Diabetes care最新文献

Objective: We compare the risk of postpartum diabetes in people with early antenatal prediabetes, HbA1c 5.9-6.4% (41-47 mmol/mol), versus those with HbA1c <5.9% (41 mmol/mol) who developed gestational diabetes mellitus (GDM) in later pregnancy. Secondly, we perform an exploratory analysis of lipid profiling to guide antenatal and postpartum management decisions for people with antenatal prediabetes.

Research design and methods: We analyze a prospective cohort study conducted in New Zealand. The "antenatal prediabetes" group was identified during 2017-2022 (n = 355). The comparator "GDM" group was identified in 2017 (n = 490). Postpartum laboratory data were collected from electronic health records until November 2025. Progression to diabetes was evaluated using multivariate analysis.

Results: Compared with GDM, adjusted hazard ratios for postpartum type 2 diabetes following antenatal prediabetes were 4.5 (2.8-7.3) to 16.7 (10.8-25.8) for HbA1c 5.9% (41 mmol/mol) to 6.2-6.4% (44-47 mmol/mol), P < 0.001. HbA1c was the strongest predictor of type 2 diabetes, followed by BMI and Pacific ethnicity. Lipid profiles in the antenatal prediabetes cohort varied according to postpartum diagnosis: glucokinase monogenic diabetes was associated with lower serum triglycerides, mean 53.1 mg/dL (0.6 mmol/L), versus type 2 diabetes, 183.4 mg/dL (2.07 mmol/L), P = 0.012, or versus no diabetes, 165.6 mg/dL (1.87 mmol/L), P = 0.013; in type 1 diabetes, mean triglycerides were 87.7 mg/dL (0.99 mmol/L).

Conclusions: Early antenatal prediabetes is a strong predictor of rapid progression to type 2 diabetes. HbA1c at booking provides an important risk stratification tool identifying people with the greatest need for preventive intervention. Further research could evaluate lipid profiling to identify genetic and autoimmune diabetes subtypes within antenatal prediabetes.

Objective: To compare diet and physical activity during pregnancy in women with and without type 1 diabetes and assess against national dietary guidelines.

Research design and methods: Diet and physical activity were measured prospectively in 1,124 pregnancies using validated questionnaires.

Results: Diets exceeded recommended intake for fat, saturated fat, discretionary foods, sodium, vitamin C, calcium, and zinc and were below recommendations for carbohydrate, fruit, dairy, vegetables, grain foods, and lean meats and alternatives. Differences in dietary intake between women with and without type 1 diabetes were modest. Total, moderate, and vigorous physical activity decreased in the third trimester. Women with type 1 diabetes performed less vigorous intensity activity than women without type 1 diabetes.

Conclusions: Most pregnant women with and without type 1 diabetes did not meet dietary guidelines. Physical activity patterns were also mostly similar in women with and without type 1 diabetes.

Objective: Type 2 diabetes (T2D) is a significant risk factor for adverse outcomes in coronary heart disease (CHD). We investigated whether inflammation and immune dysregulation, measured using soluble urokinase plasminogen activator receptor (suPAR) and high-sensitivity C-reactive protein (hs-CRP) levels, mediate this risk.

Research design and methods: Patients with and without CHD enrolled in the Emory Cardiovascular Biobank had suPAR (ViroGates, Denmark) and hs-CRP levels measured and were followed for 1) cardiovascular death, 2) a composite of incident myocardial infarction and cardiovascular death, and 3) all-cause death. Fine and Gray or Cox proportional hazards models adjusted for demographic, clinical, and treatment variables were used. Regression-based causal mediation analyses were performed.

Results: A total of 4,324 participants (mean [SD] age 64 [11.9] years, 36% women, 31.8% with T2D) were followed for a median of 6.9 years. SuPAR levels were higher in those with T2D (median [interquartile range] 3,260 [2,503-4,463] vs. 2,792 [2,217-3,600] pg/mL). T2D was associated with a higher adjusted risk (hazard ratio [HR] 1.38; 95% CI 1.16, 1.63; P < 0.001) of cardiovascular death that was greatly attenuated (HR 1.18; 95% CI 0.99, 1.40; P = 0.1) after adjustment for suPAR, but not hs-CRP, levels. Similar findings were observed for the other outcomes. SuPAR, but not hs-CRP, levels mediated >50% of the effect of T2D on adverse outcomes.

