Genetic Evidence of Causal Relation Between Intestinal Glucose Absorption and Early Postprandial Glucose Response: A Mendelian Randomization Study
The post-prandial glucose response is an independent risk factor for type 2 diabetes. Observationally, early glucose response after an oral glucose challenge has been linked to intestinal glucose absorption, largely influenced by the expression of sodium-glucose-co-transporter-1 (SGLT1). This study...
Saved in:
| Published in | Diabetes (New York, N.Y.) Vol. 73; no. 6; pp. 983 - 992 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
American Diabetes Association
01.06.2024
|
| Subjects | |
| Online Access | Get full text |
Cover
Loading…
| Abstract | The post-prandial glucose response is an independent risk factor for type 2 diabetes. Observationally, early glucose response after an oral glucose challenge has been linked to intestinal glucose absorption, largely influenced by the expression of sodium-glucose-co-transporter-1 (SGLT1). This study utilizes Mendelian randomization (MR) to estimate the causal effect of intestinal SGLT1 expression on early glucose response. Involving 1547 subjects with class II/III obesity from the ABOS cohort, the study employs SGLT1 genotyping, oral glucose tolerance tests, and jejunal biopsies to measure SGLT1 expression. A loss-of-function SGLT1 haplotype served as the instrumental variable, with intestinal SGLT1 expression as the exposure and the change in 30-minute post-load glycemia from fasting glycemia (Δ30 glucose) as the outcome. Results showed that 12.8% of the 1,342 genotyped patients carried the SGLT1 loss-of-function haplotype, associated with a mean Δ30 glucose reduction of -0.41 mmol/L and a significant decrease in intestinal SGLT1 expression. The observational study linked a one standard deviation decrease in SGLT1 expression to a Δ30 glucose reduction of -0.097 mM/L. MR analysis paralleled these findings, associating a statistically significant reduction in genetically instrumented intestinal SGLT1 expression with a Δ30 glucose decreases of -0.353. In conclusion, the MR analysis provides genetic evidence that reducing intestinal SGLT1 expression causally lowers early post-load glucose response. This finding has a potential translational impact on managing early glucose response in type 2 diabetes. |
|---|---|
| AbstractList | The post-prandial glucose response is an independent risk factor for type 2 diabetes. Observationally, early glucose response after an oral glucose challenge has been linked to intestinal glucose absorption, largely influenced by the expression of sodium-glucose-co-transporter-1 (SGLT1). This study utilizes Mendelian randomization (MR) to estimate the causal effect of intestinal SGLT1 expression on early glucose response. Involving 1547 subjects with class II/III obesity from the ABOS cohort, the study employs SGLT1 genotyping, oral glucose tolerance tests, and jejunal biopsies to measure SGLT1 expression. A loss-of-function SGLT1 haplotype served as the instrumental variable, with intestinal SGLT1 expression as the exposure and the change in 30-minute post-load glycemia from fasting glycemia (Δ30 glucose) as the outcome. Results showed that 12.8% of the 1,342 genotyped patients carried the SGLT1 loss-of-function haplotype, associated with a mean Δ30 glucose reduction of -0.41 mmol/L and a significant decrease in intestinal SGLT1 expression. The observational study linked a one standard deviation decrease in SGLT1 expression to a Δ30 glucose reduction of -0.097 mM/L. MR analysis paralleled these findings, associating a statistically significant reduction in genetically instrumented intestinal SGLT1 expression with a Δ30 glucose decreases of -0.353. In conclusion, the MR analysis provides genetic evidence that reducing intestinal SGLT1 expression causally lowers early post-load glucose response. This finding has a potential translational impact on managing early glucose response in type 2 diabetes. The postprandial glucose response is an