@article {437,
	title = {Asprosin is a centrally acting orexigenic hormone.},
	journal = {Nat Med},
	volume = {23},
	year = {2017},
	month = {2017 Dec},
	pages = {1444-1453},
	abstract = {<p>Asprosin is a recently discovered fasting-induced hormone that promotes hepatic glucose production. Here we demonstrate that asprosin in the circulation crosses the blood-brain barrier and directly activates orexigenic AgRP neurons via a cAMP-dependent pathway. This signaling results in inhibition of downstream anorexigenic proopiomelanocortin (POMC)-positive neurons in a GABA-dependent manner, which then leads to appetite stimulation and a drive to accumulate adiposity and body weight. In humans, a genetic deficiency in asprosin causes a syndrome characterized by low appetite and extreme leanness; this is phenocopied by mice carrying similar mutations and can be fully rescued by asprosin. Furthermore, we found that obese humans and mice had pathologically elevated concentrations of circulating asprosin, and neutralization of asprosin in the blood with a monoclonal antibody reduced appetite and body weight in obese mice, in addition to improving their glycemic profile. Thus, in addition to performing a glucogenic function, asprosin is a centrally acting orexigenic hormone that is a potential therapeutic target in the treatment of both obesity and diabetes.</p>},
	keywords = {Adolescent, Adult, Animals, Appetite Depressants, Appetite Regulation, Female, Humans, Hypothalamus, Male, Mice, Mice, Inbred C57BL, Mice, Transgenic, Microfilament Proteins, Neurons, Peptide Fragments, Peptide Hormones, Rats, Signal Transduction, Young Adult},
	issn = {1546-170X},
	doi = {10.1038/nm.4432},
	author = {Duerrschmid, Clemens and He, Yanlin and Wang, Chunmei and Li, Chia and Bournat, Juan C and Romere, Chase and Saha, Pradip K and Lee, Mark E and Phillips, Kevin J and Jain, Mahim and Jia, Peilin and Zhao, Zhongming and Farias, Monica and Wu, Qi and Milewicz, Dianna M and Sutton, V Reid and Moore, David D and Butte, Nancy F and Krashes, Michael J and Xu, Yong and Chopra, Atul R}
}
@article {66,
	title = {Asprosin, a Fasting-Induced Glucogenic Protein Hormone.},
	journal = {Cell},
	volume = {165},
	year = {2016},
	month = {2016 Apr 21},
	pages = {566-79},
	abstract = {<p>Hepatic glucose release into the circulation is vital for brain function and survival during periods of fasting and is modulated by an array of hormones that precisely regulate plasma glucose levels. We have identified a fasting-induced protein hormone that modulates hepatic glucose release. It is the C-terminal cleavage product of profibrillin, and we name it Asprosin. Asprosin is secreted by white adipose, circulates at nanomolar levels, and is recruited to the liver, where it activates the G protein-cAMP-PKA pathway, resulting in rapid glucose release into the circulation. Humans and mice with insulin resistance show pathologically elevated plasma asprosin, and its loss of function via immunologic or genetic means~has a profound glucose- and insulin-lowering effect secondary to reduced hepatic glucose release. Asprosin represents a glucogenic protein hormone, and therapeutically targeting it may be beneficial in type II diabetes and metabolic syndrome. </p>},
	keywords = {Adipose Tissue, White, Amino Acid Sequence, Animals, Antibodies, Circadian Rhythm, Cyclic AMP, Cyclic AMP-Dependent Protein Kinases, Fasting, Female, Fetal Growth Retardation, Glucose, Humans, Insulin, Liver, Male, Mice, Mice, Inbred C57BL, Mice, Obese, Microfilament Proteins, Molecular Sequence Data, Peptide Fragments, Peptide Hormones, Progeria, Recombinant Proteins, Sequence Alignment},
	issn = {1097-4172},
	doi = {10.1016/j.cell.2016.02.063},
	author = {Romere, Chase and Duerrschmid, Clemens and Bournat, Juan and Constable, Petra and Jain, Mahim and Xia, Fan and Saha, Pradip K and Del Solar, Maria and Zhu, Bokai and York, Brian and Sarkar, Poonam and Rendon, David A and Gaber, M Waleed and LeMaire, Scott A and Coselli, Joseph S and Milewicz, Dianna M and Sutton, V Reid and Butte, Nancy F and Moore, David D and Chopra, Atul R}
}
