BACKGROUND:Since obesity and its associated metabolic dysregulation are recognized risk factors for cognitive decline, this study investigated whether semaglutide, a glucagon-like peptide-1 receptor agonist proven to have cardiometabolic benefits, could provide potential neuroprotective effects on brain structure and function. METHODS:In a prospective, single-arm intervention study, 26 adults with overweight or obesity received 1.0 mg semaglutide weekly for 24 weeks. Multimodal assessments were performed pre- and post-intervention, including structural and functional MRI for analysing grey matter volume (GMV), fractional amplitude of low-frequency fluctuations (fALFF), and regional homogeneity (ReHo). Cognitive function was evaluated using standardized computerized tasks (the Flanker and N-back). Additionally, comprehensive metabolic profiles were assessed, including markers of glucose and lipid metabolism along with inflammatory cells. RESULTS:Semaglutide treatment significantly improved systemic metabolic health, inducing weight loss and reducing glycolipid levels and leukocyte counts. Neuroimaging revealed targeted neurobiological effects in the left temporal lobe: specifically, increased GMV in the left inferior temporal gyrus and decreased fALFF in the left middle and superior temporal gyri alongside reduced ReHo in the left middle temporal gyrus. These neural changes occurred despite no significant improvement in cognitive task performance. Importantly, the alterations in brain structure and function were not statistically correlated with the degree of weight loss or metabolic improvement. CONCLUSIONS:A 24-week semaglutide intervention induces significant neurobiological remodelling in the left temporal lobe of adults with overweight or obesity. These central effects are independent of the drug's systemic metabolic improvements, offering new evidence for its potential neuroprotective role.

Berberine demonstrates protective effects against diabetic kidney disease (DKD), yet its underlying mechanisms remain incompletely understood. This study investigated whether berberine alleviates DKD through modulation of the gut microbiota and the sodium butyrate-mediated HDAC1/GPX4 axis (Histone deacetylase 1 / glutathione peroxidase 4). In diabetic (db/db) mice, berberine treatment significantly ameliorated renal injury, reduced proteinuria and serum creatinine, increased the abundance of the butyrate producing bacterium Lachnospiraceae and plasma butyrate levels, while downregulating renal HDAC1 and upregulating GPX4 expression. In high glucose (HG) stimulated human renal glomerular endothelial cells (HRGECs), sodium butyrate enhanced cell viability, improved tube formation, and suppressed lipid peroxidation, effects counteracted by the ferroptosis inducer RSL3. Sodium butyrate inhibited HG-induced HDAC1 expression, increased H3K9 acetylation, and enriched H3K9ac binding to the GPX4 promoter. Overexpression of HDAC1 attenuated sodium butyrate's protective effects against HG-induced injury and ferroptosis. In conclusion, berberine attenuates DKD by increasing sodium butyrate, which modulates the HDAC1/GPX4 axis to inhibit ferroptosis in glomerular endothelial cells, providing a novel mechanistic insight and potential therapeutic strategy.

Objective Placenta-derived inflammation plays a vital role in the pathophysiology of gestational diabetes mellitus (GDM). IL-32 is a novel pro-inflammatory cytokine and metabolic regulator involved in the development of metabolic disease. We investigated the effect of IL-32 in GDM. Materials and Methods First-trimester C-reactive protein (CRP) level was monitored in a case-control study of 186 women with GDM and 186 women without. Placental tissue was lysed and analyzed by high-resolution liquid chromatography-tandem mass spectrometry. Circulating level of inflammatory cytokines IL-32, IL-6, and TNF-α were measured by ELISA kits. The expression of placenta-derived macrophages, inflammatory cytokines, and related pathway proteins were assessed by reverse transcriptase-quantitative PCR, western blot, immunohistochemistry, or immunofluorescence. Results First-trimester CRP level in peripheral blood was closely associated with glucose and insulin resistance index and was an independent correlation with the development of GDM. High-resolution liquid chromatography-tandem mass spectrometry revealed that placenta-derived CRP expression was dramatically elevated in women with GDM. Interestingly, the expression of placenta-derived IL-32 was also increased and located in the macrophages of placental tissue. Meanwhile, the expression of IL-6, TNF-α, and p-p38 were up-regulated in the placental tissues with GDM. Either IL-6 or TNF-α was colocated with IL-32 in the placental tissue. Importantly, circulating IL-32 throughout pregnancy was increased in GDM and was related to placental-derived IL-32 expression, circulating IL-6, and TNF-α, glucose and insulin resistance index. Conclusion Increased circulating IL-32 throughout pregnancy was closely associated with placenta macrophage-derived IL-32 expression and GDM. First trimester IL-32 level in peripheral blood may serve to predict the development of GDM.