independent risk factor for type 2 diabetes. Observationally, early glucose response after an oral glucose challenge has been linked to intestinal glucose absorption, largely influenced by the expression of sodium-glucose cotransporter 1 (SGLT1). This study uses Mendelian randomization (MR) to estimate the causal effect of intestinal SGLT1 expression on early glucose response. Involving 1,547 subjects with class II/III obesity from the Atlas Biologique de l'Obésité Sévère cohort, the study uses SGLT1 genotyping, oral glucose tolerance tests, and jejunal biopsies to measure SGLT1 expression. A loss-of-function SGLT1 haplotype serves as the instrumental variable, with intestinal SGLT1 expression as the exposure and the change in 30-min postload glycemia from fasting glycemia (Δ30 glucose) as the outcome. Results show that 12.8% of the 1,342 genotyped patients carried the SGLT1 loss-of-function haplotype, associated with a mean Δ30 glucose reduction of -0.41 mmol/L and a significant decrease in intestinal SGLT1 expression. The observational study links a 1-SD decrease in SGLT1 expression to a Δ30 glucose reduction of -0.097 mmol/L. MR analysis parallels these findings, associating a statistically significant reduction in genetically instrumented intestinal SGLT1 expression with a Δ30 glucose decrease of -0.353. In conclusion, the MR analysis provides genetic evidence that reducing intestinal SGLT1 expression causally lowers early postload glucose response. This finding has a potential translational impact on managing early glucose response to prevent or treat type 2 diabetes.The postprandial glucose response is an independent risk factor for type 2 diabetes. Observationally, early glucose response after an oral glucose challenge has been linked to intestinal glucose absorption, largely influenced by the expression of sodium-glucose cotransporter 1 (SGLT1). This study uses Mendelian randomization (MR) to estimate the causal effect of intestinal SGLT1 expression on early glucose response. Involving 1,547 subjects with class II/III obesity from the Atlas Biologique de l'Obésité Sévère cohort, the study uses SGLT1 genotyping, oral glucose tolerance tests, and jejunal biopsies to measure SGLT1 expression. A loss-of-function SGLT1 haplotype serves as the instrumental variable, with intestinal SGLT1 expression as the exposure and the change in 30-min postload glycemia from fasting glycemia (Δ30 glucose) as the outcome. Results show that 12.8% of the 1,342 genotyped patients carried the SGLT1 loss-of-function haplotype, associated with a mean Δ30 glucose reduction of -0.41 mmol/L and a significant decrease in intestinal SGLT1 expression. The observational study links a 1-SD decrease in SGLT1 expression to a Δ30 glucose reduction of -0.097 mmol/L. MR analysis parallels these findings, associating a statistically significant reduction in genetically instrumented intestinal SGLT1 expression with a Δ30 glucose decrease of -0.353. In conclusion, the MR analysis provides genetic evidence that reducing intestinal SGLT1 expression causally lowers early postload glucose response. This finding has a potential translational impact on managing early glucose response to prevent or treat type 2 diabetes. The postprandial glucose response is an independent risk factor for type 2 diabetes. Observationally, early glucose response after an oral glucose challenge has been linked to intestinal glucose absorption, largely influenced by the expression of sodium–glucose cotransporter 1 (SGLT1). This study uses Mendelian randomization (MR) to estimate the causal effect of intestinal SGLT1 expression on early glucose response. Involving 1,547 subjects with class II/III obesity from the Atlas Biologique de l'Obésité Sévère cohort, the study uses SGLT1 genotyping, oral glucose tolerance tests, and jejunal biopsies to measure SGLT1 expression. A loss-of-function SGLT1 haplotype serves as the instrumental variable, with intestinal SGLT1 expression as the exposure and the change in 30-min