Artificial sweeteners have become ubiquitous additives in the food supply, and yet the safety of their regular consumption remains controversial. The present study examined whether intakes of aspartame or saccharin are related to aberrations in the plasma metabolome indicating disruptions in metabolism.
A cohort of 2160 male and female participants, mean age 32.1 years, was included in the analysis. Liquid chromatography and mass-spectrometry assessed 549 unique plasma metabolites. Diet was assessed using a validated questionnaire that allowed for estimation of aspartame and saccharin intakes. A generalized linear regression model evaluated associations of saccharin or aspartame intake with plasma metabolites with adjustment for potential confounders and multiple comparisons. Multiple sensitivity analyses and propensity score matching were conducted.
Heavy aspartame intake (≥ 5 servings/day) was associated with plasma levels (per SD) of saccharin (β = 0.90; q = 9.0E-36), myo-inositol (β = 0.27; q = 3.7E-04), caffeine (β = 0.31; q = 4.1E-04), and five metabolites of caffeine including 1,7-dimethyluric acid (β = 0.37; q = 7.1E-06), 1-methylurate (β = 0.36; q = 7.1E-06), 5-acetylamino-6-amino-3-methyluracil (β = 0.38; q = 3.2E-6), theophylline (β = 0.36; q = 9.1E-06), and 1-methylxanthine (β = 0.32; q = 2.0E-03). Saccharin intake was associated with plasma levels of saccharin alone (β = 0.29; q = 1.8E-10). No associations with sugars, carbohydrates, lipids, amino acids, or other metabolites that would suggest metabolic perturbations were observed with either artificial sweetener; sensitivity analyses supported these findings.
In the largest metabolomics study to date, no link was found between metabolic disruptions and either aspartame or saccharin intake. We cannot exclude the possibility that more extreme intakes may be related to metabolic disruptions among consumers of artificial sweeteners.
This study aims to explore the effect of the ketogenic diet (KD) on the occurrence of end-stage renal disease (ESRD) and the longitudinal relationship between circulating β-hydroxybutyrate (β-OHB) and kidney outcomes.
We used the dietary ketogenic ratio (DKR) to estimate the nutritional ketosis probability of KD and analyzed the association with ESRD using NHANES cross-sectional data by Spearman correlation coefficient and multivariate logistic regression model. We also used the Kaplan–Meier method, Cox regression analysis, and restricted cubic splines (RCS) to analyze the relationship between circulating β-OHB and renal outcomes in the T2DM-DKD longitudinal cohort of West China Hospital. Mendelian randomization (MR) was also employed to evaluate potential causal associations.
The cross-sectional analysis revealed that non-ESRD patients had significantly higher baseline age, BMI, serum albumin, and DKR values, with a weak negative correlation between DKR and serum creatinine (ρ = −0.072, p = 0.011). Logistic regression consistently indicated a reduced ESRD prevalence in higher DKR quartiles. In the longitudinal study, elevated β-OHB levels were associated with improved renal survival and a lower risk of ESRD, with RCS analysis identifying the lowest risk at approximately 0.25 mmol/L. MR analyses supported these findings, showing inverse correlations between genetically predicted β-OHB and creatinine (p = 0.007) and cystatin c (p < 0.001).
These findings suggest that KD may be associated with a lower incidence of ESRD in DKD patients, with elevated β-OHB levels independently associated with a reduced risk of ESRD, warranting further research to confirm causality and elucidate underlying mechanisms.
Type 1 diabetes mellitus (T1DM) is a chronic autoimmune disorder where the immune system targets and destroys insulin-producing β-cells in the pancreas. It generally emerges during childhood or adolescence, but individuals of any age can be affected. In contrast to Type 2 diabetes mellitus (T2DM) which is often associated with lifestyle factors, T1DM cannot be prevented and necessitates lifelong management. Currently, there is no definitive cure for T1DM, and patients rely on continuous insulin injections for their entire lives. Ongoing developments in insulin treatment, such as insulin pumps, continuous glucose monitoring, and hybrid closed-loop systems, offer promising alternatives. Despite advancements in intensive glycemic control that have reduced the occurrence of microvascular and macrovascular complications, a significant number of T1DM patients still these issues. Extensive research efforts are crucial to achieve early detection, prevent the loss of β-cells, and devise improved treatment strategies to enhance the quality of life and prognosis for those affected. This review explores the most noteworthy and recent advancements in the field of T1DM.