This study aimed to assess whether the Haptoglobin (Hp) genotype influences the relationship between hemoglobin (Hb) levels and the development of gestational diabetes mellitus (GDM). Additionally, it sought to evaluate the interaction and joint association of Hb levels and Hp genotype with GDM risk. This retrospective study involved 358 women with GDM and 1324 women with normal glucose tolerance (NGT). Peripheral blood leukocytes were collected from 360 individuals at 14–16 weeks’ gestation for Hp genotyping. GDM was diagnosed between 24–28 weeks’ gestation. Interactive moderating effect, joint analysis, and mediation analysis were performed to evaluate the crosslink of Hb levels and Hp genotype with GDM risk. Women who developed GDM had significantly higher Hb levels throughout pregnancy compared to those with NGT. Increase first-trimester Hb concentration was associated with a progressive rise in GDM incidence, glucose levels, glycosylated hemoglobin levels, Homeostasis Model Assessment for Insulin Resistance (HOMA-IR) values, cesarean delivery rates, and composite neonatal outcomes. Spline regression showed a significant linear association of GDM incidence with continuous first-trimester Hb level when the latter exceeded 122 g/L. Increased first-trimester Hb concentration was an independent risk factor for GDM development after adjusting for potential confounding factors in both the overall population and a matched case-control group. The Hp2–2 genotype was more prevalent among pregnant women with GDM when first-trimester Hb exceeded 122 g/L. Significant multiplicative and additive interactions were identified between Hb levels and Hp genotype for GDM risk, adjusted for age and pre-pregnancy BMI. The odds ratio (OR) for GDM development increased incrementally when stratified by Hb levels and Hp genotype. Moreover, first-trimester Hb level partially mediated the association between Hp genotype and GDM risk. Increased first-trimester Hb levels were closely associated with the development of GDM and adverse pregnancy outcomes, with this association moderated by the Hp2–2 genotype.

Background Chronic inflammation plays a vital role in the development of gestational diabetes mellitus (GDM). Studies in mouse models show that neutrophil serine proteases (NSPs), neutrophil elastase (NE) and proteinase-3 (PR3) are important drivers of chronic inflammation with consequent metabolic disturbances. This study evaluated the association of NE and PR3 with GDM development and adverse fetal outcomes. Method(s) This was a prospective cohort study. Serum PR3 and NE concentration was measured in all enrolled pregnant women in the first and the second trimester to determine the connection between NSPs and GDM and adverse fetal outcomes. Logistic regression, spline regression and linear regression analyses were applied to investigate the association of NE or PR3 with GDM development and adverse fetal outcomes. The concentration of NE and PR3 in placental biopsies was evaluated by semi-quantitative analysis of immunohistochemistry staining. Result(s) NE or PR3 concentration in the first trimester, rather than the second, increased more significantly in women with GDM than in those without, regardless of pre-pregnancy body mass index and age. There was a stepwise increase in GDM occurrence as well as comprehensive adverse fetal outcomes across tertiles of NE and PR3. NE and PR3 were positively associated with neutrophil count, pre-pregnancy BMI, plasma glucose level and newborn weight. Logistic regression revealed NE or PR3 to be independent risk factors for the development of GDM and comprehensive adverse fetal outcomes. Spline regression showed a significant increased risk of GDM occurrence and comprehensive adverse fetal outcomes when serum NE concentration exceeded 417.60 ng/mL and a similar result for PR3 and GDM occurrence when the latter exceeded 88.52 ng/mL. Immunohistochemistry data confirmed that enriched NE and PR3 content in placental tissue may have contributed to the development of GDM. Conclusion(s) This work demonstrates that excessive first-trimester NE and PR3 increase the risk of GDM development and comprehensive adverse fetal outcomes.