postload glycemia from fasting glycemia (Δ30 glucose) as the outcome. Results show that 12.8% of the 1,342 genotyped patients carried the SGLT1 loss-of-function haplotype, associated with a mean Δ30 glucose reduction of −0.41 mmol/L and a significant decrease in intestinal SGLT1 expression. The observational study links a 1-SD decrease in SGLT1 expression to a Δ30 glucose reduction of −0.097 mmol/L. MR analysis parallels these findings, associating a statistically significant reduction in genetically instrumented intestinal SGLT1 expression with a Δ30 glucose decrease of −0.353. In conclusion, the MR analysis provides genetic evidence that reducing intestinal SGLT1 expression causally lowers early postload glucose response. This finding has a potential translational impact on managing early glucose response to prevent or treat type 2 diabetes. The postprandial glucose response is an independent risk factor for type 2 diabetes. Observationally, early glucose response after an oral glucose challenge has been linked to intestinal glucose absorption, largely influenced by the expression of sodium–glucose cotransporter 1 (SGLT1). This study uses Mendelian randomization (MR) to estimate the causal effect of intestinal SGLT1 expression on early glucose response. Involving 1,547 subjects with class II/III obesity from the Atlas Biologique de l’Obésité Sévère cohort, the study uses SGLT1 genotyping, oral glucose tolerance tests, and jejunal biopsies to measure SGLT1 expression. A loss-of-function SGLT1 haplotype serves as the instrumental variable, with intestinal SGLT1 expression as the exposure and the change in 30-min postload glycemia from fasting glycemia (Δ30 glucose) as the outcome. Results show that 12.8% of the 1,342 genotyped patients carried the SGLT1 loss-of-function haplotype, associated with a mean Δ30 glucose reduction of −0.41 mmol/L and a significant decrease in intestinal SGLT1 expression. The observational study links a 1-SD decrease in SGLT1 expression to a Δ30 glucose reduction of −0.097 mmol/L. MR analysis parallels these findings, associating a statistically significant reduction in genetically instrumented intestinal SGLT1 expression with a Δ30 glucose decrease of −0.353. In conclusion, the MR analysis provides genetic evidence that reducing intestinal SGLT1 expression causally lowers early postload glucose response. This finding has a potential translational impact on managing early glucose response to prevent or treat type 2 diabetes |
| Author | Lefebvre, Philippe Marciniak, Camille Lestavel, Sophie Derudas, Bruno Raverdy, Violeta Goutchtat, Rebecca Oukhouya Daoud, Naima Peschard, Simon Caiazzo, Robert Dubois-Chevalier, Julie Staels, Bart Bauvin, Pierre Verkindt, Helene Touche, Veronique Gheeraert, Celine Pattou, François Baud, Gregory Le Roux, Carel W. |
| AuthorAffiliation | 1 European Genomic Institute for Diabetes, University Lille, Lille, France 2 U1011 Nuclear Receptors, Metabolic and Cardiovascular Diseases, Institut Pasteur de Lille, CHU Lille, INSERM, University Lille, Lille, France 5 Diabetes Complications Research Centre, University College Dublin, Dublin, Ireland 3 U1190 Translational Research on Diabetes, Institut Pasteur de Lille, CHU Lille, INSERM, University Lille, Lille, France 4 Department of General and Endocrine Surgery, CHU Lille, Lille, France |
| AuthorAffiliation_xml | – name: 2 U1011 Nuclear Receptors, Metabolic and Cardiovascular Diseases, Institut Pasteur de Lille, CHU Lille, INSERM, University Lille, Lille, France – name: 4 Department of General and Endocrine Surgery, CHU Lille, Lille, France – name: 5 Diabetes Complications Research Centre, University College Dublin, Dublin, Ireland – name: 3 U1190 Translational Research on Diabetes, Institut Pasteur de Lille, CHU Lille, INSERM, University Lille, Lille, France – name: 1 European Genomic Institute for Diabetes, University Lille, Lille, France |