Periodontal disease is a prevalent and chronic inflammatory condition increasingly recognized for its systemic implications beyond oral health. While traditionally confined to dentistry, recent evidence reveals strong associations between periodontitis and chronic systemic conditions such as cardiovascular disease, diabetes mellitus, rheumatoid arthritis, inflammatory bowel disease, Alzheimer's disease, and various cancers. Mechanistic studies have identified plausible biological pathways, including systemic dissemination of periodontal pathogens and immune mediators, which can exacerbate distant organ inflammation and dysfunction. Experimental models highlight how oral bacteria influence immune responses, disrupt gut and vascular homeostasis, and contribute to oncogenesis and autoimmunity. Notably, bidirectional relationships, such as those between periodontitis and diabetes, underscore the need for integrated care approaches. Effective periodontal therapy has demonstrated systemic benefits, including improved glycemic control and reduced inflammation. Given the mounting evidence, periodontal disease should be approached as a critical component of systemic health, necessitating interdisciplinary collaboration among healthcare providers to optimize patient outcomes and public health.
Early short-term intensive insulin therapy may induce sustained glycemic remission in type 2 diabetes. However, patients' responses vary greatly. Exploring key factors to improve glycemic control and predict the probability of remission precisely is meaningful for future treatment.
Patients with newly diagnosed type 2 diabetes receiving 2–3 weeks of intensive insulin therapy were followed up for at least 1 year in three randomized clinical trials. Data of theirs were extracted with the same inclusion criteria and divided into training and validation sets. A nomogram was constructed in the training set and tested in the internal validation set.
Among 302 patients with transient intensive insulin therapy, 162 (53.64%) patients achieved the 1-year glycemic remission. Severe hyperglycemia at baseline did not impede future remission, as the remission rate was 60.70% in those with HbA1c greater than 13%. Three parameters were identified as predictive factors in the nomogram: fasting glucose after short-term insulin treatment, mean glucose during insulin therapy, and postprandial glucose/fasting glucose ratio at baseline. The odds ratios were 0.06 (95% CI, 0.02–0.25), 0.41 (0.18–0.93) and 6.55 (1.39–30.89), respectively. Incorporating these factors, the nomogram achieved an accuracy of 81.50%.
Short-term intensive insulin therapy assists patients with newly diagnosed type 2 diabetes and significant hyperglycemia to achieve glycemic remission. A rigorous control of glucose during insulin treatment favors future remission. We construct a nomogram to predict sustained glycemic remission, which may help determine whether subsequent medication is needed and thus reduce both overtreatment and therapeutic inertia.
Whether diverse metabolic statuses within a similar body mass index (BMI) category associate with different in vitro fertilization (IVF) outcomes.
A retrospective cohort study.
Wenzhou, Zhengjiang Province, China.
This retrospective cohort study prescreened 16 458 women who underwent their first IVF and fresh embryo transfer cycle between January 2010 and December 2021.
Metabolic status was assessed using the National Cholesterol Education Program–Adult Treatment Panel III criteria. Patients were then categorized into six groups: metabolically healthy normal weight, metabolically unhealthy normal weight, metabolically healthy overweight, metabolically unhealthy overweight, metabolically healthy obese, and metabolically unhealthy obese.
The primary outcome was live birth rate.
Regarding live birth, rates in normal weight women were initially lower for metabolically unhealthy normal weight versus metabolically healthy normal weight (44.6% vs. 48.6%), but this was not significant after multivariate adjustment. In obese women, live birth rates were similar between metabolically unhealthy obese and metabolically healthy obese (41.5% vs. 43.9%), with no adjusted difference. For secondary outcomes, metabolically unhealthy normal weight patients had lower biochemical pregnancy rates than metabolically healthy normal weight (OR: 0.86, 95% CI: 0.76–0.98); high blood pressure was a significant risk factor for this outcome in metabolically unhealthy normal weight (OR: 0.84, 95% CI: 0.72–0.98).
Our findings indicated that different cardio-metabolic risk factors but a similar BMI category may have limited adverse effects on live birth rate.