Background Advanced glycation end products (AGEs) deposited in the lens are correlated with those in the kidneys, indicating a possible value in evaluating diabetic kidney disease (DKD). This study explored the value of noninvasively measuring lens AGEs to diagnose and evaluate the severity of diabetic nephropathy in patients with type 2 diabetes mellitus (T2DM). Methodology A total of 134 T2DM patients admitted to the Fifth People's Hospital of Shanghai from March 2020 to May 2021 were selected randomly. Patients were divided into low-, medium-and high-risk groups according to the risk assessment criteria for DKD progression and into DKD and non-DKD (non-DKD) groups according to the Guidelines for the Prevention and Treatment of Diabetic Nephropathy in China. The concentrations of noninvasive AGEs in the lens in all the groups were retrospectively analyzed. Results The concentration of noninvasive lens AGEs in the high-risk patients, according to the 2012 guidelines of the Global Organization for Improving the Prognosis of Kidney Diseases, was significantly higher than that in the remaining groups. Regression analysis suggested the value of lens AGEs in diagnosing DKD and evaluating DKD severity. Cox regression analysis indicated that the noninvasive lens AGE concentration was positive correlated with the course of disease. Conclusion The receiver operating characteristic (ROC) curve suggested that using noninvasive lens AGE measurements has clinical value in the diagnosis of DKD (area under the curve 62.4%,95% confidence interval (CI) 52.4%–73.9%, p = 0.014) and in assessing the severity of DKD (area under the curve 83.2%, 95% CI 74.1%–92.3%, P < 0.001). Noninvasive lens AGE testing helps screen T2DM patients for DKD and evaluate the severity of DKD.

Objective:To investigate the effects of persistent isolated hypothyroxinemia in the first and second trimester of pregnancy on complications and adverse outcomes of pregnancy.Methods:A retrospective analysis was conducted in 784 pregnant women including 111 cases of persistent isolated hypothyroxinemia in the first and second trimester of pregnancy and 673 pregnant women with normal thyroid function as control group. All women were registered and delivered in the Department of Obstetrics of our hospital from April 2016 to April 2017. The complications and adverse outcomes of pregnancy in the two groups were analyzed.Results:Age, body weight before pregnancy, body mass index(BMI), 1 h plasma glucose and 2 h plasma glucose during oral glucose tolerance test in persistent isolated hypothyroxinemia group were higher than those in control group( P<0.05), with increased incidence of anemia during pregnancy( P<0.05). However, there were no significant differences in the incidences of gestational diabetes mellitus and gestational hypertension between the two groups( P>0.05). No significant statistical differences were found in macrosomia, stillbirth, neonatal malformation, postpartum hemorrhage, acute delivery, premature delivery, fetal intrauterine development delay, and small full-term infants between the two groups( P>0.05). Logistic regression analysis showed that age( OR=1.1, 95% CI 1.0-1.1, P=0.002) and pre-pregnancy body weight( OR=1.0, 95% CI 1.0-1.1, P=0.046) were risk factors for the occurrence of persistent isolated hypothyroxinemia in the first and second trimesters of pregnancy. Persistent isolated hypothyroxinemia in the first and second trimesters was associated with anemia during pregnancy( OR=1.9, 95% CI 1.1-3.2, P=0.024). Conclusions:Pregnant women who are older and heavier before pregnancy should pay more attention to their thyroid function. Pregnant women with persistent isolated hypothyroxinemia in the first and second trimesters should be concerned for anemia.

