Metabolic Syndrome and Diabetes
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Metabolic syndrome (MetS) is associated with osteogenic transdifferentiation of vascular smooth muscle cells (VSMCs) and accumulation of arterial calcifications (ACs). Metformin (MET) inhibits this transdifferentiation in vitro. Here, we evaluate the in vivo efficacy of oral MET to reduce AC in a model of MetS. Twenty young male Wistar rats were divided into two groups: one received water and the other received water plus 20% fructose to induce MetS. After 14 days, and for another 4 weeks, MET (100 mg/kg per day) was added to half of each group’s drinking source, thus C (water), F (fructose), M (MET) and FM (fructose + MET). Serum and adipose tissue were collected. Aortas were dissected for histomorphometric and immunohistochemical analysis, ex vivo calcification studies and isolation of VSMCs to measure their alkaline phosphatase activity (ALP), collagen production, extracellular mineralization, gene expression of RUNX2 and receptor for advanced glycation end-products (AGEs) (RAGE), and elastic fiber production. F group showed parameters compatible with MetS. Aortic tunica media from F showed decreased elastic-to-muscular layer ratio, increased collagen content and increased levels of the AGEs structure carboxymethyl-lysine. Aortic arches from F presented a tendency for higher ex vivo calcification. VSMCs from F showed increased ALP, collagen secretion, mineralization and expression of RUNX2 and RAGE, and decreased elastic fiber production. All these effects were reverted by MET cotreatment (FM group). In vitro, AGEs-modified bovine serum albumin upregulated RAGE expression of control VSMCs, and this was prevented by MET in an AMP kinase-dependent manner. Thus, experimental MetS induces RAGE upregulation and osteogenic transdifferentiation of aortic VSMCs curbed by oral treatment with MET.
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Objective
To test whether postprandial hypoglycaemia is an extreme and repeatable phenotype of glucose metabolism. We also explored the genetic determinants of this phenotype.
Design and methods
We conducted this study using data from the Pinggu Metabolic Disease Study database (n = 3,345). We selected subjects after an oral glucose tolerance test (OGTT) (2 h glucose < 3 mmol/L) and compared their clinical features with those of subjects with normal glucose tolerance (NGT). In addition, we selected 75 subjects as a super-healthy control group. Whole-exome sequencing (WES) was performed on subjects with postprandial hypoglycaemic and super-healthy controls. We also evaluated several candidate genes believed to be important in pancreatic hypoglycaemia.
Results
We found 13 participants (0.39%) who had an OGTT (2 h glucose < 3 mmol/L). Ten of these patients were men (76.9%). All 13 participants had insulin >3 μU/mL when postprandial blood glucose levels were <3 mmol/L. WES analysis identified one gene, paternally expressed 3 (PEG3), which had three rare mutations in four patients (30.8%). Minor allele frequencies of rare PEG3 mutations were significantly higher in subjects with postprandial hypoglycaemia than in super-healthy controls. Among the four subjects with PEG3 gene mutations, 71.4% were men, and their body mass index was significantly lower than that of the NGT group.
Conclusions
Postprandial hypoglycaemia is an extreme and reproducible phenotype in the general population. PEG3 mutations may represent a potential genetic aetiology for postprandial hypoglycaemia. Further research with larger and more diverse populations and a broader genetic focus is needed to understand the genetic basis of postprandial hypoglycaemia.
Department of Clinical Nutrition, College of Heath Science and Technology, School of Medicine, Shanghai Jiao Tong University, Shanghai, China
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Department of Clinical Nutrition, College of Heath Science and Technology, School of Medicine, Shanghai Jiao Tong University, Shanghai, China
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Department of Clinical Nutrition, College of Heath Science and Technology, School of Medicine, Shanghai Jiao Tong University, Shanghai, China
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Department of Clinical Nutrition, College of Heath Science and Technology, School of Medicine, Shanghai Jiao Tong University, Shanghai, China
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Introduction
Gestational diabetes mellitus (GDM) significantly affects pregnancy outcomes. Therefore, it is crucial to develop prediction models since they can guide timely interventions to reduce the incidence of GDM and its associated adverse effects.
Methods
A total of 554 pregnant women were selected and their sociodemographic characteristics, clinical data and dietary data were collected. Dietary data were investigated by a validated semi-quantitative food frequency questionnaire (FFQ). We applied random forest mean decrease impurity for feature selection and the models are built using logistic regression, XGBoost, and LightGBM algorithms. The prediction performance of different models was compared by accuracy, sensitivity, specificity, area under curve (AUC) and Hosmer–Lemeshow test.
Results
Blood glucose, age, pre-pregnancy body mass index (BMI), triglycerides and high-density lipoprotein cholesterol (HDL) were the top five features according to the feature selection. Among the three algorithms, XGBoost performed best with an AUC of 0.788, LightGBM came second (AUC = 0.749), and logistic regression performed the worst (AUC = 0.712). In addition, XGBoost and LightGBM both achieved a fairly good performance when dietary information was included, surpassing their performance on the non-dietary dataset (0.788 vs 0.718 in XGBoost; 0.749 vs 0.726 in LightGBM).
