PMID- 26229531
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20150803
LR  - 20200929
IS  - 1687-8337 (Print)
IS  - 1687-8345 (Electronic)
IS  - 1687-8337 (Linking)
VI  - 2015
DP  - 2015
TI  - Consequence of Menin Deficiency in Mouse Adipocytes Derived by In Vitro 
      Differentiation.
PG  - 149826
LID - 10.1155/2015/149826 [doi]
LID - 149826
AB  - Lipoma in patients with the multiple endocrine neoplasia type 1 (MEN1) syndrome 
      is a type of benign fat-cell tumor that has biallelic inactivation of MEN1 that 
      encodes menin and could serve as a model to investigate normal and pathologic 
      fat-cell (adipocyte) proliferation and function. The role of menin and its target 
      genes in adipocytes is not known. We used in vitro differentiation to derive 
      matched normal and menin-deficient adipocytes from wild type (WT) and menin-null 
      (Men1-KO) mouse embryonic stem cells (mESCs), respectively, or 3T3-L1 cells 
      without or with menin knockdown to investigate cell size, lipid content, and gene 
      expression changes. Adipocytes derived from Men1-KO mESCs or after menin 
      knockdown in 3T3-L1 cells showed a 1.5-1.7-fold increase in fat-cell size. Global 
      gene expression analysis of mESC-derived adipocytes showed that lack of menin 
      downregulated the expression of many differentially methylated genes including 
      the tumor suppressor long noncoding RNA Meg3 but upregulated gene expression from 
      the prolactin gene family locus. Our results show that menin deficiency leads to 
      fat-cell hypertrophy and provide model systems that could be used to study the 
      regulation of fat-cell size.
FAU - Parekh, Vaishali I
AU  - Parekh VI
AD  - Metabolic Diseases Branch, National Institute of Diabetes and Digestive and 
      Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
FAU - Modali, Sita D
AU  - Modali SD
AD  - Metabolic Diseases Branch, National Institute of Diabetes and Digestive and 
      Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
FAU - Desai, Shruti S
AU  - Desai SS
AD  - Metabolic Diseases Branch, National Institute of Diabetes and Digestive and 
      Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
FAU - Agarwal, Sunita K
AU  - Agarwal SK
AD  - Metabolic Diseases Branch, National Institute of Diabetes and Digestive and 
      Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
LA  - eng
GR  - ZIA DK075035/Intramural NIH HHS/United States
PT  - Journal Article
DEP - 20150702
PL  - Egypt
TA  - Int J Endocrinol
JT  - International journal of endocrinology
JID - 101516376
PMC - PMC4503551
EDAT- 2015/08/01 06:00
MHDA- 2015/08/01 06:01
PMCR- 2015/07/02
CRDT- 2015/08/01 06:00
PHST- 2015/04/03 00:00 [received]
PHST- 2015/06/17 00:00 [revised]
PHST- 2015/06/18 00:00 [accepted]
PHST- 2015/08/01 06:00 [entrez]
PHST- 2015/08/01 06:00 [pubmed]
PHST- 2015/08/01 06:01 [medline]
PHST- 2015/07/02 00:00 [pmc-release]
AID - 10.1155/2015/149826 [doi]
PST - ppublish
SO  - Int J Endocrinol. 2015;2015:149826. doi: 10.1155/2015/149826. Epub 2015 Jul 2.