Improvements in Insulin Resistance and Glucose Metabolism Related to Breastfeeding Are Not Mediated by Subclinical Inflammation.

IF 3.4 3区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Metabolites Pub Date : 2024-11-09 DOI:10.3390/metabo14110608
Julia Martins de Oliveira, Patrícia Médici Dualib, Alexandre Archanjo Ferraro, Rosiane Mattar, Sérgio Atala Dib, Bianca de Almeida-Pititto
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Abstract

Background: Lactation is known to improve insulin resistance, but this phenomenon remains poorly understood. Our goal was to evaluate whether subclinical inflammation could mediate the association between breastfeeding (BF) and improvement in glucose metabolism and markers of insulin resistance (MIRs) in the postpartum. Methods: A total of 95 adult women (≥18 years) with a BMI ≥ 25 kg/m2 from the outpatient clinic of the Federal University of São Paulo were followed from early pregnancy until 60 to 180 days postpartum. The patients were divided based on their BF status: BF and non-BF groups. A latent variable termed SubInf was created incorporating inflammation-related biomarkers: adiponectin, E-selectin, branched-chain amino acids, zonulin, copeptin, and lipopolysaccharides. The association of BR with MIRs in the postpartum was evaluated through linear regression analysis, and mediation analysis was performed to evaluate the role of SubInf in this association. Results: The groups were similar regarding gestational diabetes mellitus (GDM) prevalence, pre-gestational BMI, caloric intake, physical activity, and postpartum weight loss. The BF group presented lower levels of triglycerides (TGs), fasting glucose, fasting insulin, TG/HDLcholesterol ratio (TG/HDL), TyG index, and HOMA-IR compared to the non-BF group. A linear regression analysis adjusted for scholarity, parity, pre-gestational BMI, GDM, weight gain during pregnancy, and mode of delivery revealed an inverse association between BF and fasting glucose [-6.30 (-10.71 to -1.89), p = 0.005), HOMA-IR [-0.28 (-0.50 to -0.05), p = 0.017], TyG index [-0.04 (-0.06 to -0.01), p = 0.002], and TG/HDL ratio [-0.23 (-0.46 to -0.01), p = 0.001]. In the mediation analysis, SubInf did not mediate the indirect effect of BF on MIRs. Conclusions: In overweight and obese women, an association between BF and improvement in MIRs in the postpartum was seen, corroborating that BF should be stimulated, especially in these cardiometabolic high-risk women. Subclinical inflammation did not seem to mediate this association.

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与母乳喂养相关的胰岛素抵抗和葡萄糖代谢改善并非由亚临床炎症介导
背景:众所周知,母乳喂养可改善胰岛素抵抗,但人们对这一现象仍知之甚少。我们的目标是评估亚临床炎症是否会介导母乳喂养(BF)与产后糖代谢和胰岛素抵抗标志物(MIRs)改善之间的关联。研究方法对圣保罗联邦大学门诊部的 95 名体重指数≥ 25 kg/m2 的成年女性(≥ 18 岁)进行了从怀孕初期到产后 60 至 180 天的跟踪调查。患者根据其母乳喂养状况分为母乳喂养组和非母乳喂养组:母乳喂养组和非母乳喂养组。创建了一个称为 SubInf 的潜变量,其中包含与炎症相关的生物标记物:脂肪连蛋白、E-选择素、支链氨基酸、zonulin、 copeptin 和脂多糖。通过线性回归分析评估了BR与产后MIRs的关系,并进行了中介分析以评估SubInf在这种关系中的作用。结果两组在妊娠糖尿病(GDM)发病率、妊娠前体重指数、热量摄入、体力活动和产后体重减轻方面相似。与非 BF 组相比,BF 组的甘油三酯 (TGs)、空腹血糖、空腹胰岛素、TG/HDL 胆固醇比值 (TG/HDL)、TyG 指数和 HOMA-IR 水平较低。经学者、奇偶性、妊娠前体重指数、GDM、孕期体重增加和分娩方式调整后的线性回归分析表明,BF 与空腹血糖呈负相关 [-6.30 (-10.71 to -1.89), p = 0.005)、HOMA-IR [-0.28 (-0.50 to -0.05),p = 0.017]、TyG 指数 [-0.04 (-0.06 to -0.01),p = 0.002]、TG/HDL 比值 [-0.23 (-0.46 to -0.01),p = 0.001]。在中介分析中,SubInf 没有中介 BF 对 MIRs 的间接影响。结论:在超重和肥胖妇女中,BF 与产后 MIRs 的改善之间存在关联,这证实了应促进 BF,尤其是对这些心脏代谢高风险妇女。亚临床炎症似乎与这种关联无关。
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来源期刊
Metabolites
Metabolites Biochemistry, Genetics and Molecular Biology-Molecular Biology
CiteScore
5.70
自引率
7.30%
发文量
1070
审稿时长
17.17 days
期刊介绍: Metabolites (ISSN 2218-1989) is an international, peer-reviewed open access journal of metabolism and metabolomics. Metabolites publishes original research articles and review articles in all molecular aspects of metabolism relevant to the fields of metabolomics, metabolic biochemistry, computational and systems biology, biotechnology and medicine, with a particular focus on the biological roles of metabolites and small molecule biomarkers. Metabolites encourages scientists to publish their experimental and theoretical results in as much detail as possible. Therefore, there is no restriction on article length. Sufficient experimental details must be provided to enable the results to be accurately reproduced. Electronic material representing additional figures, materials and methods explanation, or supporting results and evidence can be submitted with the main manuscript as supplementary material.
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