| Author_xml | – sequence: 1 givenname: Simon surname: Peschard fullname: Peschard, Simon – sequence: 2 givenname: Violeta orcidid: 0000-0001-5754-2028 surname: Raverdy fullname: Raverdy, Violeta – sequence: 3 givenname: Pierre surname: Bauvin fullname: Bauvin, Pierre – sequence: 4 givenname: Rebecca surname: Goutchtat fullname: Goutchtat, Rebecca – sequence: 5 givenname: Veronique surname: Touche fullname: Touche, Veronique – sequence: 6 givenname: Bruno surname: Derudas fullname: Derudas, Bruno – sequence: 7 givenname: Celine surname: Gheeraert fullname: Gheeraert, Celine – sequence: 8 givenname: Julie surname: Dubois-Chevalier fullname: Dubois-Chevalier, Julie – sequence: 9 givenname: Robert surname: Caiazzo fullname: Caiazzo, Robert – sequence: 10 givenname: Gregory surname: Baud fullname: Baud, Gregory – sequence: 11 givenname: Camille surname: Marciniak fullname: Marciniak, Camille – sequence: 12 givenname: Helene surname: Verkindt fullname: Verkindt, Helene – sequence: 13 givenname: Naima surname: Oukhouya Daoud fullname: Oukhouya Daoud, Naima – sequence: 14 givenname: Carel W. orcidid: 0000-0001-5521-5445 surname: Le Roux fullname: Le Roux, Carel W. – sequence: 15 givenname: Philippe orcidid: 0000-0002-9366-5129 surname: Lefebvre fullname: Lefebvre, Philippe – sequence: 16 givenname: Bart orcidid: 0000-0002-3784-1503 surname: Staels fullname: Staels, Bart – sequence: 17 givenname: Sophie orcidid: 0000-0001-7839-4757 surname: Lestavel fullname: Lestavel, Sophie – sequence: 18 givenname: François surname: Pattou fullname: Pattou, François |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/38498375$$D View this record in MEDLINE/PubMed |
| BookMark | eNpdks9u1DAQxi1URLeFAy-ALHGBQ4r_JLHNpVpWy7ZSEWgBiZvlxBNwlbWDnbTaPgZPXG-3VAXNYTSan74ZzXxH6MAHDwi9pOSEcS7e2YbxgkhSPUEzqrgqOBM_DtCMEMoKKpQ4REcpXRJC6hzP0CGXpZJcVDP0ZwUeRtfi5ZWz4FvAocMLMyXT4zX0ZnTB4w8wXgN4fO5HSKPzubfqpzYkwPMmhTjcUcZbvDSx3-IvIY1DzLV7RK4hDcEneI_n-BN4C70zHq8zFTbuZj_o6zjZ7XP0tDN9ghf3-Rh9_7j8tjgrLj6vzhfzi6LldTkWlBnCZG04MUaCqhqojTVCGibajkqlOqgqYhSz0CghZM1aUTLZKU4rW1rLj9HpXneYmg3YFvwYTa-H6DYmbnUwTv_b8e6X_hmuNKWUKCF5VnhzrxDD7ymfRm9caqHvjYcwJc1ULRXLL2IZff0fehmmmC-ZNCd1WStRkTpTrx6v9LDL339l4O0eaGNIKUL3gFCid17QOy_onRf4LW7yqH4 |
| Cites_doi | 10.1152/ajpgi.00286.2014 10.1016/S2213-8587(13)70050-0 10.1172/JCI105534 10.1093/ije/dyr036 10.1210/jc.2015-3906 10.1210/clinem/dgz258 10.1210/jc.2018-02166 10.1186/s12920-019-0536-1 10.1016/j.coph.2020.10.017 10.1038/nmeth842 10.1002/(SICI)1097-0258(19980430)17:8<857::AID-SIM777>3.0.CO;2-E 10.1016/j.cmet.2016.01.018 10.1038/ng0296-216 10.2337/dc13-0592 10.1016/j.cell.2015.11.001 10.1136/bmj.k601 10.1210/jc.2014-3144 10.2337/dc23-S002 10.1038/ng1547 10.1038/s41591-022-01790-7 10.1016/j.isci.2023.106057 10.1016/j.jacc.2018.07.061 10.1097/SLA.0000000000001915 10.1111/j.1467-789X.2012.01011.x 10.2337/dc10-2414 10.1002/gepi.21758 10.1016/S2213-8587(22)00005-5 10.1038/s41598-020-76769-w 10.1111/j.1365-2796.2006.01746.x 10.1152/ajpgi.00310.2001 10.1001/jama.2021.18236 10.1210/JC.2015-2482 10.1210/jc.2017-00348 10.1016/j.diabres.2012.08.002 |
| ContentType | Journal Article |
| Copyright | 2024 by the American Diabetes Association. Copyright American Diabetes Association Jun 2024 2024 by the American Diabetes Association 2024 |
| Copyright_xml | – notice: 2024 by the American Diabetes Association. – notice: Copyright American Diabetes Association Jun 2024 – notice: 2024 by the American Diabetes Association 2024 |
| DBID | AAYXX CITATION NPM K9. NAPCQ 7X8 5PM |
| DOI | 10.2337/db23-0805 |
| DatabaseName | CrossRef PubMed ProQuest Health & Medical Complete (Alumni) Nursing & Allied Health Premium MEDLINE - Academic PubMed Central (Full Participant titles) |
| DatabaseTitle | CrossRef PubMed ProQuest Health & Medical Complete (Alumni) Nursing & Allied Health Premium MEDLINE - Academic |
| DatabaseTitleList | PubMed MEDLINE - Academic ProQuest Health & Medical Complete (Alumni) |
| Database_xml | – sequence: 1 dbid: NPM name: PubMed url: https://proxy.k.utb.cz/login?url=http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed sourceTypes: Index Database |
| DeliveryMethod | fulltext_linktorsrc |
