PMID- 23168387
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20121122
LR  - 20211021
IS  - 2044-4052 (Electronic)
IS  - 2044-4052 (Linking)
VI  - 2
IP  - 5
DP  - 2012 May 28
TI  - Menin liver-specific hemizygous mice challenged with high fat diet show increased 
      weight gain and markers of metabolic impairment.
PG  - e34
LID - 10.1038/nutd.2012.7 [doi]
AB  - OBJECTIVE: The menin tumor suppressor protein is abundantly expressed in the 
      liver, although no function has been identified because of lack of tumor 
      development in multiple endocrine neoplasia type 1 (Men1) null livers. We examine 
      the phenotype of mice lacking one functional allele of Men1 (consistent with the 
      phenotype in humans with MEN1 syndrome) challenged with high fat diet (HFD) to 
      elucidate a metabolic function for hepatic menin. METHODS: In this study, we 
      challenged mice harboring a liver-specific hemizygous deletion of Men1 (HETs) 
      alongside wild-type (WT) counterparts with HFD for 3 months and monitored the 
      severity of metabolic changes. We demonstrate that the HET mice challenged with 
      HFD for 3 months show an increased weight gain with decreased glucose tolerance 
      compared with WT counterparts. Along with these changes, there was a more severe 
      serum hormone profile involving increased serum insulin, glucose and glucagon, 
      all hallmarks of the type 2 diabetic phenotype. In concert with increased serum 
      hormones, we found that these mice have significantly increased liver 
      triglycerides coupled with increased liver steatosis and inflammatory markers. 
      Quantitative real-time PCR and western blotting studies show increases in enzymes 
      involved with lipogenesis and hepatic glucose production. CONCLUSION: We conclude 
      that hepatic menin is required for regulation of diet-induced metabolism, and our 
      studies indicate a protective role for the Men1 gene in the liver when challenged 
      with HFD.
FAU - Wuescher, L
AU  - Wuescher L
AD  - Department of Physiology and Pharmacology, Center for Diabetes and Endocrine 
      Research, University of Toledo College of Medicine, Toledo, OH, USA.
FAU - Angevine, K
AU  - Angevine K
FAU - Patel, P R
AU  - Patel PR
FAU - Mensah-Osman, E
AU  - Mensah-Osman E
LA  - eng
PT  - Journal Article
DEP - 20120528
PL  - England
TA  - Nutr Diabetes
JT  - Nutrition & diabetes
JID - 101566341
PMC - PMC3366066
EDAT- 2012/11/22 06:00
MHDA- 2012/11/22 06:01
PMCR- 2012/05/01
CRDT- 2012/11/22 06:00
PHST- 2012/11/22 06:00 [entrez]
PHST- 2012/11/22 06:00 [pubmed]
PHST- 2012/11/22 06:01 [medline]
PHST- 2012/05/01 00:00 [pmc-release]
AID - nutd20127 [pii]
AID - 10.1038/nutd.2012.7 [doi]
PST - epublish
SO  - Nutr Diabetes. 2012 May 28;2(5):e34. doi: 10.1038/nutd.2012.7.