AIMS:The role of Neutrophil elastase (NE) and proteinase 3 (PR3) in the occurrence and severity of stroke and acute myocardial infarction (AMI) have not been explored in type 2 diabetes mellitus (T2DM). This study aimed to investigate the relationship and predictive ability of NE and PR3 in the development of stroke and AMI in patients with T2DM, and to explore the pattern of NE and PR3 in atherosclerotic plaques.METHODS:465 patients with T2DM (stroke or AMI, n = 234; non stroke or AMI, n = 231) were recruited. Clinical characteristics, and NE and PR3 concentration were measured in all subjects. Semi-quantitative analysis of immunohistochemistry staining for NE and PR3 was performed in detached emboli and stable plaques.RESULTS:Patients with stroke or AMI had a higher level of NE and PR3, with a more pronounced increase in more severe cases (higher mRS score in stroke and Gensini score in AMI) and associated with clinical markers. An increase in NE and PR3 was an independent risk factor for stroke (OR = 4.318, P = 0.017; OR = 2.979, P = 0.048, respectively) and AMI (OR = 8.385, P = 0.015; OR = 5.540, P = 0.047). Finally, immunohistochemistry staining revealed that the NE and PR3 positive area increased significantly in detached emboli compared with stable plaques.CONCLUSION:Increased NE and PR3 was associated with occurrence and severity of stroke and AMI in patients with T2DM. Enriched NE and PR3 in detached emboli may be associated with plaque vulnerability.

CONTEXT:The immune system plays a central role in the pathophysiology of gestational diabetes mellitus (GDM). Monocytes, the main innate immune cells, are especially important in the maintenance of a normal pregnancy. OBJECTIVE:Here, we investigated the potential effect of monocytes in GDM. METHODS:Monocyte count was monitored throughout pregnancy in 214 women with GDM and 926 women without in a case-control and cohort study. Circulating levels of inflammatory cytokines, placenta-derived macrophages, and their products were measured. RESULTS:Throughout pregnancy, monocyte count was significantly decreased in women with GDM, and was closely associated with glucose level, insulin resistance, and newborn weight. First-trimester monocyte count outperformed that of the second and third trimester as a risk factor and diagnostic predictor of GDM and macrosomia both in the case-control and cohort study. In addition, our cohort study showed that as first-trimester monocyte count decreased, GDM and macrosomia incidence, glucose level, and newborn weight increased in a stepwise manner. Risk of GDM started to decrease rapidly when first-trimester monocyte count exceeded 0.48 × 109/L. Notably, CD206 and interleukin 10 (IL-10) were significantly lower, whereas CD80, CD86, tumor necrosis factor α (TNF-α), and interleukin 6 (IL-6) were higher both in GDM placental tissue and peripheral blood. First-trimester monocyte count was positively related to IL-10 and CD206, but negatively related to CD80, CD86, TNF-α, and IL-6. CONCLUSION:Decreased monocyte count throughout pregnancy was closely associated with the development of GDM, macrosomia, and the chronic inflammatory state of GDM. First-trimester monocyte count has great potential as an early diagnostic marker of GDM.