Conclusion
XGBoost and LightGBM algorithms outperform logistic regression in predicting GDM among Chinese pregnant women. In addition, dietary data may have a positive effect on improving model performance, which deserves more in-depth investigation with larger sample size.
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Aim
Incretin therapies, including dipeptidyl peptidase-4 inhibitors (DPP-4is) and glucagon-like peptide-1 receptor agonists (GLP-1RAs), are crucial for type 2 diabetes treatment. Evidence of their association with gallbladder, biliary diseases, and liver injury remains inconsistent. This study evaluated the association between incretin therapies and hepatobiliary adverse events using the FDA’s Adverse Event Reporting System (FAERS) data.
Methods
Case reports involving incretin therapies and hepatobiliary events from January 2006 to December 2023 were extracted from FAERS. The association between these agents and hepatobiliary adverse events (hAEs) was analyzed using reporting odds ratios and empirical Bayesian geometric means. Descriptive analyses were conducted to characterize the demographic and clinical features of the hAE cases. Additionally, subgroup analyses calculated reporting odds ratios to evaluate the strength of the association between specific incretin drugs and hAEs.
Results
Among 68,351 case reports associated with incretin-based therapies, 1327 (1.941%) involved hepatobiliary adverse events. DPP-4 inhibitors demonstrated statistically significant associations with multiple hepatobiliary events, like cholelithiasis, chronic cholecystitis, and biliary diseases. In contrast, GLP-1 receptor agonists showed weaker associations, primarily linked to gallbladder and biliary disease risks. Subgroup analyses revealed stronger positive correlations with hepatobiliary events for liraglutide and semaglutide among GLP-1 agonists, and for sitagliptin, linagliptin, and vildagliptin among DPP-4 inhibitors. The pooled reporting odds ratio of 2.85 indicated a positive correlation between these drugs and studied adverse events.
Conclusions
This study found statistically significant associations between DPP-4 inhibitors and hepatobiliary adverse events like cholelithiasis and cholecystitis. GLP-1 agonists showed weaker gallbladder/biliary disorder links but higher acute cholecystitis risk. Subgroup analyses revealed varying correlations among specific drugs, potentially dose-dependent. Further large-scale studies are needed to evaluate class effect differences and elucidate mechanisms for guiding clinical use.
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Rama Medical College Hospital, Hapur, Uttar Pradesh, India
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Queen Elizabeth Hospital Birmingham, University Hospitals Birmingham NHS Foundation Trust, Birmingham, UK
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Objectives
To investigate the utility and effectiveness of a school outreach programme in areas of lower socioeconomic status to improve understanding of common endocrine topics and the medical profession.
Methods
Two secondary school outreach sessions were conducted in July 2022. Students were invited to attend lectures delivered by medical professionals and engage in poster-making sessions using the knowledge they had gained throughout the day. Participants completed anonymised pre- and post-session surveys. Outcomes were identified using Kirkpatrick’s training evaluation model. Self-reported perceptions and beliefs (Kirkpatrick’s level 2a) were compared using chi-square tests. Thematic analysis of team-led poster presentations was performed.
Results
Of the 254 participants included, the response rates of pre- and post-session questionnaires were 75.6% and 56.2%, respectively. The outreach day increased students’ understanding of obesity and diabetes, polycystic ovary syndrome, and Health Technology. The most well-received activities from the outreach day were voted to be the poster challenge (43.4%) and poster presentation (14.7%). Following the session, there was a trend towards an increased understanding of medical careers and interest in pursuing a medical career, although these did not reach statistical significance.
Conclusions
Outreach programmes could be a practical and effective approach to engaging prospective medical applicants from areas of lower socioeconomic status. Further studies are required to expand outreach programmes and investigate the efficacy of school engagement programmes.
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Norwegian Institute of Public Health, Oslo, Norway
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Department of Obstetrics & Gynecology, Oslo University Hospital, Oslo, Norway
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Department of Endocrinology, Institute of Clinical Medicine, University of Oslo, Oslo, Norway
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Objective
Increasing numbers of pregnancies are complicated by pregestational diabetes mellitus, especially type 2 diabetes (T2DM). Some studies have reported similar or greater risks of adverse pregnancy outcomes among women with T2DM relative to type 1 diabetes (T1DM). We aimed to compare the risk of four pregnancy complications: pre-eclampsia, preterm delivery, macrosomia, and perinatal mortality, in pregnant women with T2DM vs T1DM in high-income countries.
Design
Systematic review with meta-analyses.
Methods
Systematic literature searches in Medline and Embase were performed. We included observational studies with original data of outcome occurrence in both women with pregestational T2DM and T1DM. Two researchers independently evaluated full-text studies for inclusion and assessed the risk of bias using the Newcastle–Ottawa scale. Finally, we performed four meta-analyses.
Results
We included 35 publications in total. Meta-analyses demonstrated that, compared to T1DM, T2DM was associated with a lower risk of pre-eclampsia (risk ratio (RR): 0.76; 95% CI: 0.68–0.85), preterm delivery (RR: 0.69; 95% CI: 0.62–0.77), and macrosomia (RR: 0.75; 95% CI: 0.60–0.94). Perinatal mortality was more likely in pregnancies with T2DM (RR: 1.26; 95% CI: 1.06–1.50).
