Necdin and E2F4 Are Modulated by Rosiglitazone Therapy in Diabetic Human Adipose and Muscle Tissue

Goldfine, Allison B.; Crunkhorn, Sarah; Costello, Maura; Gami, Hiral; Landaker, Edwin J.; Niinobe, Michio; Yoshikawa, Kunio; Lo, David; Warren, Amy J.; Jimenez-Chillaron, Jose; Patti, Mary Elizabeth

doi:10.2337/diabetes.55.03.06.db05-1015

Cited by 22 publications

(21 citation statements)

References 58 publications

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“…We observed that both pref-1 (dlk1) and necdin are down-regulated in both brown and white primary cells. Given the lack of consistency between the different models, we can conclude that there may be substantial differences between the early differentiation transcriptional program characterized in artificially immortalized cell lines (11,45) and the primary brown preadipocyte differentiation program investigated in the present work. In addition, our data contrast with general pRB-E2F brown adipocyte differentiation model (47) developed by using mouse embryo fibroblasts.…”

Section: ) (B)mentioning

confidence: 76%

“…Pref-1 and necdin have been described as being potential regulators of brown preadipocyte differentiation (11). Necdin has been shown to promote differentiation of skeletal muscle (44) and to be modulated during adipocyte differentiation (45,46). Specifically, necdin down-regulation appears to promote adipogenesis in immortalized brown preadipocytes (11), whereas overexpression in 3T3-L1 white preadipocytes prevents differentiation (45).…”

Section: ) (B)mentioning

confidence: 99%

“…Necdin has been shown to promote differentiation of skeletal muscle (44) and to be modulated during adipocyte differentiation (45,46). Specifically, necdin down-regulation appears to promote adipogenesis in immortalized brown preadipocytes (11), whereas overexpression in 3T3-L1 white preadipocytes prevents differentiation (45). However, necdin expression increases in the 3T3-L1 adipocyte cell model (45) during differentiation (but is concurrently associated with inhibition of differentiation when expressed at artificially high levels; ref.…”

Section: ) (B)mentioning

confidence: 99%

“…However, necdin expression increases in the 3T3-L1 adipocyte cell model (45) during differentiation (but is concurrently associated with inhibition of differentiation when expressed at artificially high levels; ref. 45). We observed that both pref-1 (dlk1) and necdin are down-regulated in both brown and white primary cells.…”

Section: ) (B)mentioning

confidence: 99%

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Myogenic gene expression signature establishes that brown and white adipocytes originate from distinct cell lineages

Timmons

Wennmalm

Larsson

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

644

520

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Attainment of a brown adipocyte cell phenotype in white adipocytes, with their abundant mitochondria and increased energy expenditure potential, is a legitimate strategy for combating obesity. The unique transcriptional regulators of the primary brown adipocyte phenotype are unknown, limiting our ability to promote brown adipogenesis over white. In the present work, we used microarray analysis strategies to study primary preadipocytes, and we made the striking discovery that brown preadipocytes demonstrate a myogenic transcriptional signature, whereas both brown and white primary preadipocytes demonstrate signatures distinct from those found in immortalized adipogenic models. We found a plausible SIRT1-related transcriptional signature during brown adipocyte differentiation that may contribute to silencing the myogenic signature. In contrast to brown preadipocytes or skeletal muscle cells, white preadipocytes express Tcf21, a transcription factor that has been shown to suppress myogenesis and nuclear receptor activity. In addition, we identified a number of developmental genes that are differentially expressed between brown and white preadipocytes and that have recently been implicated in human obesity. The interlinkage between the myocyte and the brown preadipocyte confirms the distinct origin for brown versus white adipose tissue and also represents a plausible explanation as to why brown adipocytes ultimately specialize in lipid catabolism rather than storage, much like oxidative skeletal muscle tissue. microarray ͉ myocyte ͉ principal component analysis ͉ differentiation ͉ transcriptome

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Section: ) (B)mentioning

confidence: 76%

Section: ) (B)mentioning

confidence: 99%

Section: ) (B)mentioning

confidence: 99%

Section: ) (B)mentioning

confidence: 99%

See 2 more Smart Citations

Myogenic gene expression signature establishes that brown and white adipocytes originate from distinct cell lineages

Timmons

Wennmalm

Larsson

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

644

520

View full text Add to dashboard Cite

show abstract

“…In particular, Wnt signaling in pre-adipocytes maintains an undifferentiated state, while blocking Wnt signaling in myoblasts induces transdifferentiation into adipocytes (Ross et al, 2000). In addition to its role in promoting differentiation of neurons and muscle, necdin has been implicated in adipogenic differentiation (Cypess et al, 2011;Goldfine et al, 2006;Tseng et al, 2005). Ndn, the gene encoding necdin, was the most highly up-regulated gene in immortalized brown pre-adipocytes with decreased differentiation potential due to defective insulin receptor substrate (Irs)-1 signaling (Tseng et al, 2005).…”

Section: Introductionmentioning

confidence: 98%

Loss of the Prader–Willi obesity syndrome protein necdin promotes adipogenesis

Bush

Wevrick

2012

Gene

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Adipose Organ Development and Remodeling

Cinti

2018

Comprehensive Physiology

142

121

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During the last decades, research on adipose tissues has spread in parallel with the extension of obesity. Several observations converged on the idea that adipose tissues are organized in a large organ with endocrine and plastic properties. Two parenchymal components: white (WATs) and brown adipose tissues (BATs) are contained in subcutaneous and visceral compartments. Although both have endocrine properties, their function differs: WAT store lipids to allow intervals between meals, BAT burns lipids for thermogenesis. In spite of these opposite functions, they share the ability for reciprocal reversible transdifferentiation to tackle special physiologic needs. Thus, chronic need for thermogenesis induces browning and chronic positive energy balance induce whitening. Lineage tracing and data from explant studies strongly suggest other remodeling properties of this organ. During pregnancy and lactation breast WAT transdifferentiates into milk-secreting glands, composed by cells with abundant cytoplasmic lipids (pink adipocytes) and in the postlactation period pink adipocytes transdifferentiate back into WAT and BAT. The plastic properties of mature adipocytes are supported also by a liposecretion process in vitro where adult cell in culture transdifferentiate to differentiated fibroblast-like elements able to give rise to different phenotypes (rainbow adipocytes). In addition, the inflammasome system is activated in stressed adipocytes from obese adipose tissue. These adipocytes die and debris are reabsorbed by macrophages inducing a chronic low-grade inflammation, potentially contributing to insulin resistance and T2 diabetes. Thus, the plastic properties of this organ could open new therapeutic perspectives in the obesity-related metabolic disease and in breast pathologies. © 2018 American Physiological Society. Compr Physiol 8:1357-1431, 2018.

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Necdin and E2F4 Are Modulated by Rosiglitazone Therapy in Diabetic Human Adipose and Muscle Tissue

Cited by 22 publications

References 58 publications

Myogenic gene expression signature establishes that brown and white adipocytes originate from distinct cell lineages

Myogenic gene expression signature establishes that brown and white adipocytes originate from distinct cell lineages

Loss of the Prader–Willi obesity syndrome protein necdin promotes adipogenesis

Adipose Organ Development and Remodeling

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