Association of common polymorphisms with gestational diabetes mellitus in Japanese women: A case-control study

Kasuga, Yoshifumi; Hata, Kenichiro; Tajima, Atsushi; Ochiai, Daigo; Saisho, Yoshifumi; Matsumoto, Tadashi; Arata, Naoko; Miyakoshi, Kei; Tanaka, Mamoru

doi:10.1507/endocrj.ej16-0431

Cited by 23 publications

(15 citation statements)

References 45 publications

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“…Of the four genetic variants (four genes) identified in the present study, several studies showed that a single polymorphism, rs266729 (ADIPOQ), was associated with decreased levels of serum adiponectin in GDM, as well as type 2 diabetes mellitus 31 . Our previous investigation showed that rs266729 (ADIPOQ) was associated with Japanese GDM 28 . Furthermore, hepatocyte nuclear factor 4 alpha (HNF4A) is known as the gene responsible for maturity onset diabetes in the young population 32 .…”

Section: Discussionmentioning

confidence: 96%

Clinical and genetic characteristics of abnormal glucose tolerance in Japanese women in the first year after gestational diabetes mellitus

Kasuga

Miyakoshi

Tajima

et al. 2018

J of Diabetes Invest

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Aims/Introduction Risk factors of type 2 diabetes mellitus in Japanese women with recent gestational diabetes mellitus are unknown. The objective of the present study was to investigate the clinical and genetic characteristics associated with postpartum abnormal glucose tolerance in Japanese women with gestational diabetes mellitus. Materials and Methods A total of 213 Japanese women with recent gestational diabetes mellitus who underwent a postpartum 2‐h oral glucose tolerance test were investigated. The association between antepartum clinical characteristics and postpartum abnormal glucose tolerance (diabetes or prediabetes based on the Japan Diabetes Society criteria) was examined. Frequencies of 45 known type 2 diabetes mellitus‐associated genetic variants were also compared between women with and without postpartum abnormal glucose tolerance. Results A total of 59 women showed postpartum abnormal glucose tolerance (prediabetes, n = 51; diabetes, n = 8). Plasma glucose levels at 1 or 2 h, the insulinogenic index and the insulin secretion‐sensitivity index‐2 of the antepartum oral glucose tolerance test were independent of postpartum abnormal glucose tolerance risk factors ( P = 0.006, P = 0.00002, P = 0.01 and P = 0.006, respectively). Four genetic variants (rs266729 [ ADIPOQ ], rs6017317 [ HNF 4A ], rs5215 [ KCNJ 11 ] and rs7177055 [ HMG 20A ]) showed a nominally significant association with postpartum abnormal glucose tolerance ( P < 0.05, respectively). Among these, three were related to insulin secretion. Postpartum abnormal glucose tolerance risk significantly increased with increasing risk‐allele number ( P = 0.0005; odds ratio 1.91). Conclusions Clinical features and genetic variants related to impaired insulin secretion are risk factors of postpartum abnormal glucose tolerance in Japanese women with recent gestational diabetes mellitus.

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Section: Discussionmentioning

confidence: 96%

Clinical and genetic characteristics of abnormal glucose tolerance in Japanese women in the first year after gestational diabetes mellitus

Kasuga

Miyakoshi

Tajima

et al. 2018

J of Diabetes Invest

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“…As the Japanese population has lower ability of insulin secretion compared with other ethnicities such as the Caucasians, the Japanese women with GDM has been shown to associate with impaired insulin secretion or beta cell dysfunction in our previous report 3 . In the Japanese GDM diagnostic strategy in the evolving COVID‐19 pandemic, which is a modification of criteria from other countries, FPG and HbA1c are listed as important for diagnosing GDM.…”

Section: Covid‐19‐gdm Covid‐19‐nft P‐value (N = 104) (N = 160)mentioning

confidence: 96%

A new diagnostic strategy for gestational diabetes during the COVID‐19 pandemic for the Japanese population

Kasuga

Saisho

Ikenoue

et al. 2020

Diabetes Metabolism Res

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“…As preproinsulin is predisposed to inefficient translocation, it is possible that TRAP might enhance its efficiency, especially given that in a pancreatic β‐cell line, mRNA encoding TRAP components are upregulated along with insulin mRNA in response to glucose stimulation . Recently, a genetic polymorphism of TRAPα has been reported to be associated with type 2 diabetes, and with gestational diabetes . Additional studies will be needed to determine if the TRAP complex plays a role in insulin biosynthesis.…”

Section: Preproinsulin Biosynthesis and Translocation Across The Er Mmentioning

confidence: 99%

“…43 Recently, a genetic polymorphism of TRAPα has been reported to be associated with type 2 diabetes, and with gestational diabetes. 44,45 Additional studies will be needed to determine if the TRAP complex plays a role in insulin biosynthesis.…”

mentioning

confidence: 99%

Biosynthesis, structure, and folding of the insulin precursor protein

Liu

Weiss

Arunagiri

et al. 2018

Diabetes Obesity Metabolism

171

165

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Insulin synthesis in pancreatic β-cells is initiated as preproinsulin. Prevailing glucose concentrations, which oscillate pre- and postprandially, exert major dynamic variation in preproinsulin biosynthesis. Accompanying upregulated translation of the insulin precursor includes elements of the endoplasmic reticulum (ER) translocation apparatus linked to successful orientation of the signal peptide, translocation and signal peptide cleavage of preproinsulin-all of which are necessary to initiate the pathway of proper proinsulin folding. Evolutionary pressures on the primary structure of proinsulin itself have preserved the efficiency of folding ("foldability"), and remarkably, these evolutionary pressures are distinct from those protecting the ultimate biological activity of insulin. Proinsulin foldability is manifest in the ER, in which the local environment is designed to assist in the overall load of proinsulin folding and to favour its disulphide bond formation (while limiting misfolding), all of which is closely tuned to ER stress response pathways that have complex (beneficial, as well as potentially damaging) effects on pancreatic β-cells. Proinsulin misfolding may occur as a consequence of exuberant proinsulin biosynthetic load in the ER, proinsulin coding sequence mutations, or genetic predispositions that lead to an altered ER folding environment. Proinsulin misfolding is a phenotype that is very much linked to deficient insulin production and diabetes, as is seen in a variety of contexts: rodent models bearing proinsulin-misfolding mutants, human patients with Mutant INS-gene-induced Diabetes of Youth (MIDY), animal models and human patients bearing mutations in critical ER resident proteins, and, quite possibly, in more common variety type 2 diabetes.

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Association of common polymorphisms with gestational diabetes mellitus in Japanese women: A case-control study

Cited by 23 publications

References 45 publications

Clinical and genetic characteristics of abnormal glucose tolerance in Japanese women in the first year after gestational diabetes mellitus

Clinical and genetic characteristics of abnormal glucose tolerance in Japanese women in the first year after gestational diabetes mellitus

A new diagnostic strategy for gestational diabetes during the COVID‐19 pandemic for the Japanese population

Biosynthesis, structure, and folding of the insulin precursor protein

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