Diabetic kidney disease (DKD) is a complication of diabetes, which is the most common cause of end-stage renal disease (dialysis). DKD has a high mortality rate, and only early detection can nip this disease in the bud. Advanced glycation end products (AGEs)are generally believed to be involved in the occurrence of DKD. Studies have shown that the lens AGEs fluorescence for noninvasive detection has high consistency with the gold standard OGTT, has high sensitivity and specificity, and could be used as a practical tool for the early screening of type 2 diabetes mellitus (T2DM).Therefore, we speculated that the noninvasive lens AGEs fluorescence detection method can be used to predict the occurrence of DKD. This study detected levels of AGEs in multiple cellular and tissues and analyzed the relationships between AGEs and lens, eyeballs, peripheral blood mononuclear cell (PBMC), serum, and kidney. Additionally, we examined the possible role of lens AGEs fluorescence in DKD screening. Our preexperimental study found that lens AGE levels in patients with T2DM were positively correlated with PBM and serum AGE levels. Lens AGE levels in patients with T2DM were negatively correlated with eGFR and positively correlated with urinary ACR. The animal and cell experiments showed that the AGE levels in the eyeballs of DM mice were also positively correlated with those in the serum and kidney. To increase the reliability of the experiment, we increased the sample size. In our results, lens AGEs levels were positively correlated with the occurrence of DKD, and the incidence of DKD in the high lens AGEs group was 2.739 times that in the low lens AGEs group. The receiver operating characteristic (ROC) curves showed that patients with T2DM with a lens AGEs value ≥ 0.306 were likely to have DKD. The area under the ROC curve of the noninvasive technique for identifying DKD was 0.757 (95% Cl: 0.677-0.838, p<0.001), and the sensitivity and specificity were 70.0% and 78.7%, respectively. These results suggest that noninvasive lens AGEs detection technology has certain clinical value in diagnosing whether patients with T2DM have DKD.

Immune dysfunction caused by environmental factors plays an important role in the development of Graves’ disease (GD), and environmental factors are closely related to the intestinal flora. Our previous study showed significant changes in the intestinal flora in GD patients compared with healthy volunteers. This study analyzed the relationships between changes in the intestinal flora, thyroid function and relevant thyroid antibodies in GD patients before and after methimazole treatment. The subjects were divided into the UGD group (18 newly diagnosed GD patients), the TGD group (10 GD patients with normal or approximately normal thyroid function after methimazole treatment) and the NC group (11 healthy volunteers). Their fresh stool samples were sent for 16S rRNA gene amplification and Illumina platform sequencing. The correlations of the relative abundance of Bifidobacterium with the levels of TRAb, TgAb and TPOAb in the NC group and the UGD group were analyzed. A total of 1,562,445 high-quality sequences were obtained. In the UGD group, the abundances of Bifidobacterium and Collinsella were higher than that in the NC group; Bacteroides abundance in the TGD group was higher than that in the NC group, while Prevotella and Dialister abundances were lower than that in the NC group; Prevotella and Collinsella abundances in the UGD group were higher than that in the TGD group. The predominant abundance distribution of Bifidobacteriaceae in the UGD group at the family level was superior to that in the NC group. The abundance of Bifidobacterium was positively correlated with the levels of TRAb, TgAb, and TPOAb. The biological diversity of the intestinal flora was reduced in GD patients. After methimazole treatment, the composition of the intestinal flora was significantly altered. The change in Bifidobacterium abundance was positively correlated with TRAb, TgAb and TPOAb, suggesting that it might be related to the immune mechanism of GD. The results of this study may deepen our understanding of the pathogenesis of GD and provide a new idea for the treatment of GD.

Background:This study aimed to investigate the association of non-alcoholic fatty liver disease (NAFLD) and liver fibrosis with osteoporosis in postmenopausal women and men over 50 years of age with type 2 diabetes (T2DM). Methods:In this study, 1243 patients with T2DM (T2DM with coexistent NAFLD, n = 760; T2DM with no NAFLD, n = 483) were analysed. Non-invasive markers, NAFLD fibrosis score (NFS) and fibrosis index based on four factors (FIB-4), were applied to evaluate NAFLD fibrosis risk. Results:There was no significant difference in bone mineral density (BMD) between the NAFLD group and the non-NAFLD group or between males and females after adjusting for age, BMI and gender. In postmenopausal women, there was an increased risk of osteoporosis (odds ratio (OR): 4.41, 95% CI: 1.04-18.70, P = 0.039) in the FIB-4 high risk group compared to the low risk group. Similarly, in women with high risk NFS, there was an increased risk of osteoporosis (OR: 5.98, 95% CI: 1.40-25.60, P = 0.043) compared to the low risk group. Among men over 50 years old, there was no significant difference in bone mineral density between the NAFLD group and the non-NAFLD group and no significant difference between bone mineral density and incidence of osteopenia or osteoporosis among those with different NAFLD fibrosis risk. Conclusion:There was a significant association of high risk for NAFLD liver fibrosis with osteoporosis in postmenopausal diabetic women but not men. In clinical practice, gender-specific evaluation of osteoporosis is needed in patients with T2DM and coexistent NAFLD.

