PMID- 34200102
OWN - NLM
STAT- MEDLINE
DCOM- 20210728
LR  - 20210728
IS  - 2072-6643 (Electronic)
IS  - 2072-6643 (Linking)
VI  - 13
IP  - 6
DP  - 2021 Jun 4
TI  - Dietary Macronutrient Intake May Influence the Effects of TCF7L2 rs7901695 
      Genetic Variants on Glucose Homeostasis and Obesity-Related Parameters: A 
      Cross-Sectional Population-Based Study.
LID - 10.3390/nu13061936 [doi]
LID - 1936
AB  - Transcription factor-7-like 2 (TCF7L2) is one of the most important 
      susceptibility genes for type 2 diabetes mellitus (T2DM). The aim of our 
      cross-sectional population-based study was to analyze whether daily macronutrient 
      intake may influence the effects of the TCF7L2 rs7901695 genotype on glucose 
      homeostasis and obesity-related parameters. We recruited 810 participants (47.5% 
      men and 52.5% women), 18-79 years old (mean age, 42.1 (+/-14.5) years), who were 
      genotyped for the common TCF7L2 rs7901695 single-nucleotide polymorphism (SNP), 
      and anthropometric measurements, body composition, body fat distribution 
      (visceral (VAT) and subcutaneous adipose tissue (SAT) content), blood glucose and 
      insulin concentrations after fasting and during OGTTs, and HbA1c were assessed. 
      The VAT/SAT ratio, HOMA-IR (homeostatic model assessment of insulin resistance), 
      HOMA-B (homeostatic model assessment of beta-cell function), and CIR30 (corrected 
      insulin response) were calculated. The daily macronutrient intake was evaluated 
      based on 3-day food-intake diaries. Daily physical activity was evaluated based 
      on a validated questionnaire. We performed ANOVA or Kruskal-Wallis tests, and 
      multivariate linear regression models were created to evaluate the effects of 
      dietary macronutrient intake on glucose homeostasis and obesity-related 
      parameters in carriers of the investigated genotypes. This study was registered 
      at ClinicalTrials.gov as NCT03792685. The TT-genotype carriers stratified to the 
      upper protein intake quantiles presented higher HbA1c levels than the CT- and 
      CC-genotype participants in the same quantiles (p = 0.038 and p = 0.022, 
      respectively). Moreover, we observed higher HOMA-IR (p = 0.014), as well as 
      significantly higher blood glucose and insulin concentrations, during the OGTTs 
      for those in the upper quantiles, when compared to subjects from the lower 
      quantiles of protein intake, while the CC-genotype carriers presented 
      significantly lower HbA1c (p = 0.033) and significantly higher CIR30 (p = 0.03). 
      The linear regression models revealed that an increase in energy derived from 
      proteins in TT carriers was associated with higher HbA1c levels (beta = 0.37 (95% 
      CI: 0.01-0.74, p = 0.05)), although, in general, carrying the TT genotype, but 
      without considering protein intake, showed an opposite tendency-to lower HbA1c 
      levels (beta = -0.22 (95% CI: 0.47 to -0.01, p = 0.05). Among the subjects 
      stratified to the lower quantile of carbohydrate intake, the TT-genotype 
      individuals presented higher HbA1c (p = 0.041), and the CC-genotype subjects 
      presented higher VAT (p = 0.033), lower SAT (p = 0.033), and higher VAT/SAT 
      ratios (p = 0.034). In both the CC- and TT-genotype carriers, we noted higher VAT 
      (p = 0.012 and p = 0.0006, respectively), lower SAT (p = 0.012 and p = 0.0006, 
      respectively) and higher VAT/SAT ratios (p = 0.016 and p = 0.00062, respectively) 
      when dietary fat provided more than 30% of total daily energy intake, without any 
      differences in total body fat content. Our findings suggest that associations of 
      the common TCF7L2 SNP with glucose homeostasis and obesity-related parameters may 
      be dependent on daily macronutrient intake, which warrants further investigations 
      in a larger population, as well as interventional studies.
FAU - Bauer, Witold
AU  - Bauer W
AUID- ORCID: 0000-0003-0776-6714
AD  - Clinical Research Centre, Medical University of Bialystok, Marii 
      Sklodowskiej-Curie 24A, 15-276 Bialystok, Poland.
FAU - Adamska-Patruno, Edyta
AU  - Adamska-Patruno E
AUID- ORCID: 0000-0002-8805-0744
AD  - Clinical Research Centre, Medical University of Bialystok, Marii 
      Sklodowskiej-Curie 24A, 15-276 Bialystok, Poland.
