PMID- 19931559
OWN - NLM
STAT- MEDLINE
DCOM- 20100427
LR  - 20220311
IS  - 1872-6321 (Electronic)
IS  - 0165-0173 (Linking)
VI  - 62
IP  - 2
DP  - 2010 Mar
TI  - Molecular mechanisms underlying anorexia nervosa: focus on human gene association 
      studies and systems controlling food intake.
PG  - 147-64
LID - 10.1016/j.brainresrev.2009.10.007 [doi]
AB  - Anorexia nervosa (AN) is a complex multi-factorial disease with high 
      heritability. The psychological AN symptoms are poorly connected with specific 
      molecular mechanisms. Here we review the molecular basis of AN with the focus on 
      human genetic association studies; we put these in the experimental biological 
      context with emphasis on molecular systems controlling food intake and body 
      weight in a direct or indirect manner. We systematically searched for human 
      genetic studies related to AN and grouped data into main categories/systems 
      reflecting their major known roles: (1) Systems related to mental disorders 
      (serotonin, brain-derived neurotrophic factor (BDNF), norepinephrine (NE), 
      glutamate (NMDA) receptor and SK3 channel, KCCN3). (2) Hunger regulatory systems 
      (leptin, AGRP, MSH, melanocortin 4 receptor (MC4R), NPY, ghrelin, cholecystokinin 
      (CCK). (3) Feeding motivation- and reward-related systems (opioids, OPRD1, 
      cannabinoids (anandamide (AEA), THC, CBR1), dopamine, DRD2, DRD3, DRD4, 
      catecholamine-O-methyl transferase (COMT). (4) Systems regulating energy 
      metabolism (uncoupling proteins 2 and 3 (UCP2 and UCP3). (5) Neuroendocrine 
      systems with emphasis on sex hormones (estrogen receptor-beta (ESR2). (6) The 
      immune system and inflammatory response (tumor necrosis factor-alpha 
      (TNF-alpha)). Overall, we found that in total 175 association studies have been 
      performed on AN cohorts on 128 different polymorphisms related to 43 genes. We 
      review the strongest associations, identify some genes that have an important 
      role in regulating BMI whose possible relationship to AN has not been 
      investigated and discuss the potential targets for pharmacological interventions.
FAU - Rask-Andersen, Mathias
AU  - Rask-Andersen M
AD  - Department of Neuroscience, Functional Pharmacology, Uppsala University, BMC, Box 
      593, 75124 Uppsala, Sweden.
FAU - Olszewski, Pawel K
AU  - Olszewski PK
FAU - Levine, Allen S
AU  - Levine AS
FAU - Schioth, Helgi B
AU  - Schioth HB
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20091118
PL  - Netherlands
TA  - Brain Res Rev
JT  - Brain research reviews
JID - 101300366
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Gonadal Steroid Hormones)
RN  - 0 (Neurotransmitter Agents)
RN  - 0 (Peptides)
SB  - IM
MH  - Anorexia Nervosa/*genetics/*physiopathology
MH  - Appetite Regulation/*genetics
MH  - Body Weight/genetics
MH  - Brain-Derived Neurotrophic Factor/genetics/metabolism
MH  - Energy Metabolism/genetics
MH  - *Genetic Predisposition to Disease
MH  - Genome-Wide Association Study/*methods
MH  - Gonadal Steroid Hormones/genetics/metabolism
MH  - Humans
MH  - Neurotransmitter Agents/genetics/metabolism
MH  - Peptides/genetics/metabolism
RF  - 111
EDAT- 2009/11/26 06:00
MHDA- 2010/04/28 06:00
CRDT- 2009/11/26 06:00
PHST- 2009/07/28 00:00 [received]
PHST- 2009/10/08 00:00 [revised]
PHST- 2009/10/08 00:00 [accepted]
PHST- 2009/11/26 06:00 [entrez]
PHST- 2009/11/26 06:00 [pubmed]
PHST- 2010/04/28 06:00 [medline]
AID - S0165-0173(09)00123-4 [pii]
AID - 10.1016/j.brainresrev.2009.10.007 [doi]
PST - ppublish
SO  - Brain Res Rev. 2010 Mar;62(2):147-64. doi: 10.1016/j.brainresrev.2009.10.007. 
      Epub 2009 Nov 18.