| Discipline | Medicine |
| EISSN | 1939-327X |
| EndPage | 992 |
| ExternalDocumentID | PMC11109783 38498375 10_2337_db23_0805 |
| Genre | Journal Article |
| GrantInformation_xml | – fundername: ; grantid: ANR-16-RHUS-0006_PreciNASH – fundername: ; grantid: ANR-10-LABX-0046 |
| GroupedDBID | --- .55 .XZ 08P 0R~ 18M 29F 2WC 354 4.4 53G 5GY 5RE 5RS 5VS 6PF 8R4 8R5 AAFWJ AAQQT AAWTL AAYEP AAYXX ABOCM ACGFO ACGOD ACPRK ADBBV AEGXH AENEX AERZD AHMBA AIAGR AIZAD ALIPV ALMA_UNASSIGNED_HOLDINGS BAWUL BES BTFSW CITATION CS3 DIK DU5 E3Z EBS EDB EMOBN EX3 F5P FRP GX1 H13 HZ~ IAO IEA IHR INH INR IOF IPO K2M KQ8 L7B M5~ O5R O5S O9- OHH OK1 OVD P2P PCD Q2X RHI RPM SJN SV3 TDI TEORI TR2 VVN W8F WH7 WOQ WOW X7M YFH YHG YOC ZY1 ~KM NPM K9. NAPCQ 7X8 5PM |
| ID | FETCH-LOGICAL-c364t-12a0286a30aa8e95be6ada78a27cf1899fe550a92deb977862c7428f9315d4dd3 |
| ISSN | 0012-1797 1939-327X |
| IngestDate | Thu Aug 21 18:35:07 EDT 2025 Fri Jul 11 11:11:02 EDT 2025 Mon Jun 30 10:44:30 EDT 2025 Mon Jul 21 06:00:33 EDT 2025 Tue Jul 01 04:15:15 EDT 2025 |
| IsDoiOpenAccess | true |
| IsOpenAccess | true |
| IsPeerReviewed | true |
| IsScholarly | true |
| Issue | 6 |
| Language | English |
| License | 2024 by the American Diabetes Association. Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. More information is available at https://www.diabetesjournals.org/journals/pages/license. |
| LinkModel | OpenURL |
| MergedId | FETCHMERGED-LOGICAL-c364t-12a0286a30aa8e95be6ada78a27cf1899fe550a92deb977862c7428f9315d4dd3 |
| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 V.R. and S.L. contributed equally as first/last authors. |
| ORCID | 0000-0001-5521-5445 0000-0001-5754-2028 0000-0002-9366-5129 0000-0001-7839-4757 0000-0002-3784-1503 |
| OpenAccessLink | https://pubmed.ncbi.nlm.nih.gov/PMC11109783 |
| PMID | 38498375 |
| PQID | 3064697506 |
| PQPubID | 34443 |
| PageCount | 10 |
| ParticipantIDs | pubmedcentral_primary_oai_pubmedcentral_nih_gov_11109783 proquest_miscellaneous_2968922332 proquest_journals_3064697506 pubmed_primary_38498375 crossref_primary_10_2337_db23_0805 |
| ProviderPackageCode | CITATION AAYXX |
| PublicationCentury | 2000 |
| PublicationDate | 2024-06-01 |
| PublicationDateYYYYMMDD | 2024-06-01 |
| PublicationDate_xml | – month: 06 year: 2024 text: 2024-06-01 day: 01 |
| PublicationDecade | 2020 |
| PublicationPlace | United States |
| PublicationPlace_xml | – name: United States – name: New York |
| PublicationTitle | Diabetes (New York, N.Y.) |
| PublicationTitleAlternate | Diabetes |
| PublicationYear | 2024 |
| Publisher | American Diabetes Association |
| Publisher_xml | – name: American Diabetes Association |
| References | Gunderson (2024052018520512000_B21) 2005; 37 Zubiaga (2024052018520512000_B14) 2023; 26 Martín (2024052018520512000_B32) 1996; 12 Newcombe (2024052018520512000_B31) 1998; 17 Margerie (2024052018520512000_B24) 2019; 12 Nair (2024052018520512000_B1) 2022; 28 Powell (2024052018520512000_B15) 2020; 105 ElSayed (2024052018520512000_B18) 2023; 46 Cavalot (2024052018520512000_B4) 2011; 34 Seidelmann (2024052018520512000_B23) 2018; 72 Dyer (2024052018520512000_B11) 2002; 282 Raverdy (2024052018520512000_B17) 2016; 264 International Diabetes Federation Guideline Development Group (2024052018520512000_B3) 2014; 103 Blaak (2024052018520512000_B2) 2012; 13 Tahrani (2024052018520512000_B7) 2013; 1 Wright (2024052018520512000_B10) 1998; 275 Skrivankova (2024052018520512000_B30) 2021; 326 Nguyen (2024052018520512000_B33) 2015; 100 Wright (2024052018520512000_B9) 2007; 261 Wu (2024052018520512000_B6) 2020; 55 Zeevi (2024052018520512000_B36) 2015; 163 Hemani (2024052018520512000_B28) 2018 Raverdy (2024052018520512000_B16) 2022; 10 Burgess (2024052018520512000_B26) 2013; 37 Tricò (2024052018520512000_B5) 2019; 104 Færch (2024052018520512000_B8) 2013; 36 Vandel (2024052018520512000_B25) 2020; 10 Burgess (2024052018520512000_B29) 2011; 40 Baud (2024052018520512000_B13) 2016; 23 Vanderheiden (2024052018520512000_B19) 2016; 101 Seltzer (2024052018520512000_B20) 1967; 46 Dobbins (2024052018520512000_B35) 2015; 308 Fiorentino (2024052018520512000_B12) 2017; 102 Davies (2024052018520512000_B27) 2018; 362 Marathe (2024052018520512000_B34) 2015; 100 Steemers (2024052018520512000_B22) 2006; 3 |