Objective:To Investigate comprehensive predictive ability of first-trimester complete blood count combined with maternal characteristics for gestational diabetes mellitus (GDM).Methods:From May 2015 to July 2018, 1 412 pregnant women were retrospectively screened at the Fifth People′s Hospital of Shanghai, Fudan University. We recruited 258 women who developed GDM and 1 154 women who had normal glucose level during pregnancy. At the first visit, clinical data and complete blood count result were obtained. GDM prediction models were established through logistic regression analysis of GDM related risk factors and the prediction abilities of each model were compared.Results:Logistic regression analyses identified age, pre-pregnancy body mass index, previous GDM history, family history of diabetes mellitus, the neutrophil-to-lymphocyte ratio, leukocyte, neutrophil, and monocyte counts were significantly independent predictors of GDM. In the entire cohort, the predictive ability of neutrophil and monocyte counts together with maternal basal characteristics model for the development of GDM [areas under the receiver operating characteristic curve (AUC-ROC)=0.809, integrated discrimination improvement (IDI)=0.056, P=0.001] was the best among various models (basal characteristics model, AUC-ROC=0.753; Monocyte count+ basal characteristics model, AUC-ROC=0.764; neutrophil count + basal characteristics model, AUC-ROC=0.775). Similar results obtained by the same way in all pregnant women without previous GDM history. Conclusion:It could improve the prediction of GDM with model incorporated maternal characteristics and first-trimester neutrophil and monocyte counts.

Background Although insulin therapy achieves effective glycemic control, it may aggravate hyperinsulinemia. Nonetheless the benefits of insulin as first-line treatment for women with GDM are controversial. This work aimed to investigate the effect of insulin on maternal GDM. Methods This retrospective cohort study recruited 708 women with GDM of whom 616 underwent lifestyle intervention and 92 were prescribed insulin therapy. Differences in variables between the two groups were analyzed by univariate analysis and multivariate analysis. Propensity score matching was used to control for age, pre-pregnancy BMI, time and BP at GDM diagnosis, and family history of diabetes and hypertension. Paired sample test was applied to evaluate the changes in BP after intervention in the two groups of women. Results There was no significant difference in mode of delivery, newborn weight or incidence of macrosomia between women prescribed insulin and those who adopted lifestyle modifications. Insulin therapy was associated with a slight increase in maternal weight compared with the lifestyle intervention group and was attributed to short-term treatment (about 12 weeks). In addition, insulin therapy remarkably increased maternal blood pressure, an effect that persisted after matching age, pre-pregnancy BMI, time and BP at GDM diagnosis, and family history of diabetes and hypertension. Between commencing insulin therapy and delivery, systolic blood pressure significantly increased by 6mmHg ( P = 0.015) and diastolic blood pressure by 9 mmHg ( P < 0.001). Increase in BP was significantly higher in the insulin group compared with the lifestyle intervention group ( P < 0.001). Logistic regression analysis with enter selection confirmed that insulin therapy was closely correlated with development of gestational hypertension (GH). Conclusions This work suggested that short-term insulin therapy for GDM was associated with a slight increase in maternal weight but a significant risk of increasing maternal blood pressure.

