002. PMID 19452636. S2CID 3837217.
- ^ Shimizu, H.; Oh-i, S.; Hashimoto, K.; Nakata, M.; Yamamoto, S.; Yoshida, N.; Eguchi, H.; Kato, I.; et al. (2008). "Peripheral Administration of Nesfatin-1 Reduces Food Intake in Mice: The Leptin-Independent Mechanism". Endocrinology. 150 (2): 662–71. doi:10.1210/en.2008-0598. PMID 19176321.
- ^ Zhang, Z.; Li, L.; Yang, M.; Liu, H.; Boden, G.; Yang, G. (2011). "Increased Plasma Levels of Nesfatin-1 in Patients with Newly Diagnosed Type 2 Diabetes Mellitus". Experimental and Clinical Endocrinology & Diabetes. 120 (2): 91–95. doi:10.1055/s-0031-1286339. PMID 22020667.
- ^ Yang, M.; Zhang, Z.; Wang, C.; Li, K.; Li, S.; Boden, G.; Li, L.; Yang, G. (2012). "Nesfatin-1 Action in the Brain Increases Insulin Sensitivity Through Akt/AMPK/TORC2 Pathway in Diet-Induced Insulin Resistance". Diabetes. 61 (8): 1959–68. doi:10.2337/db11-1755. PMC 3402309. PMID 22688332.
- ^ Stengel, A.; Goebel, M.; Wang, L.; Rivier, J.; Kobelt, P.; Monnikes, H.; Lambrecht, N. W. G.; Tache, Y. (2009). "Central Nesfatin-1 Reduces Dark-Phase Food Intake and Gastric Emptying in Rats: Differential Role of Corticotropin-Releasing Factor2 Receptor". Endocrinology. 150 (11): 4911–9. doi:10.1210/en.2009-0578. PMC 2775975. PMID 19797401.
External links
- nesfatin-1+protein,+rat at the U.S. National Library of Medicine Medical Subject Headings (MeSH)