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          Abstract

          OBJECTIVE

          Roux-en-Y gastric bypass (RYGB) and pregnancy markedly alter glucose metabolism, but evidence on glucose metabolism in pregnancy after RYGB is limited. Thus, the aims of the Bariatric Surgery and Consequences for Mother and Baby in Pregnancy study were to investigate interstitial glucose (IG) profiles during pregnancy, risk factors associated with hypoglycemia, and the association between fetal growth and hypoglycemia in pregnant women previously treated with RYGB, compared with control participants.

          RESEARCH DESIGN AND METHODS

          Twenty-three pregnant women with RYGB and 23 BMI- and parity-matched pregnant women (control group) were prospectively studied with continuous glucose monitoring in their first, second, and third trimesters, and 4 weeks postpartum. Time in range (TIR) was defined as time with an IG level of 3.5–7.8 mmol/L.

          RESULTS

          Women with RYGB were 4 years (interquartile range [IQR] 0–7) older than control participants. Pregnancies occurred 30 months (IQR 15–98) after RYGB, which induced a reduction in BMI from 45 kg/m 2 (IQR 42–54) presurgery to 32 kg/m 2 (IQR 27–39) prepregnancy. Women with RYGB spent decreased TIR (87.3–89.5% vs. 93.3–96.1%; P < 0.01) owing to an approximately twofold increased time above range and increased time below range (TBR) throughout pregnancy and postpartum compared with control participants. Women with increased TBR had a longer surgery-to-conception interval, lower nadir weight, and greater weight loss after RYGB. Finally, women giving birth to small-for-gestational age neonates experienced slightly increased TBR.

          CONCLUSIONS

          Women with RYGB were more exposed to hypoglycemia and hyperglycemia during pregnancy compared with control participants. Further research should investigate whether hypoglycemia during pregnancy in women with RYGB is associated with decreased fetal growth.

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          Most cited references30

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          Clinical Targets for Continuous Glucose Monitoring Data Interpretation: Recommendations From the International Consensus on Time in Range

          Improvements in sensor accuracy, greater convenience and ease of use, and expanding reimbursement have led to growing adoption of continuous glucose monitoring (CGM). However, successful utilization of CGM technology in routine clinical practice remains relatively low. This may be due in part to the lack of clear and agreed-upon glycemic targets that both diabetes teams and people with diabetes can work toward. Although unified recommendations for use of key CGM metrics have been established in three separate peer-reviewed articles, formal adoption by diabetes professional organizations and guidance in the practical application of these metrics in clinical practice have been lacking. In February 2019, the Advanced Technologies & Treatments for Diabetes (ATTD) Congress convened an international panel of physicians, researchers, and individuals with diabetes who are expert in CGM technologies to address this issue. This article summarizes the ATTD consensus recommendations for relevant aspects of CGM data utilization and reporting among the various diabetes populations.
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            Cellular mechanisms for insulin resistance in normal pregnancy and gestational diabetes.

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              Longitudinal changes in glucose metabolism during pregnancy in obese women with normal glucose tolerance and gestational diabetes mellitus.

              This study prospectively evaluated the longitudinal changes in insulin sensitivity, insulin response, and endogenous (primarily hepatic) glucose production and suppression during insulin infusion in women with normal glucose tolerance (control) and gestational diabetes mellitus before and during a planned pregnancy. Eight control subjects and 7 subjects in whom gestational diabetes mellitus developed were evaluated with an oral glucose tolerance test, an intravenous glucose tolerance test, and hyperinsulinemic-euglycemic clamp with infusion of [6,6 (2)H2 ]glucose before conception and at 12 to 14 and 34 to 36 weeks' gestation. Insulin response was estimated as the area under the curve during the intravenous glucose tolerance test. Basal endogenous glucose production was estimated from isotope tracer dilution during steady state with [6,6 (2)H2 ]glucose and suppression during insulin infusion. Insulin sensitivity to glucose was defined as the glucose infusion rate required to maintain euglycemia during steady-state insulin infusion. Body composition was estimated with hydrodensitometry. Data were analyzed with 2-way analysis of variance with repeated measures for 2 groups. There were increases in first-phase (P =.006) and second-phase (P =. 0001) insulin responses in both groups with advancing gestation, but the increase in second-phase response was significantly greater (P =. 02) in the gestational diabetes mellitus group than in the control group. Basal glucose production increased significantly (P =.0001) with advancing gestation, and there was resistance to suppression during insulin infusion in both groups (P =.0001). There was less suppression of endogenous glucose production however, in the gestational diabetes mellitus group than in the control group (P =. 01). Insulin sensitivity decreased with advancing gestation in both groups (P =.0001), and there was lower insulin sensitivity in the gestational diabetes mellitus group than in the control group (P =. 04). Significant decreases in insulin sensitivity with time (P =. 0001) and between groups (P =.03) remained when the data were adjusted for differences in insulin concentration or residual hepatic glucose production. Obese women in whom gestational diabetes mellitus develops have a significant increase in insulin response but decreases in insulin sensitivity and suppression of hepatic glucose production during insulin infusion with advancing gestation with respect to a matched control group. These metabolic abnormalities in glucose metabolism are the hallmarks of type 2 diabetes, for which these women are at increased risk in later life.
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                Author and article information

                Journal
                Diabetes Care
                Diabetes Care
                diabetes care
                Diabetes Care
                American Diabetes Association
                0149-5992
                1935-5548
                March 2023
                5 December 2022
                5 December 2022
                : 46
                : 3
                : 502-510
                Affiliations
                [1] 1Steno Diabetes Center Odense, Odense University Hospital, Odense, Denmark
                [2] 2Department of Clinical Research, University of Southern Denmark, Odense, Denmark
                [3] 3Steno Diabetes Center Aarhus, Aarhus University Hospital, Aarhus, Denmark
                [4] 4Department of Internal Medicine, Regional Hospital West Jutland, Herning, Denmark
                [5] 5Danish Diabetes Academy, Odense University Hospital, Odense, Denmark
                [6] 6Department of Endocrinology, Odense University Hospital, Odense, Denmark
                [7] 7Department of Gynecology and Obstetrics, Odense University Hospital, Odense, Denmark
                [8] 8Department of Endocrinology, Hospital of South West Jutland, Esbjerg, Denmark
                [9] 9Department of Regional Health Research, University of Southern Denmark, Odense, Denmark
                Author notes
                Corresponding author: Louise L. Stentebjerg, Louise.Laage.Stentebjerg2@ 123456rsyd.dk
                Author information
                https://orcid.org/0000-0003-1419-0223
                https://orcid.org/0000-0002-8964-9564
                https://orcid.org/0000-0002-4255-5544
                https://orcid.org/0000-0003-2997-2228
                https://orcid.org/0000-0001-5084-6053
                https://orcid.org/0000-0002-4285-5459
                https://orcid.org/0000-0002-3298-9824
                Article
                221357
                10.2337/dc22-1357
                10020020
                36477853
                7a036df0-2945-49b7-9c35-62506ab9bb86
                © 2023 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.

                History
                : 11 July 2022
                : 07 November 2022
                Funding
                Funded by: Danish Diabetes Academy, Novo Nordisk;
                Award ID: NNF17SA
                Funded by: Region of Southern Denmark;
                Categories
                Original Article

                Endocrinology & Diabetes
                Endocrinology & Diabetes

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