目的 探讨妊娠前体重指数(BMI)、妊娠年龄及妊娠早期甘油三酯(TG)水平对妊娠期糖尿病(GDM)的预测价值.方法 收集于我院常规产检和住院分娩的孕妇162例,按照妊娠24～28周口服葡萄糖耐量试验(OGTT)结果将其分为对照组(89例)与GDM组(73例).比较两组孕妇的临床资料及妊娠早期生化指标,采用logistic多因素回归分析筛选GDM发生的独立危险因素,采用受试者工作特征(ROC)曲线评估相关指标对GDM的预测价值.结果 GDM组孕妇的年龄、BMI及妊娠早期空腹血糖、TG、载脂蛋白、白细胞计数、中性粒细胞计数、淋巴细胞计数、血小板计数、ALT、血尿酸均明显高于对照组,而妊娠早期总胆红素、直接胆红素水平均明显低于对照组(P<0.05).妊娠前BMI、妊娠年龄、妊娠早期TG较高均为GDM的独立危险因素(P<0.05).预测GDM发生的妊娠前BMI、妊娠年龄、妊娠早期TG的最佳界值分别为22.53 kg/m2、32.5岁和1.72 mmol/L.结论 妊娠前BMI、妊娠年龄、妊娠早期TG水平较高是GDM发生的独立危险因素,提示妊娠前减重、适龄生育有助于减少GDM的发生.

目的 探讨正常糖耐量孕妇孕前体质量指数(body mass index,BMI)及孕期体重增长对新生儿体重的影响.方法 选取2016年1月～2017年12月在复旦大学附属上海市第五人民医院和上海市闵行区吴泾医院的正常糖耐量妊娠初产妇746例,根据美国国家科学院研究所(Institute of Medicine,IOM)指南(2009年)对孕前BMI及体重增长情况进行分组,分析孕前BMI、孕期体重增长与新生儿体重的关系.结果 随着孕前BMI及孕期体重增长,新生儿体重逐渐增长,消瘦组新生儿体重为(3178.56±486.59)g,正常组为(3350.75±449.10)g,超重组为(3488.36±406.25)g,肥胖组为(3581.50±534.44)g(P<0.05);孕期体重低增长组新生儿体重为(3223.37±434.71)g,正常增长组为(3343.11±433.38)g,高增长组为(3521.56±451.85)g(P<0.05).预测巨大儿的受试者工作特征曲线(receiver operator characteristic curve,ROC)所得的孕前BMI切点值为23.24 kg/m2,孕期体重增长的切点值为14.75 kg.结论 孕前肥胖及孕期体重增长过多可导致新生儿体重过快增长,控制孕前BMI和孕期体重增长对于减少巨大胎儿的出生非常重要.

Tiange Sun (  tiangesun@fudan.edu.cn ) Fifth People's Hospital of Shanghai Fudan University https://orcid.org/0000-0003-1955-5121 Fanhua Meng Fifth People's Hospital of Shanghai Fudan University Shufei Zang Fifth People's Hospital of Shanghai Fudan University Yue Li Fifth People's Hospital of Shanghai Fudan University Rui Zhang Fifth People's Hospital of Shanghai Fudan University Zhiyan Yu Fifth People's Hospital of Shanghai Fudan University Xinmei Huang Fifth People's Hospital of Shanghai Fudan University Fang Wang Fifth People's Hospital of Shanghai Fudan University Liwen Zhang Fifth People's Hospital of Shanghai Fudan University Jun Liu Fifth People's Hospital of Shanghai Fudan University

