scholarly journals Consequence of Menin Deficiency in Mouse Adipocytes Derived by In Vitro Differentiation

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Vaishali I. Parekh ◽  
Sita D. Modali ◽  
Shruti S. Desai ◽  
Sunita K. Agarwal
Keyword(s):  
Gene Expression ◽  
Cell Size ◽  
Noncoding Rna ◽  
Embryonic Stem ◽  
Model Systems ◽  
In Vitro Differentiation ◽  
Fat Cell ◽  
Fat Cell Size ◽  
Differentially Methylated Genes

Lipoma in patients with the multiple endocrine neoplasia type 1 (MEN1) syndrome is a type of benign fat-cell tumor that has biallelic inactivation ofMEN1that 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.

Influence of Aging and Menstrual Status on Subcutaneous Fat Cell Lipolysis

2019 ◽  
Vol 105 (4) ◽  
pp. e955-e962 ◽  
Author(s):  
Mikael Rydén ◽  
Hui Gao ◽  
Peter Arner
Keyword(s):  
Cell Size ◽  
Subcutaneous Fat ◽  
Elderly Subjects ◽  
Fat Cell ◽  
Menstrual Status ◽  
Fat Cell Size ◽  
Phosphodiesterase 3B ◽  
Cell Mobilization ◽  
Over Time

Abstract Context Aging is accompanied by inhibited fat cell mobilization of fatty acids through lipolysis, which may contribute to decreased energy expenditure in elderly subjects. However, the influence of menstrual status is unknown. Objective To investigate the role of menstrual status on changes in lipolysis induced by aging. Design A longitudinal investigation with a mean 13-year interval. Setting Ambulatory study at a clinical academic unit. Participants Eighty-two continuously recruited women between 24 and 62 years of age and with body mass index 21 to 48 kg/m2 at first examination. Twenty-nine women continued to have normal menstruation, 42 developed irregular menstruation/menopause, and 11 had a perimenstrual/menopausal phenotype already at the first examination. Main outcome measure Lipolysis measured as glycerol release from isolated subcutaneous fat cells incubated in vitro. Results On average, body weight/body fat mass levels did not change over time. In all 3 groups, aging was associated with a similar decrease in spontaneous (basal) and catecholamine-stimulated lipolysis. The latter was due to decreased signal transduction through stimulatory beta adrenoceptors and increased alpha-2-adrenoceptor–mediated antilipolytic effects. Gene microarray data from adipose tissue at baseline and follow-up (n = 53) showed that a limited set of lipolysis-linked genes, including phosphodiesterase-3B, were altered over time, but this was independent of menstrual status. Fat cell size also decreased during aging, but this could not explain the decrease in lipolysis. Conclusions In women, the rate of fat cell lipolysis decreases during aging due to multiple alterations in spontaneous (basal) and catecholamine-induced lipolysis. This is independent of changes in menstrual status or fat cell size.

Changes in fat cell size and in vitro lipolytic activity of abdominal and gluteal adipocytes after a one-year cross—sex hormone administration in transsexuals

Metabolism ◽  
1999 ◽  
Vol 48 (11) ◽  
pp. 1371-1377 ◽  
Author(s):  
Jolanda M.H. Elbers ◽  
Sigrid de Jong ◽  
Tom Teerlink ◽  
Henk Asscheman ◽  
Jacob C. Seidell ◽  
...  
Keyword(s):  
Cell Size ◽  
Lipolytic Activity ◽  
Sex Hormone ◽  
Fat Cell ◽  
Hormone Administration ◽  
Fat Cell Size ◽  
One Year

scholarly journals The Lysine Methylase SMYD3 Modulates Mesendodermal Commitment during Development

Cells ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 1233
Author(s):  
Raffaella Fittipaldi ◽  
Pamela Floris ◽  
Valentina Proserpio ◽  
Franco Cotelli ◽  
Monica Beltrame ◽  
...  
Keyword(s):  
Embryonic Stem ◽  
Stem Cell Differentiation ◽  
Model Systems ◽  
Embryonic Stem Cell Differentiation ◽  
In Vitro Differentiation ◽  
Cancer Models ◽  
Lineage Markers

SMYD3 (SET and MYND domain containing protein 3) is a methylase over-expressed in cancer cells and involved in oncogenesis. While several studies uncovered key functions for SMYD3 in cancer models, the SMYD3 role in physiological conditions has not been fully elucidated yet. Here, we dissect the role of SMYD3 at early stages of development, employing mouse embryonic stem cells (ESCs) and zebrafish as model systems. We report that SMYD3 depletion promotes the induction of the mesodermal pattern during in vitro differentiation of ESCs and is linked to an upregulation of cardiovascular lineage markers at later stages. In vivo, smyd3 knockdown in zebrafish favors the upregulation of mesendodermal markers during zebrafish gastrulation. Overall, our study reveals that SMYD3 modulates levels of mesendodermal markers, both in development and in embryonic stem cell differentiation.

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