Glucagon-like peptide-1 receptor agonists (GLP-1 RAs) have demonstrated substantial weight loss effects among patients with diabetes and obesity. However, given the rapid weight loss induced, there is concern about the total change in body composition, including lean body mass (LBM). Current literature on these effects contains significant heterogeneity, with some studies reporting a loss of 40%–60% of LBM and others reporting 15% or less. To combat this, selective androgen receptor modulators (SARMs) have become a popular candidate. Given their androgen receptor selectivity, SARMs have notable anabolic properties and proposed improved safety profiles over traditional anabolic compounds. Several of these agents, such as enobosarm, have been investigated in clinical trials involving older patient populations or patients with cachexia or sarcopenia secondary to chronic diseases. Furthermore, other agents to maintain or enhance LBM, such as antimyostatin agents, are also under investigation. Exploring this potential synergy could lead to better weight loss and body composition management in patients using GLP-1 RAs for diabetes or weight loss therapy. This review aims to evaluate the potential benefits and uses of SARMs in ameliorating the body composition changes induced by GLP-1 RAs. Other investigational agents to retain or increase muscle mass and the future possibilities of these drugs will be discussed.
To examine the association between non-traditional lipid parameters and adverse pregnancy outcomes (APOs) in women with gestational diabetes mellitus (GDM) and the mediating role of maternal serum metabolites during pregnancy.
This prospective observational study enrolled 399 women with GDM. Multivariate logistic regression was used to examine the association between non-traditional lipid parameters and APOs risk. Additionally, we assessed the mediating role of single and composite maternal serum metabolites during pregnancy using causal mediation analysis and high-dimensional mediation analysis, respectively.
APOs were observed in 12.0% (N = 48) of participants. Seven non-traditional lipid parameters, except for the RC/HDL-C ratio, were associated with APOs risk, with the highest estimate for the atherogenic index of plasma (AIP) (OR = 3.873, 95% CI: 1.079–13.934, p = 0.037) after adjusting for confounders. Maternal metabolic markers mediated these associations, with mediation effect proportions of 21.9%–39.4%. Seven key metabolic markers were identified as potential mediators primarily involved in the biosynthesis of the unsaturated fatty acids pathway. Gene set variation analysis revealed significant differences in the positive regulation of this pathway between the APO and normal pregnancy outcome groups (p = 0.015).
Non-traditional lipid parameters were positively associated with APOs risk in women with GDM. Maternal serum metabolites, predominantly involved in the biosynthesis of unsaturated fatty acids, contribute to these associations.
It has been shown that offspring of type 2 diabetic parents have a high risk for developing diabetes and atherosclerosis, but the exact mechanism is unclear. In the present study, the possible association between oxidative stress and subclinical atherosclerosis serum markers in this population was investigated.
LDL/HDL ratio, triglyceride-glucose index (TyG), atherogenic index of plasma (AIP), single-point insulin sensitivity estimator (SPISE) index, oxidized LDL (Ox-LDL), intercellular adhesion molecules (ICAM-1 and E-selectin), as well as the marker of oxidative DNA damage were compared among 150 offspring of diabetic parents (90 normoglycemic and normotolerant offspring, 31 offspring with impaired fasting glucose (IFG), and 29 offspring with impaired glucose tolerance (IGT)), and 40 age-and sex-matched healthy control individuals. The control subjects were among individuals with no family history of diabetes.
All three groups with diabetic parents, that is, norm-offspring, IFG, and IGT groups, had higher serum levels of Ox-LDL, ICAM-1, and 8-hydroxy-2′-deoxyguanosine (8-OHdG) than the controls. In the whole population, ICAM-1 correlated with Ox-LDL, fasting plasma glucose (FPG) and 8-OHdG, and Ox-LDL correlated with LDL/HDL, fasting plasma glucose, TyG index, and 8-OHdG after adjustment for age, sex, and BMI.
This study shows that subclinical atherosclerosis and oxidative DNA damage are present in normotolerant normoglycemic offspring of type 2 diabetic parents, and they progress with impaired fasting glucose and/or impaired glucose tolerance. Also, our results indicate that a marker of subclinical atherosclerosis, ICAM-1, was directly correlated with the DNA damage marker, 8-OHdG.
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