| References_xml | – volume: 308 start-page: G946 year: 2015 ident: 2024052018520512000_B35 article-title: Selective sodium-dependent glucose transporter 1 inhibitors block glucose absorption and impair glucose-dependent insulinotropic peptide release publication-title: Am J Physiol Gastrointest Liver Physiol doi: 10.1152/ajpgi.00286.2014 – volume: 1 start-page: 140 year: 2013 ident: 2024052018520512000_B7 article-title: SGLT inhibitors in management of diabetes publication-title: Lancet Diabetes Endocrinol doi: 10.1016/S2213-8587(13)70050-0 – volume: 46 start-page: 323 year: 1967 ident: 2024052018520512000_B20 article-title: Insulin secretion in response to glycemic stimulus: relation of delayed initial release to carbohydrate intolerance in mild diabetes mellitus publication-title: J Clin Invest doi: 10.1172/JCI105534 – volume: 40 start-page: 755 year: 2011 ident: 2024052018520512000_B29 article-title: Avoiding bias from weak instruments in Mendelian randomization studies publication-title: Int J Epidemiol doi: 10.1093/ije/dyr036 – volume: 101 start-page: 1798 year: 2016 ident: 2024052018520512000_B19 article-title: Mechanisms of action of liraglutide in patients with type 2 diabetes treated with high-dose insulin publication-title: J Clin Endocrinol Metab doi: 10.1210/jc.2015-3906 – volume: 275 start-page: G879 year: 1998 ident: 2024052018520512000_B10 article-title: I. Glucose galactose malabsorption publication-title: Am J Physiol – volume: 105 start-page: e1235 year: 2020 ident: 2024052018520512000_B15 article-title: Sotagliflozin decreases postprandial glucose and insulin concentrations by delaying intestinal glucose absorption publication-title: J Clin Endocrinol Metab doi: 10.1210/clinem/dgz258 – volume: 104 start-page: 2131 year: 2019 ident: 2024052018520512000_B5 article-title: Intestinal glucose absorption is a key determinant of 1-hour postload plasma glucose levels in nondiabetic subjects publication-title: J Clin Endocrinol Metab doi: 10.1210/jc.2018-02166 – volume: 12 start-page: 80 year: 2019 ident: 2024052018520512000_B24 article-title: Hepatic transcriptomic signatures of statin treatment are associated with impaired glucose homeostasis in severely obese patients publication-title: BMC Med Genomics doi: 10.1186/s12920-019-0536-1 – volume: 55 start-page: 116 year: 2020 ident: 2024052018520512000_B6 article-title: Role of intestinal glucose absorption in glucose tolerance publication-title: Curr Opin Pharmacol doi: 10.1016/j.coph.2020.10.017 – volume: 3 start-page: 31 year: 2006 ident: 2024052018520512000_B22 article-title: Whole-genome genotyping with the single-base extension assay publication-title: Nat Methods doi: 10.1038/nmeth842 – volume: 17 start-page: 857 year: 1998 ident: 2024052018520512000_B31 article-title: Two-sided confidence intervals for the single proportion: comparison of seven methods publication-title: Stat Med doi: 10.1002/(SICI)1097-0258(19980430)17:8<857::AID-SIM777>3.0.CO;2-E – volume: 23 start-page: 547 year: 2016 ident: 2024052018520512000_B13 article-title: Bile diversion in Roux-en-Y gastric bypass modulates sodium-dependent glucose intestinal uptake publication-title: Cell Metab doi: 10.1016/j.cmet.2016.01.018 – volume: 12 start-page: 216 year: 1996 ident: 2024052018520512000_B32 article-title: Defects in Na+/glucose cotransporter (SGLT1) trafficking and function cause glucose-galactose malabsorption publication-title: Nat Genet doi: 10.1038/ng0296-216 – volume: 36 start-page: 3691 year: 2013 ident: 2024052018520512000_B8 article-title: Impact of glucose tolerance status, sex, and body size on glucose absorption patterns during OGTTs publication-title: Diabetes Care doi: 10.2337/dc13-0592 – volume: 163 start-page: 1079 year: 2015 ident: 2024052018520512000_B36 