FAU - Krasowska, Urszula
AU  - Krasowska U
AUID- ORCID: 0000-0002-2612-8796
AD  - Clinical Research Centre, Medical University of Bialystok, Marii 
      Sklodowskiej-Curie 24A, 15-276 Bialystok, Poland.
FAU - Moroz, Monika
AU  - Moroz M
AD  - Clinical Research Centre, Medical University of Bialystok Clinical Hospital, 
      Marii Sklodowskiej-Curie 24A, 15-276 Bialystok, Poland.
FAU - Fiedorczuk, Joanna
AU  - Fiedorczuk J
AD  - Clinical Research Centre, Medical University of Bialystok Clinical Hospital, 
      Marii Sklodowskiej-Curie 24A, 15-276 Bialystok, Poland.
FAU - Czajkowski, Przemyslaw
AU  - Czajkowski P
AUID- ORCID: 0000-0001-8968-4063
AD  - Clinical Research Centre, Medical University of Bialystok, Marii 
      Sklodowskiej-Curie 24A, 15-276 Bialystok, Poland.
FAU - Bielska, Dorota
AU  - Bielska D
AD  - Department of Family Medicine, Medical University of Bialystok, Mieszka I 4b, 
      15-054 Bialystok, Poland.
FAU - Gorska, Maria
AU  - Gorska M
AD  - Department of Endocrinology, Diabetology and Internal Medicine, Medical 
      University of Bialystok, Marii Sklodowskiej-Curie 24A, 15-276 Bialystok, Poland.
FAU - Kretowski, Adam
AU  - Kretowski A
AUID- ORCID: 0000-0002-4522-4978
AD  - Clinical Research Centre, Medical University of Bialystok, Marii 
      Sklodowskiej-Curie 24A, 15-276 Bialystok, Poland.
AD  - Clinical Research Centre, Medical University of Bialystok Clinical Hospital, 
      Marii Sklodowskiej-Curie 24A, 15-276 Bialystok, Poland.
AD  - Department of Endocrinology, Diabetology and Internal Medicine, Medical 
      University of Bialystok, Marii Sklodowskiej-Curie 24A, 15-276 Bialystok, Poland.
LA  - eng
SI  - ClinicalTrials.gov/NCT03792685
GR  - 4774/B/P01/2009/37/Polish Ministry of Science and Higher Education/
PT  - Journal Article
DEP - 20210604
PL  - Switzerland
TA  - Nutrients
JT  - Nutrients
JID - 101521595
RN  - 0 (Blood Glucose)
RN  - 0 (Insulin)
RN  - 0 (TCF7L2 protein, human)
RN  - 0 (Transcription Factor 7-Like 2 Protein)
RN  - IY9XDZ35W2 (Glucose)
SB  - IM
MH  - Adolescent
MH  - Adult
MH  - Aged
MH  - Blood Glucose/analysis
MH  - Body Composition
MH  - Body Fat Distribution
MH  - Cross-Sectional Studies
MH  - *Eating/physiology
MH  - Female
MH  - Genotype
MH  - Glucose/*metabolism
MH  - Homeostasis/physiology
MH  - Humans
MH  - Insulin/blood
MH  - Male
MH  - Middle Aged
MH  - Obesity/diet therapy/*genetics/metabolism
MH  - Polymorphism, Single Nucleotide/*genetics
MH  - Transcription Factor 7-Like 2 Protein/*genetics/physiology
MH  - Young Adult
PMC - PMC8230266
OTO - NOTNLM
OT  - TCF7L2 gene
OT  - body fat content
OT  - glucose homeostasis
OT  - macronutrient intake
OT  - obesity
OT  - rs7901695 single nucleotide polymorphism
OT  - type 2 diabetes risk
COIS- The authors declare no conflict of interest.
EDAT- 2021/07/03 06:00
MHDA- 2021/07/29 06:00
PMCR- 2021/06/04
CRDT- 2021/07/02 01:06
PHST- 2021/03/23 00:00 [received]
PHST- 2021/05/28 00:00 [revised]
PHST- 2021/06/04 00:00 [accepted]
PHST- 2021/07/02 01:06 [entrez]
PHST- 2021/07/03 06:00 [pubmed]
PHST- 2021/07/29 06:00 [medline]
PHST- 2021/06/04 00:00 [pmc-release]
AID - nu13061936 [pii]
AID - nutrients-13-01936 [pii]
AID - 10.3390/nu13061936 [doi]
PST - epublish
SO  - Nutrients. 2021 Jun 4;13(6):1936. doi: 10.3390/nu13061936.