Maternal smoking, nutritional factors at different life stage, and the risk of incident type 2 diabetes: a prospective study of the UK Biobank
Background This study aims to investigate potential interactions between maternal smoking around birth (MSAB) and type 2 diabetes (T2D) pathway-specific genetic risks in relation to the development of T2D in offspring. Additionally, it seeks to determine whether and how nutritional factors during different life stages may modify the association between MSAB and risk of T2D. Methods This study included 460,234 participants aged 40 to 69 years, who were initially free of T2D from the UK Biobank. MSAB and breastfeeding were collected by questionnaire. The Alternative health eating index(AHEI) and dietary inflammation index(DII) were calculated. The polygenic risk scores(PRS) of T2D and pathway-specific were established, including β-cell function, proinsulin, obesity, lipodystrophy, liver function and glycated haemoglobin(HbA1c). Cox proportion hazards models were performed to evaluate the gene/diet-MSAB interaction on T2D. The relative excess risk due to additive interaction (RERI) were calculated. Results During a median follow-up period of 12.7 years, we identified 27,342 cases of incident T2D. After adjustment for potential confounders, participants exposed to MSAB had an increased risk of T2D (HR=1.11, 95%CI:1.08-1.14), and this association remained significant among the participants with breastfeeding (HR= HR=1.10, 95%CI: 1.06-1.14). Moreover, among the participants in the highest quartile of AHEI or in the lowest quartile of DII, the association between MSAB and the increased risk of T2D become non-significant (HR=0.94, 95%CI: 0.79-1.13 for AHEI; HR=1.09, 95%CI:0.99-1.20 for DII). Additionally, the association between MSAB and risk of T2D became non-significant among the participants with lower genetic risk of lipodystrophy (HR=1.06, 95%CI:0.99-1.14), and exposed to MSAB with a higher genetic risk for β-cell dysfunction or lipodystrophy additively elevated the risk of T2D(RERI=0.18, 95%CI:0.06-0.30 for β-cell function; RERI=0.16, 95%CI:0.04-0.28 for lipodystrophy). Conclusions This study indicates that maintaining a high dietary quality or lower dietary inflammation in diet may reduce the risk of T2D associated with MSAB, and the combination of higher genetic risk of β-cell dysfunction or lipodystrophy and MSAB significantly elevate the risk of T2D in offspring..
| Medienart: |
E-Artikel |
|---|
| Erscheinungsjahr: |
2024 |
|---|---|
| Erschienen: |
2024 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:22 |
|---|---|
| Enthalten in: |
BMC medicine - 22(2024), 1 vom: 02. Feb. |
| Sprache: |
Englisch |
|---|
| Beteiligte Personen: |
Jiang, Wenbo [VerfasserIn] |
|---|
| Links: |
Volltext [kostenfrei] |
|---|
| Themen: |
Breastfeeding |
|---|
| Anmerkungen: |
© The Author(s) 2024 |
|---|
| doi: |
10.1186/s12916-024-03256-8 |
|---|
| funding: |
|
|---|---|
| Förderinstitution / Projekttitel: |
|
| PPN (Katalog-ID): |
SPR054614627 |
|---|
| LEADER | 01000naa a22002652 4500 | ||
|---|---|---|---|
| 001 | SPR054614627 | ||
| 003 | DE-627 | ||
| 005 | 20240202064712.0 | ||
| 007 | cr uuu---uuuuu | ||
| 008 | 240202s2024 xx |||||o 00| ||eng c | ||
| 024 | 7 | |a 10.1186/s12916-024-03256-8 |2 doi | |
| 035 | |a (DE-627)SPR054614627 | ||
| 035 | |a (SPR)s12916-024-03256-8-e | ||
| 040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
| 041 | |a eng | ||
| 100 | 1 | |a Jiang, Wenbo |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Maternal smoking, nutritional factors at different life stage, and the risk of incident type 2 diabetes: a prospective study of the UK Biobank |