Conclusion
A summation of the research literature demonstrated that, compared to T1DM, women with T2DM had a lower risk of pre-eclampsia, preterm delivery, and macrosomia, but a higher risk of perinatal mortality.
Significance statement
Our review of pregnant women with diabetes suggests a higher risk of perinatal mortality for cases with maternal type 2 diabetes, even though the risks of pre-eclampsia, preterm delivery, and macrosomia were higher in cases with type 1 diabetes. Hence, the prevention of the development of type 2 diabetes and focus on improved gestational and diabetic care could be beneficial for fetal health.
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Background
Evidence has demonstrated that visceral fat area (VFA) and subcutaneous fat area (SFA) have different influences on cardiovascular disease (CVD) risk in patients with type 2 diabetes mellitus (T2DM). We aimed to investigate the relationship between the visceral fat area (VFA), the subcutaneous fat area (SFA) ratio (V/S), and carotid atherosclerosis (CAS) in patients with T2DM.
Methods
From January 2018 to May 2023, 1838 patients with T2DM admitted to the National Metabolic Management Centre in our hospital were assigned to two groups based on comorbid CAS. Dual bioelectrical impedance analysis was used to measure the VAF and SFA, and the V/S was calculated. Patient characteristics and serum biochemical indices were compared between groups. Factors influencing comorbid CAS were determined, and correlations between V/S and other clinical indices were analyzed.
Results
The group with comorbid CAS included 858 individuals and 980 without comorbid CAS. Those with comorbid CAS were older and had a longer disease duration, more significant systolic blood pressure, and greater V/S. The proportions of patients with comorbid hypertension increased significantly with the V/S ratio. The V/S ratio positively correlated with triglyceride (TG), low-density lipoprotein cholesterol levels, and waist circumference. According to binary logistic regression analysis, V/S was an independent risk factor for CAS.
Conclusion
Elevated V/S is an independent risk factor for CAS in patients with T2DM.
Tanaka Medical Clinic, Yoichi, Japan
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Institute for Clinical Research, NHO Kure Medical Center and Chugoku Cancer Center, Hiroshima, Japan
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Department of Cellular Physiology and Signal Transduction, Sapporo Medical University School of Medicine, Sapporo, Japan
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Background
Fatty acid-binding protein 4 (FABP4) is an adipokine that plays significant roles in the development of insulin resistance and atherosclerosis. High levels of soluble tumor necrosis factor receptors (TNFRs) including TNFR1 and TNFR2 are associated with renal dysfunction and increased mortality in patients with diabetes mellitus (DM). However, the association between circulating levels of FABP4 and TNFRs remains unclear.
Methods
We investigated the associations of FABP4 with TNFRs and metabolic markers in Japanese patients with type 1 DM (T1DM, n = 76, men/women: 31/45) and type 2 DM (T2DM, n = 575, men/women: 312/263).
Results
FABP4 concentration was positively correlated with levels of TNFR1 and TNFR2 in both patients with T1DM and those with T2DM. Multivariable regression analyses showed that there were independent associations of FABP4 concentration with body mass index (BMI) and estimated glomerular filtration rate (eGFR) after adjustment for age and sex in both patients with T1DM and those with T2DM. FABP4 concentration was independently associated with circulating levels of TNFR1 and TNFR2 after adjustment for the confounders in patients with T2DM but not in those with T1DM. Similarly, levels of TNFR1 and TNFR2 were independently associated with FABP4 concentration after adjustment for age, sex, systolic blood pressure, duration of DM and levels of eGFR, high-density lipoprotein cholesterol, and C-reactive protein in patients with T2DM but not in those with T1DM.
Conclusion
FABP4 concentration is independently associated with levels of TNFRs in patients with DM, but the association is more evident in patients with T2DM than in those with T1DM.
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Glucose-like peptide-1 (GLP-1) is a vital hormone in the intestines that regulates glucose metabolism. Although pancreatic-derived factor (PANDER) overexpression is known to suppress GLP-1, the underlying mechanisms are unclear. Our study aims to uncover how PANDER influences GLP-1 synthesis and secretion. We established a PANDER overexpression model in STC-1 intestinal cells, confirming its inhibitory effect on GLP-1 secretion. This effect was reversed in PANDER-knockout cells. Additionally, a negative correlation between PANDER and GLP-1 was observed in patients with a history of gestational diabetes. Subsequently, through whole transcriptome gene sequencing in PANDER-overexpressed STC-1 cells, we discovered that the activation of IL-6 and its related STAT3 signaling pathway was significantly inhibited, and this finding was validated by Western blotting and quantitative reverse transcription PCR. Finally, rescue experiments confirmed that the IL-6-related STAT3/Akt/GSK3β/β-catenin signaling pathway mediates the negative regulatory effect of PANDER on GLP-1. Taken together, our data identify IL-6 as a bridge connecting PANDER and GLP-1 in the STC-1 cells, demonstrating potential therapeutic targets for diabetes treatment by targeting the PANDER–IL-6–GLP-1 axis.
