Association of genetic variations of PRDM16 with metabolic syndrome in a general Xinjiang Uygur population

Zhang, Ju Hong; Li, Nan Fang; Yan, Zhi Tao; Zhang, De Lian; Wang, Hong Mei; Guo, Yan; Zhou, Lin

doi:10.1007/s12020-011-9547-1

Cited by 12 publications

(8 citation statements)

References 6 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Brown adipogenesis from white preadipocytes or myoblasts was successfully induced by the ectopic expression of PRDM16 (Seale et al, 2007), and BAT from PRDM16 -/- mice exhibited an abnormal morphology and reduced expression of brown fat markers (Seale et al, 2008). Recently, association of PRDM16 with metabolic syndrome was also suggested (Zhang et al, 2012). Considering the rapid rise in importance of PRDM16 in energy homeostasis, finding the signaling molecules that control the expression of PRDM16 are warranted, and in this respect, it is valuable to further identify a missing link between PRDM16 and clozapine or quetiapine in brown adipocytes.…”

Section: Resultsmentioning

confidence: 99%

Inhibition of mouse brown adipocyte differentiation by second-generation antipsychotics

Cho

Kwak

et al. 2012

Exp Mol Med

View full text Add to dashboard Cite

Brown adipose tissue is specialized to burn lipids for thermogenesis and energy expenditure. Second-generation antipsychotics (SGA) are the most commonly used drugs for schizophrenia with several advantages over first-line drugs, however, it can cause clinically-significant weight gain. To reveal the involvement of brown adipocytes in SGA-induced weight gain, we compared the effect of clozapine, quetiapine, and ziprasidone, SGA with different propensities to induce weight gain, on the differentiation and the expression of brown fat-specific markers, lipogenic genes and adipokines in a mouse brown preadipocyte cell line. On Oil Red-O staining, the differentiation was inhibited almost completely by clozapine (40 µM) and partially by quetiapine (30 µM). Clozapine significantly down-regulated the brown adipogenesis markers PRDM16, C/EBPβ, PPARγ2, UCP-1, PGC-1α, and Cidea in dose- and time-dependent manners, whereas quetiapine suppressed PRDM16, PPARγ2, and UCP-1 much weakly than clozapine. Clozapine also significantly inhibited the mRNA expressions of lipogenic genes ACC, SCD1, GLUT4, aP2, and CD36 as well as adipokines such as resistin, leptin, and adiponectin. In contrast, quetiapine suppressed only resistin and leptin but not those of lipogenic genes and adiponectin. Ziprasidone (10 µM) did not alter the differentiation as well as the gene expression patterns. Our results suggest for the first time that the inhibition of brown adipogenesis may be a possible mechanism to explain weight gain induced by clozapine and quetiapine.

show abstract

Section: Resultsmentioning

confidence: 99%

Inhibition of mouse brown adipocyte differentiation by second-generation antipsychotics

Cho

Kwak

et al. 2012

Exp Mol Med

View full text Add to dashboard Cite

show abstract

“…The potential role of PRDM16 in migraine is unclear. PRDM16 was originally identified associated with myelodysplastic syndrome and acute myeloid leukemia, but recent research has found its regulatory role in brown fat development and may be related to metabolic syndrome . The protein encoded by this gene is a zinc finger transcription factor and contains an N‐terminal PR domain.…”

Section: Discussionmentioning

confidence: 99%

PRDM16 rs2651899 Variant Is a Risk Factor for Chinese Common Migraine Patients

Lin

et al. 2013

Headache

View full text Add to dashboard Cite

show abstract

“…Genome-wide association studies have linked mutations of PRDM16 to migraines; however, its specific role is remains to be elucidated [20][21][22]. In addition, PRDM16 has been implicated in obesity, metabolic syndrome [23][24][25], and hypertension [26]. While the mechanism and specific role of PRDM16 in these disorders is not known, these observations support the premise that PRDM16 has quite diverse functions in tissue homeostasis.…”

Section: Other Disordersmentioning

confidence: 88%

PRDM16 in Development and Disease

Pisano¹

2014

Human Genet Embryol

View full text Add to dashboard Cite

PRDM16 is a member of the PRDM family of transcription co-regulators characterized by a PR domain (positive regulatory domain) that is similar to the SET domain found in lysine histone methyltransferases. Most PRDM proteins also contain one or more zinc finger domains that can confer direct DNA binding, in addition to other domains that mediate binding to additional transcription factors and cofactors. PRDM16 was originally identified from studies of (1;3)(p36;q21)-positive leukaemia's but has subsequently been implicated in several developmental processes, including differentiation of muscle cell precursors into brown adipocyte fat cells. Such differentiation, regulated in part by the enzyme tyrosine-protein kinase-2 (Tyk2), has gained recent attention as a means to reduce obesity via manipulating the production of TYK2 and/or PRDM16. In addition, PRDM16 is also involved in hematopoietic stem cell maintenance and craniofacial development. This review focuses on our current understanding of the role of PRDM16 in each of these processes and highlights some of the challenges for future studies.

show abstract

Association of genetic variations of PRDM16 with metabolic syndrome in a general Xinjiang Uygur population

Cited by 12 publications

References 6 publications

Inhibition of mouse brown adipocyte differentiation by second-generation antipsychotics

Inhibition of mouse brown adipocyte differentiation by second-generation antipsychotics

PRDM16 rs2651899 Variant Is a Risk Factor for Chinese Common Migraine Patients

PRDM16 in Development and Disease

Contact Info

Product

Resources

About