article-title: Personalized nutrition by prediction of glycemic responses publication-title: Cell doi: 10.1016/j.cell.2015.11.001 – volume: 362 start-page: k601 year: 2018 ident: 2024052018520512000_B27 article-title: Reading Mendelian randomisation studies: a guide, glossary, and checklist for clinicians publication-title: BMJ doi: 10.1136/bmj.k601 – volume: 100 start-page: 968 year: 2015 ident: 2024052018520512000_B33 article-title: Accelerated intestinal glucose absorption in morbidly obese humans: relationship to glucose transporters, incretin hormones, and glycemia publication-title: J Clin Endocrinol Metab doi: 10.1210/jc.2014-3144 – volume: 46 start-page: S19 year: 2023 ident: 2024052018520512000_B18 article-title: 2. Classification and diagnosis of diabetes: Standards of Care in Diabetes–2023 publication-title: Diabetes Care doi: 10.2337/dc23-S002 – volume: 37 start-page: 549 year: 2005 ident: 2024052018520512000_B21 article-title: A genome-wide scalable SNP genotyping assay using microarray technology publication-title: Nat Genet doi: 10.1038/ng1547 – volume: 28 start-page: 982 year: 2022 ident: 2024052018520512000_B1 article-title: Heterogeneity in phenotype, disease progression and drug response in type 2 diabetes publication-title: Nat Med doi: 10.1038/s41591-022-01790-7 – volume: 26 start-page: 106057 year: 2023 ident: 2024052018520512000_B14 article-title: Oral metformin transiently lowers post-prandial glucose response by reducing the apical expression of sodium-glucose co-transporter 1 in enterocytes publication-title: iScience doi: 10.1016/j.isci.2023.106057 – volume: 72 start-page: 1763 year: 2018 ident: 2024052018520512000_B23 article-title: Genetic variants in SGLT1, glucose tolerance, and cardiometabolic risk publication-title: J Am Coll Cardiol doi: 10.1016/j.jacc.2018.07.061 – volume: 264 start-page: 878 year: 2016 ident: 2024052018520512000_B17 article-title: Incidence and predictive factors of postprandial hyperinsulinemic hypoglycemia after Roux-en-Y gastric bypass: a five year longitudinal study publication-title: Ann Surg doi: 10.1097/SLA.0000000000001915 – volume: 13 start-page: 923 year: 2012 ident: 2024052018520512000_B2 article-title: Impact of postprandial glycaemia on health and prevention of disease publication-title: Obes Rev doi: 10.1111/j.1467-789X.2012.01011.x – volume: 34 start-page: 2237 year: 2011 ident: 2024052018520512000_B4 article-title: Postprandial blood glucose predicts cardiovascular events and all-cause mortality in type 2 diabetes in a 14-year follow-up: lessons from the San Luigi Gonzaga Diabetes Study publication-title: Diabetes Care doi: 10.2337/dc10-2414 – volume: 37 start-page: 658 year: 2013 ident: 2024052018520512000_B26 article-title: Mendelian randomization analysis with multiple genetic variants using summarized data publication-title: Genet Epidemiol doi: 10.1002/gepi.21758 – volume: 10 start-page: 167 year: 2022 ident: 2024052018520512000_B16 article-title: Data-driven subgroups of type 2 diabetes, metabolic response, and renal risk profile after bariatric surgery: a retrospective cohort study publication-title: Lancet Diabetes Endocrinol doi: 10.1016/S2213-8587(22)00005-5 – volume: 10 start-page: 19835 year: 2020 ident: 2024052018520512000_B25 article-title: GIANT: galaxy-based tool for interactive analysis of transcriptomic data publication-title: Sci Rep doi: 10.1038/s41598-020-76769-w – volume: 261 start-page: 32 year: 2007 ident: 2024052018520512000_B9 article-title: Active sugar transport in health and disease publication-title: J Intern Med doi: 10.1111/j.1365-2796.2006.01746.x – volume: 282 start-page: G241 year: 2002 ident: 2024052018520512000_B11 article-title: Expression of monosaccharide transporters in intestine of diabetic humans publication-title: Am J Physiol Gastrointest Liver Physiol doi: 10.1152/ajpgi.00310.2001 – volume: 326 start-page: 1614 year: 2021 ident: 2024052018520512000_B30 article-title: Strengthening the reporting of observational studies in epidemiology using