Background: Intestinal flora is associated with Graves’ disease (GD). This study explored the association of serum 25(OH)D with the diversity of the intestinal flora and serum IL-17 in GD patients. Methods: Patients newly diagnosed with GD at 2 centers between 2018 and 2021 were consecutively included. According to their 25(OH)D levels, they were divided into the deficiency group, the insufficiency group, and the sufficiency group. Some patients with vitamin D deficiency or insufficiency were randomly selected and were matched with healthy volunteers (normal control [NC]) in terms of sex, age, and case number. The diversity and differential species of the intestinal flora and serum IL-17 levels were compared. Results: Serum 25(OH)D negatively correlated with serum IL-17, the platelet/lymphocyte ratio, and TSH receptor antibody. The diversity of the intestinal flora decreased in the GD group, with noticeable differences in the composition of the intestinal flora when compared with the NC group. At the phylum level, the GD group exhibited a significantly lower abundance of Firmicutes but a higher abundance of Actinobacteria. At the genus level, the GD group exhibited higher relative abundances of Bifidobacterium, Collinsella, and Pediococcus but lower abundances of Roseburia and Dialister. Conclusions: The changes in the vitamin D level and the composition of the intestinal flora may partially contribute to the development of GD.

Objective The aim of this study was to evaluate the effect of TFR2 on iron storage in type 2 diabetes. Methods A cross-sectional study was conducted among 1938 participants from the Jiangchuan Community of Shanghai. A total of 784 participants with T2DM and 1154 normal participants (non-T2DM) were enrolled in this study. Serum ferritin, fasting blood glucose, postprandial blood glucose, and HbA1C (glycated hemoglobin A1c) levels were determined. Eighteen Wistar male rats were randomly assigned into three groups (n = 6/group): rats in a high-fat diet streptozotocin (HFD+STZ) group were fed with HFD for 4 weeks and intraperitoneally injected with streptozotocin (STZ); rats in a control group were fed with a standard diet for 4 weeks and intraperitoneally injected with buffer; rats in an STZ group were fed with a standard diet for 4 weeks and intraperitoneally injected with streptozotocin. Glucose tolerance test was performed at the end of the study. Blood samples and liver tissues were assessed for liver TFR2, blood glucose, serum ferritin, and iron levels. Results The mean serum ferritin level of T2DM participants was significantly higher than that of the control group (227 (140–352) vs 203.5 (130.5–312) ng/mL, P < 0.05). Serum ferritin level was an independent risk factor for T2DM (high ferritin group vs low ferritin group, 1.304 (1.03–1.651), P < 0.05). Diabetic rats showed reduced liver TFR2 levels, with increased serum ferritin levels. Conclusion T2DM participants exhibited iron disorder with elevated serum ferritin levels. Elevated serum ferritin levels in diabetic rats were accompanied by reduced liver TFR2 levels.

Background: Previous studies have reported an association between iron deficiency (ID) and increased thyroid peroxidase antibody (TPO-ab) during early pregnancy. The objective of this study was to explore the relationship between ID and thyroid dysfunction, as well as thyroid autoantibodies, during the second trimester of pregnancy. Methods: A total of 1592 pregnant women (13-28 weeks gestation) were enrolled in this cross-sectional study. According to serum ferritin (SF) concentrations, they were divided into ID (SF <20 μg/L) or non-ID (SF ≥20 μg/L) groups. Logistic regression analysis was used to evaluate the association between ID and subclinical hypothyroidism (thyroid-stimulating hormone [TSH] >4.0 mIU/L and free thyroxine [FT4] within the reference range) and thyroid autoimmunity. Results: The prevalence of ID was 23.43% (373/1592). Compared with the non-ID group, the ID group had lower FT4 levels (13.94 [8.91-29.82] vs 14.63 [8.22-47.24] pmol/L, p<0.001]) and higher TSH levels (1.85 [0.01-7.84] vs 1.69 [0.01-10.2] mIU/L, p<0.05). Logistic regression analysis confirmed ID as a risk factor for increased thyroglobulin antibody (TG-ab) (odds ratio 1.974; 95% confidence interval 1.065, 3.657; p<0.05), but not for subclinical hypothyroidism or increased TPO-ab. Conclusions: ID is associated with increased TG-ab during the second trimester of pregnancy.