Conclusions: The impact of T2D on adverse outcomes is significantly mediated through chronic inflammation and immune dysregulation, estimated using suPAR levels. Whether novel therapies for reducing suPAR levels will impact CHD risk in T2D warrants further investigation.

Objective: Maturity-onset diabetes of the young (MODY) caused by pathogenic variants in HNF1A is a common form of monogenic diabetes. Sulfonylurea drugs are considered first-line treatment of HNF1A-MODY (MODY3), but intensified treatment is often needed. HNF1A encodes a transcription factor involved in the regulation of the sodium-glucose cotransporter 2 (SGLT2). Accordingly, the glucose-lowering efficacy of SGLT2 inhibitors in HNF1A-MODY is questionable. Here, we assess the glucose-lowering effect of the SGLT2 inhibitor empagliflozin as an add-on for treatment of individuals with HNF1A-MODY.

Research design and methods: MOD3ST-TRIAL was a randomized, double-blind, placebo-controlled crossover trial. Adults with HNF1A-MODY treated with at least one glucose-lowering drug were randomized to be treated with empagliflozin 25 mg for 4 weeks followed by a 2-week washout period and then received placebo for 4 weeks or the opposite sequence. The primary outcome was mean glucose concentration assessed by 10 days of continuous glucose monitoring (CGM).

Results: Nineteen individuals were randomized and 18 participants (n = 10 women [56%]; median [Q1, Q3] HbA1c 7.5% [7.0, 8.4] % (58 [53, 68] mmol/mol), mean (SD) CGM glucose concentration 10.4 (2.5) mmol/L) completed the study. Compared with placebo, empagliflozin lowered the mean glucose level 2.3 mmol/L (95% CI 1.3 to 3.3; P = 0.0001). There were no significant differences in hypoglycemic outcomes. Adverse events were generally mild and transient, and no severe adverse events or study drug discontinuations were attributable to empagliflozin.

Conclusions: Empagliflozin used for 4 weeks in adjunction with other glucose-lowering treatments markedly improved glycemia compared with placebo in individuals with HNF1A-MODY without significantly increasing risk of hypoglycemia or unexpected adverse effects.

Objective: To investigate whether maternal diabetes in pregnancy was associated with altered neonatal global IgG repertoire and early-life infections in offspring.

Research design and methods: This study included 2,702 mother-infant pairs enrolled at birth and followed longitudinally at the Boston Medical Center. Maternal diabetes and infant infections were extracted from electronic medical records. Cord blood IgG antibodies against a wide range of microbes were quantified using Phage ImmunoPrecipitation Sequencing.

Results: Overall, 327 infants (12.1%) were born to mothers with gestational diabetes mellitus (GDM) and 138 (5.1%) to mothers with pregestational diabetes mellitus (PDM). Of these, 416 infants (15.4%) and 1,425 infants (52.7%) had at least one infection in the neonatal period and the first 6 months of life, respectively. Compared with no diabetes, both maternal GDM (risk ratio [RR] 1.20, 95% CI 1.09-1.32) and PDM (RR 1.28, 95% CI 1.12-1.47) were significantly associated with an elevated risk of infections in infants during the first 6 months. These associations were particularly pronounced among infants born preterm, delivered via cesarean section, or with lower IgG repertoire diversity. Additionally, PDM was associated with a lower newborn's global IgG repertoire diversity, compared with no diabetes, with the effect more marked among infants whose mothers had prepregnancy overweight or obesity.

Conclusions: This study provides strong evidence of an increased infection risk in the infants of mothers with diabetes and a reduced IgG repertoire diversity in those of PDM mothers. Lower IgG diversity exacerbated the diabetes-infection link. These findings suggest that maternal metabolic conditions may impact an infant's passive immunity and susceptibility to infections.