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Common genetic variants in the FETUB locus, genetically predicted fetuin-B levels, and risk of insulin resistance in obese Chinese adults.

Abstract Elevated serum fetuin-B is suggested to be associated with insulin resistance, but it is unknown if this association is causal. The aim of this study was to explore the potential causal relationship between fetuin-B and insulin resistance.We used Mendelian randomization analysis by incorporating information of genetic variants in FETUB and serum fetuin-B concentrations with insulin resistance in 1148 obese Chinese adults.Common genetic variants (FETUB rs4686434, rs6785067, and rs3733159) were significantly associated with serum fetuin-B concentrations but not with insulin resistance. Higher serum fetuin-B levels were significantly associated with increased homeostasis model assessment of insulin resistance (HOMA-IR) (0.17 [95%CI: 0.01 to 0.32, P = .037] 10 mol IU L higher per SD). However, Mendelian randomization analysis using 3 single-nucleotide polymorphisms as instrumental variables did not support a significant association between genetically predicted fetuin-B levels and HOMA-IR (-0.09 [95%CI: -0.62 to 0.44, P = .738] 10 mol IU L lower per SD). The regression coefficients for measured and genetically predicted fetuin-B concentrations on HOMA-IR were significantly different (P <.001).This study suggests the association between fetuin-B and insulin resistance may not be causal. Future studies on the nongenetic determinants of serum fetuin-B concentration to assess if such unmeasured factors may confound the association between fetuin-B and insulin resistance as well as more pathway analysis for this association are warranted.
PMID
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Authors

Mayor MeshTerms

Genetic Variation

Keywords
Journal Title medicine
Publication Year Start




PMID- 29390354
OWN - NLM
STAT- MEDLINE
DCOM- 20180212
LR  - 20180212
IS  - 1536-5964 (Electronic)
IS  - 0025-7974 (Linking)
VI  - 96
IP  - 50
DP  - 2017 Dec
TI  - Common genetic variants in the FETUB locus, genetically predicted fetuin-B
      levels, and risk of insulin resistance in obese Chinese adults.
PG  - e9234
LID - 10.1097/MD.0000000000009234 [doi]
AB  - Elevated serum fetuin-B is suggested to be associated with insulin resistance,
      but it is unknown if this association is causal. The aim of this study was to
      explore the potential causal relationship between fetuin-B and insulin
      resistance.We used Mendelian randomization analysis by incorporating information 
      of genetic variants in FETUB and serum fetuin-B concentrations with insulin
      resistance in 1148 obese Chinese adults.Common genetic variants (FETUB rs4686434,
      rs6785067, and rs3733159) were significantly associated with serum fetuin-B
      concentrations but not with insulin resistance. Higher serum fetuin-B levels were
      significantly associated with increased homeostasis model assessment of insulin
      resistance (HOMA-IR) (0.17 [95%CI: 0.01 to 0.32, P = .037] 10 mol IU L higher per
      SD). However, Mendelian randomization analysis using 3 single-nucleotide
      polymorphisms as instrumental variables did not support a significant association
      between genetically predicted fetuin-B levels and HOMA-IR (-0.09 [95%CI: -0.62 to
      0.44, P = .738] 10 mol IU L lower per SD). The regression coefficients for
      measured and genetically predicted fetuin-B concentrations on HOMA-IR were
      significantly different (P &lt;.001).This study suggests the association between
      fetuin-B and insulin resistance may not be causal. Future studies on the
      nongenetic determinants of serum fetuin-B concentration to assess if such
      unmeasured factors may confound the association between fetuin-B and insulin
      resistance as well as more pathway analysis for this association are warranted.
CI  - Copyright (c) 2017 The Authors. Published by Wolters Kluwer Health, Inc. All
      rights reserved.
FAU - Li, Zhibin
AU  - Li Z
AD  - Xiamen Diabetes Institute.
AD  - Epidemiology Research Unit, the First Affiliated Hospital.
AD  - School of Public Health.
FAU - Liu, Changqin
AU  - Liu C
AD  - Xiamen Diabetes Institute.
AD  - Department of Endocrinology and Diabetes, the First Affiliated Hospital, Xiamen
      University.
AD  - Department of Endocrinology and Diabetes, the Teaching Hospital of Fujian Medical
      University, Xiamen, China.
FAU - Shi, Xiulin
AU  - Shi X
AD  - Department of Endocrinology and Diabetes, the First Affiliated Hospital, Xiamen
      University.
FAU - Chen, Zheng
AU  - Chen Z
AD  - Department of Endocrinology and Diabetes, the First Affiliated Hospital, Xiamen
      University.
FAU - Wang, Dongmei
AU  - Wang D
AD  - School of Public Health.
FAU - Li, Long
AU  - Li L
AD  - Xiamen Diabetes Institute.
FAU - Tu, Yichang
AU  - Tu Y
AD  - Xiamen Diabetes Institute.
FAU - Lin, Mingzhu
AU  - Lin M
AD  - Department of Endocrinology and Diabetes, the First Affiliated Hospital, Xiamen
      University.
FAU - Liu, Suhuan
AU  - Liu S
AD  - Xiamen Diabetes Institute.
FAU - Yang, Shuyu
AU  - Yang S
AD  - Xiamen Diabetes Institute.
AD  - Department of Endocrinology and Diabetes, the First Affiliated Hospital, Xiamen
      University.
FAU - Li, Xuejun
AU  - Li X
AD  - Xiamen Diabetes Institute.
AD  - Department of Endocrinology and Diabetes, the First Affiliated Hospital, Xiamen
      University.
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Medicine (Baltimore)
JT  - Medicine
JID - 2985248R
RN  - 0 (Biomarkers)
RN  - 0 (Fetuin-B)
SB  - AIM
SB  - IM
MH  - Adult
MH  - Anthropometry
MH  - Biomarkers/blood
MH  - China
MH  - Female
MH  - Fetuin-B/*genetics
MH  - *Genetic Variation
MH  - Genotype
MH  - Humans
MH  - Insulin Resistance/*genetics
MH  - Male
MH  - Mendelian Randomization Analysis
MH  - Obesity/blood/*genetics
MH  - Polymorphism, Single Nucleotide
MH  - Risk Factors
MH  - Surveys and Questionnaires
EDAT- 2018/02/03 06:00
MHDA- 2018/02/13 06:00
CRDT- 2018/02/03 06:00
PHST- 2018/02/03 06:00 [entrez]
PHST- 2018/02/03 06:00 [pubmed]
PHST- 2018/02/13 06:00 [medline]
AID - 10.1097/MD.0000000000009234 [doi]
AID - 00005792-201712150-00104 [pii]
PST - ppublish
SO  - Medicine (Baltimore). 2017 Dec;96(50):e9234. doi: 10.1097/MD.0000000000009234.