| 264 | 1 | |c 2024 | |
| 336 | |a Text |b txt |2 rdacontent | ||
| 337 | |a Computermedien |b c |2 rdamedia | ||
| 338 | |a Online-Ressource |b cr |2 rdacarrier | ||
| 500 | |a © The Author(s) 2024 | ||
| 520 | |a Background This study aims to investigate potential interactions between maternal smoking around birth (MSAB) and type 2 diabetes (T2D) pathway-specific genetic risks in relation to the development of T2D in offspring. Additionally, it seeks to determine whether and how nutritional factors during different life stages may modify the association between MSAB and risk of T2D. Methods This study included 460,234 participants aged 40 to 69 years, who were initially free of T2D from the UK Biobank. MSAB and breastfeeding were collected by questionnaire. The Alternative health eating index(AHEI) and dietary inflammation index(DII) were calculated. The polygenic risk scores(PRS) of T2D and pathway-specific were established, including β-cell function, proinsulin, obesity, lipodystrophy, liver function and glycated haemoglobin(HbA1c). Cox proportion hazards models were performed to evaluate the gene/diet-MSAB interaction on T2D. The relative excess risk due to additive interaction (RERI) were calculated. Results During a median follow-up period of 12.7 years, we identified 27,342 cases of incident T2D. After adjustment for potential confounders, participants exposed to MSAB had an increased risk of T2D (HR=1.11, 95%CI:1.08-1.14), and this association remained significant among the participants with breastfeeding (HR= HR=1.10, 95%CI: 1.06-1.14). Moreover, among the participants in the highest quartile of AHEI or in the lowest quartile of DII, the association between MSAB and the increased risk of T2D become non-significant (HR=0.94, 95%CI: 0.79-1.13 for AHEI; HR=1.09, 95%CI:0.99-1.20 for DII). Additionally, the association between MSAB and risk of T2D became non-significant among the participants with lower genetic risk of lipodystrophy (HR=1.06, 95%CI:0.99-1.14), and exposed to MSAB with a higher genetic risk for β-cell dysfunction or lipodystrophy additively elevated the risk of T2D(RERI=0.18, 95%CI:0.06-0.30 for β-cell function; RERI=0.16, 95%CI:0.04-0.28 for lipodystrophy). Conclusions This study indicates that maintaining a high dietary quality or lower dietary inflammation in diet may reduce the risk of T2D associated with MSAB, and the combination of higher genetic risk of β-cell dysfunction or lipodystrophy and MSAB significantly elevate the risk of T2D in offspring. | ||
| 650 | 4 | |a Maternal smoking |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Breastfeeding |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Nutritional factors |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Genetic susceptibility |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Type 2 diabetes |7 (dpeaa)DE-He213 | |
| 700 | 1 | |a Tang, Yiwei |4 aut | |
| 700 | 1 | |a Yang, Ruiming |4 aut | |
| 700 | 1 | |a Long, Yujia |4 aut | |
| 700 | 1 | |a Sun, Changhao |4 aut | |
| 700 | 1 | |a Han, Tianshu |4 aut | |
| 700 | 1 | |a Wei, Wei |4 aut | |
| 773 | 0 | 8 | |i Enthalten in |t BMC medicine |d London : BioMed Central, 2003 |g 22(2024), 1 vom: 02. Feb. |w (DE-627)SPR02834149X |w (DE-600)2131669-7 |x 1741-7015 |7 nnns |
| 773 | 1 | 8 | |g volume:22 |g year:2024 |g number:1 |g day:02 |g month:02 |
| 856 | 4 | 0 | |u https://dx.doi.org/10.1186/s12916-024-03256-8 |z kostenfrei |3 Volltext |
| 912 | |a GBV_USEFLAG_A | ||
| 912 | |a GBV_SPRINGER | ||
| 951 | |a AR | ||
| 952 | |d 22 |j 2024 |e 1 |b 02 |c 02 | ||