Protein kinase C/ζ (<i>PRKCZ</i>) Gene is associated with type 2 diabetes in Han population of North China and analysis of its haplotypes

Li, Yun Feng; Sun, Hong; Wu, Guo Dong; Du, Wei; Zuo, Jun; Shen, Yan; Qiang, Bo; Yao, Zhi; Wang, Heng; Huang, Wei; Chen, Zhu; Xiong, Mo; Yue, Meng; Fang, F

doi:10.3748/wjg.v9.i9.2078

Cited by 10 publications

(5 citation statements)

References 26 publications

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“…The protein kinase C epsilon zeta ( PRKCZ ) is believed to be involved in the translocation of the GLUT4 protein and in the insulin-signalling pathway downstream of PI 3-kinase. Certain SNPs in PRKCZ gene were shown to be associated with T2DM risk in Han Chinese population [ 57 ]. A study was conducted to assess the correlation between T2DM and the DNA methylation of nine CpG sites in the promoter of the PRKCZ gene.…”

Section: Single or Multiple Gene Studiesmentioning

confidence: 99%

The role of DNA methylation in the pathogenesis of type 2 diabetes mellitus

et al. 2020

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Diabetes mellitus (DM) is a chronic condition characterised by β cell dysfunction and persistent hyperglycaemia. The disorder can be due to the absence of adequate pancreatic insulin production or a weak cellular response to insulin signalling. Among the three types of DM, namely, type 1 DM (T1DM), type 2 DM (T2DM), and gestational DM (GDM); T2DM accounts for almost 90% of diabetes cases worldwide. Epigenetic traits are stably heritable phenotypes that result from certain changes that affect gene function without altering the gene sequence. While epigenetic traits are considered reversible modifications, they can be inherited mitotically and meiotically. In addition, epigenetic traits can randomly arise in response to environmental factors or certain genetic mutations or lesions, such as those affecting the enzymes that catalyse the epigenetic modification. In this review, we focus on the role of DNA methylation, a type of epigenetic modification, in the pathogenesis of T2DM.

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Section: Single or Multiple Gene Studiesmentioning

confidence: 99%

The role of DNA methylation in the pathogenesis of type 2 diabetes mellitus

et al. 2020

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“…Other genes thought to be associated with type 2 diabetes include the protein kinase C/zeta ( PRKCZ ) gene among Han Chinese in North China (55), the Z +2 allele of the glucokinase gene among Mauritian Creoles (55), and HNF‐1 G319S mutation among Canadian aboriginal youth (56). Other studies have suggested that genes regulating lipid and lipoprotein metabolism may play a role, such as the G‐250A polymorphism of the hepatic lipase gene ( LIPC ) among a Finnish population (57).…”

Section: Factors Associated With the Development Of Type 2 Diabetesmentioning

confidence: 99%

Epidemiology of childhood type 2 diabetes in the developing world

2004

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Type 2 diabetes in the young is an increasing problem with potentially serious outcomes. Our understanding of the worldwide burden of this condition is incomplete, with many studies adopting different methodologies to assess the condition and reporting on specific communities or ethnic groups. Most of the data come from developed nations, with few studies from developing nations. The purpose of this review is to bring together the available data on type 2 diabetes in the young from the developing world, in order to highlight deficiencies in the knowledge of the condition and also to promote strategies to deal with it. Noted also are some of the factors associated with the condition, such as family history, genetic influences, intrauterine environment as well as the importance of birth weight, insulin resistance, obesity, and development of complications. These are of relevance in both developed and developing nations.

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“…Genome-wide association studies have identified a number of gene sequence variants associated with T2D ( 11 , 12 ). Among them, several single nucleotide polymorphisms in the PRKCZ gene have been associated with increased risk of T2D development ( 13 , 14 ). Whether these variants are positively or negatively associated with the activity or expression of the encoded protein is still unknown.…”

Section: Introductionmentioning

confidence: 99%

PKCζ Is Essential for Pancreatic β-Cell Replication During Insulin Resistance by Regulating mTOR and Cyclin-D2

et al. 2016

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Adaptive β-cell replication occurs in response to increased metabolic demand during insulin resistance. The intracellular mediators of this compensatory response are poorly defined and their identification could provide significant targets for β-cell regeneration therapies. Here we show that glucose and insulin in vitro and insulin resistance in vivo activate protein kinase C ζ (PKCζ) in pancreatic islets and β-cells. PKCζ is required for glucose- and glucokinase activator–induced proliferation of rodent and human β-cells in vitro. Furthermore, either kinase-dead PKCζ expression (KD-PKCζ) or disruption of PKCζ in mouse β-cells blocks compensatory β-cell replication when acute hyperglycemia/hyperinsulinemia is induced. Importantly, KD-PKCζ inhibits insulin resistance–mediated mammalian target of rapamycin (mTOR) activation and cyclin-D2 upregulation independent of Akt activation. In summary, PKCζ activation is key for early compensatory β-cell replication in insulin resistance by regulating the downstream signals mTOR and cyclin-D2. This suggests that alterations in PKCζ expression or activity might contribute to inadequate β-cell mass expansion and β-cell failure leading to type 2 diabetes.

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Protein kinase C/ζ (PRKCZ) Gene is associated with type 2 diabetes in Han population of North China and analysis of its haplotypes

Abstract: PRKCZ gene may be associated with type 2 diabetes in Han population in North China. The haplotypes at five SNP sites in this gene may be responsible for this association.

Cited by 10 publications

References 26 publications

The role of DNA methylation in the pathogenesis of type 2 diabetes mellitus

The role of DNA methylation in the pathogenesis of type 2 diabetes mellitus

Epidemiology of childhood type 2 diabetes in the developing world

PKCζ Is Essential for Pancreatic β-Cell Replication During Insulin Resistance by Regulating mTOR and Cyclin-D2

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