PMID- 38468500
OWN - NLM
STAT- MEDLINE
DCOM- 20240402
LR  - 20240407
IS  - 2233-6087 (Electronic)
IS  - 2233-6079 (Print)
IS  - 2233-6079 (Linking)
VI  - 48
IP  - 2
DP  - 2024 Mar
TI  - One-Carbon Metabolism Nutrients, Genetic Variation, and Diabetes Mellitus.
PG  - 170-183
LID - 10.4093/dmj.2023.0272 [doi]
AB  - Diabetes mellitus (DM) affects about 9.3% of the population globally. 
      Hyperhomocysteinemia (HHcy) has been implicated in the pathogenesis of DM, owing 
      to its promotion of oxidative stress, beta-cell dysfunction, and insulin resistance. 
      HHcy can result from low status of one-carbon metabolism (OCM) nutrients (e.g., 
      folate, choline, betaine, vitamin B6, B12), which work together to degrade 
      homocysteine by methylation. The etiology of HHcy may also involve genetic 
      variation encoding key enzymes in OCM. This review aimed to provide an overview 
      of the existing literature assessing the link between OCM nutrients status, 
      related genetic factors, and incident DM. We also discussed possible mechanisms 
      underlying the role of OCM in DM development and provided recommendations for 
      future research and practice. Even though the available evidence remains 
      inconsistent, some studies support the potential beneficial effects of intakes or 
      blood levels of OCM nutrients on DM development. Moreover, certain variants in 
      OCM-related genes may influence metabolic handling of methyl-donors and 
      presumably incidental DM. Future studies are warranted to establish the causal 
      inference between OCM and DM and examine the interaction of OCM nutrients and 
      genetic factors with DM development, which will inform the personalized 
      recommendations for OCM nutrients intakes on DM prevention.
FAU - Zhu, Jie
AU  - Zhu J
AD  - Nutrition and Foods Program, School of Family and Consumer Sciences, Texas State 
      University, San Marcos, TX, USA.
FAU - Saikia, Gunjana
AU  - Saikia G
AD  - Nutrition and Foods Program, School of Family and Consumer Sciences, Texas State 
      University, San Marcos, TX, USA.
FAU - Zhang, Xiaotao
AU  - Zhang X
AD  - Institute for Translational Epidemiology & Division of Liver Diseases, Department 
      of Medicine, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
FAU - Shen, Xiaoxi
AU  - Shen X
AD  - Department of Mathematics, Texas State University, San Marcos, TX, USA.
FAU - Kahe, Ka
AU  - Kahe K
AD  - Department of Obstetrics and Gynecology, Vagelos College of Physician and 
      Surgeons, Columbia University, New York, NY, USA.
AD  - Department of Epidemiology, Mailman School of Public Health, Columbia University, 
      New York, NY, USA.
LA  - eng
GR  - R01 DK116603/DK/NIDDK NIH HHS/United States
PT  - Journal Article
PT  - Review
DEP - 20240312
PL  - Korea (South)
TA  - Diabetes Metab J
JT  - Diabetes & metabolism journal
JID - 101556588
RN  - 935E97BOY8 (Folic Acid)
RN  - 7440-44-0 (Carbon)
SB  - IM
MH  - Humans
MH  - Folic Acid
MH  - Nutrients
MH  - *Hyperhomocysteinemia/genetics/metabolism/prevention & control
MH  - *Diabetes Mellitus/genetics
MH  - Carbon
MH  - Genetic Variation
PMC - PMC10995489
OTO - NOTNLM
OT  - Betaine
OT  - Choline
OT  - Diabetes mellitus
OT  - Folic acid
OT  - Genes
OT  - Homocysteine
OT  - Riboflavin
COIS- CONFLICTS OF INTEREST Ka Kahe is an international editorial board member of the 
      Diabetes & Metabolism Journal. He was not involved in the review process of this 
      review. Otherwise, there is no conflict of interest.
EDAT- 2024/03/12 06:42
MHDA- 2024/04/02 06:46
PMCR- 2024/03/01
CRDT- 2024/03/12 02:59
PHST- 2023/08/11 00:00 [received]
PHST- 2024/02/22 00:00 [accepted]
PHST- 2024/04/02 06:46 [medline]
PHST- 2024/03/12 06:42 [pubmed]
PHST- 2024/03/12 02:59 [entrez]
PHST- 2024/03/01 00:00 [pmc-release]
AID - dmj.2023.0272 [pii]
AID - dmj-2023-0272 [pii]
AID - 10.4093/dmj.2023.0272 [doi]
PST - ppublish
SO  - Diabetes Metab J. 2024 Mar;48(2):170-183. doi: 10.4093/dmj.2023.0272. Epub 2024 
      Mar 12.