Mendelian randomization: the STROBE-MR Statement publication-title: JAMA doi: 10.1001/jama.2021.18236 – volume: 100 start-page: 3565 year: 2015 ident: 2024052018520512000_B34 article-title: Relationships of early and late glycemic responses with gastric emptying during an oral glucose tolerance test publication-title: J Clin Endocrinol Metab doi: 10.1210/JC.2015-2482 – volume: 102 start-page: 3979 year: 2017 ident: 2024052018520512000_B12 article-title: Duodenal sodium/glucose cotransporter 1 expression under fasting conditions is associated with postload hyperglycemia publication-title: J Clin Endocrinol Metab doi: 10.1210/jc.2017-00348 – start-page: e34408 volume-title: eLife year: 2018 ident: 2024052018520512000_B28 article-title: The MR-Base platform supports systematic causal inference across the human phenome – volume: 103 start-page: 256 year: 2014 ident: 2024052018520512000_B3 article-title: Guideline for management of postmeal glucose in diabetes publication-title: Diabetes Res Clin Pract doi: 10.1016/j.diabres.2012.08.002 |
| SSID | ssj0006060 |
| Score | 2.4569216 |
| Snippet | The post-prandial glucose response is an independent risk factor for type 2 diabetes. Observationally, early glucose response after an oral glucose challenge... The postprandial glucose response is an independent risk factor for type 2 diabetes. Observationally, early glucose response after an oral glucose challenge... |
| SourceID | pubmedcentral proquest pubmed crossref |
| SourceType | Open Access Repository Aggregation Database Index Database |
| StartPage | 983 |
| SubjectTerms | Biopsy Blood glucose Diabetes Diabetes mellitus (non-insulin dependent) Genetic analysis Genetics/Genomes/Proteomics/Metabolomics Genotyping Glucose Glucose tolerance Haplotypes Intestine Risk factors Sodium-glucose cotransporter Statistical analysis |
| Title | Genetic Evidence of Causal Relation Between Intestinal Glucose Absorption and Early Postprandial Glucose Response: A Mendelian Randomization Study |
| URI | https://www.ncbi.nlm.nih.gov/pubmed/38498375 https://www.proquest.com/docview/3064697506 https://www.proquest.com/docview/2968922332 https://pubmed.ncbi.nlm.nih.gov/PMC11109783 |
| Volume | 73 |
| hasFullText | 1 |
| inHoldings | 1 |
| isFullTextHit | |
| isPrint | |
| link | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwnV1Lb9QwELaWIlW9IN4ECjKIa8rGzsvcEK8KaVGFWrS3yF47ag-brDYJh_6M_uLO2M5jS5GAS7SKvbGU77M9M5n5TMhb2NLLREVJqFOuwljKCOZcrEImk0QKnShWoqO4-J4en8XflslyNrucVpe06mh1eWtdyf-gCvcAV6yS_Qdkh4fCDfgN-MIVEIbrX2GMmtEouGr80aA2R1x2jRXrd0luQyIW6kLAdEbjs09Tl6qpt27JwPC5sVrHm7ppN1ssdpn03LpMWuNKoxcYNrfhEexXr30p50Sq1lu7nyaB3ZtH_kxCECemscVfNhJ7sR4TA35IgMTtAj8xgaAdowey--XUD05gXx8TeL_WHdAQDOgJdaaBDRaPCVhHxi3GgouQs2x521LPuBUL0IrxEKzeZNoHXsZmbTHneSzABU_G3W7IQeyb7pC7DFwM3kd6_C4Ojt3cKVHhSO-GcQ7Ifv_PXVPmN__kZprtxG45vU_ueYeDfnDseUBmpnpI9hc-peIRufIkoj2JaF1SRyLak4h6EtGRRNRTg44kokAGaklEpyQaevYkek8lHShEdyhELYUek7Mvn08_Hof-oI5wxdO4DSMmwUxNJZ9LmRuRKJNKLbNcsmxVRuDRlwYcYSmYNkqgYCFbZeD2loJHiY615k_IXlVX5hmhpc6V1gqF6aJYy0jlUWrKebzCGu-c5wF507_zYuP0WArwYxGjAjEqEKOAHPZoFH66NgW62qkAAzkNyOuhGRZT_EImK1N3TcFEmgswmDkLyFMH3jBKj3pA8h1Yhw4o1L7bUl2cW8H2CGV9s5w__-NDX5CDcQockr1225mXYO226pWl5TWuGLQg |
| linkProvider | National Library of Medicine |
| openUrl | ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Genetic+evidence+of+causal+relation+between+intestinal+glucose+absorption+and+early+postprandial+glucose+response%3A+a+Mendelian+randomization+study&rft.jtitle=Diabetes+%28New+York%2C+N.Y.%29&rft.au=Peschard%2C+Simon&rft.au=Raverdy%2C+Violeta&rft.au=Bauvin%2C+Pierre&rft.au=Goutchtat%2C+Rebecca&rft.date=2024-06-01&rft.eissn=1939-327X&rft_id=info:doi/10.2337%2Fdb23-0805&rft_id=info%3Apmid%2F38498375&rft.externalDocID=38498375 |
| thumbnail_l | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=0012-1797&client=summon |
| thumbnail_m | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=0012-1797&client=summon |
| thumbnail_s | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=0012-1797&client=summon |