Identifying Candidate Genes for Type 2 Diabetes Mellitus and Obesity through Gene Expression Profiling in Multiple Tissues or Cells

Chen, Junhui; Meng, Yuhuan; Zhou, Jishu; Zhuo, Min; Ling, Fei; Du, Hongli; Wang, Xiaoning

doi:10.1155/2013/970435

Cited by 57 publications

(50 citation statements)

References 47 publications

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“…Obesity is characterized by an increase in adipocyte numbers, excessive accumulation of body fat and constitutes a serious health threat worldwide (de Ferranti and Mozaffarian, 2008), as it can facilitate the development of metabolic syndromes such as Type 2 diabetes mellitus (Chen et al, 2013), and insulin resistance (Lee and Lee, 2014), as well as, cardiovascular and kidney disease and some forms of cancer (Sell and Eckel, 2009;Park et al, 2011;Hefetz-Sela and Scherer 2013). The prevalence of obesity has risen rapidly over the past few decades.…”

Section: Introductionmentioning

confidence: 99%

Wnt5a regulates the cell proliferation and adipogenesis via MAPK‐independent pathway in early stage of obesity

Tang

Chen

Zhang

et al. 2017

Cell Biology International

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The early stage of obesity is an important stage in the development of obesity. However, there are few studies which explored the property or changes in obesity at early stage especially involving Wnt5a. The associated gene expression of Wnt5a on cell regeneration and the effect of Wnt5a on rat adipose-derived stem cell (rASC) proliferation and adipogenesis need additional study. Here, we investigated the changes in obesity at early stage and how Wnt5a regulates rASC regeneration, proliferation, and adipogenesis. Our data revealed that obesity at early stage measured by Lee index presented a state with impaired adipogenesis and more infiltrated inflammatory cells but without significant changes in adipocyte sizes and inflammatory factors. The process might be associated with anti-canonical Wnt pathway and a reciprocal Wnt5a/JNK pathway. Besides the gene expression of Wnt5a decreased from cell passage 1 to passage 3. The cell proliferation was regulated by increasing dose of Wnt5a with the maximal effect at 50 ng/mL and 50 ng/mL Wnt5a suppressed adipogenic differentiation at middle-late stage of adipogenesis via anti-b-catenin and a mitogen-activated protein kinase (MAPK) signaling-independent manner. Accordingly, the research helps to gain further insights into the early stage of obesity and its associated changes on a cellular and molecular level.

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Section: Introductionmentioning

confidence: 99%

Wnt5a regulates the cell proliferation and adipogenesis via MAPK‐independent pathway in early stage of obesity

Tang

Chen

Zhang

et al. 2017

Cell Biology International

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“…TMBIM4 is a candidate gene for susceptibility to type 2 diabetes and obesity [28]. As metabolic diseases can arise from changes in gene expression, TMBIM4 duplication can put our patient at a higher risk of type 2 diabetes.…”

Section: Discussionmentioning

confidence: 99%

12q14 microduplication: a new clinical entity reciprocal to the microdeletion syndrome?

et al. 2020

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Background: 12q14 microdeletion syndrome is characterized by low birth weight and failure to thrive, proportionate short stature and developmental delay. The opposite syndrome (microduplication) has not yet been characterized. Our main objective is the recognition of a new clinical entity-12q14 microduplication syndrome.-as well as confirming the role of HMGA2 gene in growth regulation. Case presentation: Array Comparative Genomic Hybridization (CGH), Karyotype, Fluorescence in situ Hybridization, Quantitative-PCR analysis and Whole exome sequencing (WES) were performed in a girl presenting overgrowth and obesity. Array CGH identified a 1.5 Mb 12q14.3 microduplication involving HMGA2, GRIP1, IRAK3, MSRB3 and TMBIM4 genes. Karyotype and FISH showed that duplication was a de novo insertion of 12q14.3 region on chromosome 9p resulting in an interstitial microduplication. Q-PCR confirmed the duplication only in the proband. WES revealed no pathogenic variants. Conclusions: Phenotypic comparison with patients with 12q14 microdeletion syndrome showed a reciprocal presentation, suggesting a phenotypically recognizable 12q14 microduplication syndrome as well as confirming the role of HMGA2 gene in growth regulation. It is also indicative that other genes, such as IRAK3 and MSRB3 might have of role in weight gain and obesity.

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“…Mutations in DLD may alter its function and promote the increased production of ROS . Solute carrier family 35 member B4 (SLC35B4) transports nucleotide sugars in and out of the Golgi and has been linked with obesity . RAB3 GTPase activating protein subunit 2 (RAB3GAP2), a member of the RAB3 protein family, modulates exocytosis of hormones and neurotransmitters and mutations in this protein lead to abnormal neurodevelopment and Warburg Micro syndrome or Martsolf syndrome .…”

Section: Exrna In the Context Of Agingmentioning

confidence: 99%

Extracellular RNA in aging

2016

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Since the discovery of extracellular RNA (exRNA) in circulation and other bodily fluids, there has been considerable effort to catalog and assess whether exRNAs can be used as markers for health and disease. A variety of exRNA species have been identified including mRNA, and non-coding RNA (ncRNA) such as microRNA (miRNA), small nucleolar RNA (snRNA), transfer RNA (tRNA), and long non-coding RNA (lncRNA). Age-related changes in exRNA abundance have been observed, and it is likely some of these transcripts play a role in aging. In this review, we summarize the current state of exRNA profiling in various body fluids and discuss age-related changes in exRNA abundance that have been identified in humans and other model organisms. MiRNAs, in particular, are a major focus of current research and we will highlight and discuss the potential role specific miRNAs might play in age-related phenotypes and disease. We will also review challenges facing this emerging field and various strategies that can be used for the validation and future use of exRNAs as markers of aging and age-related disease.

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Identifying Candidate Genes for Type 2 Diabetes Mellitus and Obesity through Gene Expression Profiling in Multiple Tissues or Cells

Cited by 57 publications

References 47 publications

Wnt5a regulates the cell proliferation and adipogenesis via MAPK‐independent pathway in early stage of obesity

Wnt5a regulates the cell proliferation and adipogenesis via MAPK‐independent pathway in early stage of obesity

12q14 microduplication: a new clinical entity reciprocal to the microdeletion syndrome?

Extracellular RNA in aging

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