OBJECTIVE South Asian individuals are at elevated diabetes risk attributed to insulin resistance, insulin deficiency, and ectopic fat. The CHARISMA study compared metabolic mechanisms in South Asian, White, and African American adolescents and young adults (AYAs) to investigate early diabetes risk in South Asian individuals. RESEARCH DESIGN AND METHODS AYAs aged 12–21 years with a BMI ≥23 kg/m2 or ≥80 percentile underwent MRI/MRS to quantify fat; OGTT with minimal modeling to calculate insulin sensitivity (Si), AUC insulin secretory rate (ISR), and disposition index (DI); DXA; and glucose-potentiated arginine stimulation test. RESULTS South Asian AYAs (n = 53, median [interquartile range] age 20.3 [18.9, 21.4] years) compared with White (n = 53, 19.1 [17.6, 20.8] years) and African American (n = 49, 18.8 [17.7, 20.5] years) AYAs (P = 0.02) of similar sex, pubertal stage, and BMI-Z had higher visceral fat on MRI (P < 0.001 vs. White; P = 0.009 vs. African American) and liver fat on MRS (P < 0.001 vs. both). South Asian AYAs had lower Si (P = 0.006) and higher dynamic AUC-ISR (P = 0.003) vs. White AYAs, higher total and static AUC-ISR vs. both White and African American AYAs (P < 0.001), and lower dynamic DI vs. African American AYAs (P = 0.039). South Asian AYAs had lower insulin clearance than White (P = 0.027) and African American (P = 0.007) AYAs. First-pass hepatic insulin extraction was lower in African American than South Asian (P < 0.0001) and White (P = 0.027) AYAs. Group differences in Si, dynamic AUC-ISR, and dynamic DI lost significance when visceral or liver fat was added to models, but higher total and static AUC-ISR in South Asian AYAs persisted. CONCLUSIONS Compared with White and African American AYAs, South Asian AYAs have higher visceral and liver fat. These findings, along with lower Si and dynamic DI, suggest elevated metabolic risk in South Asian individuals, even at young ages. Higher total and static phase insulin secretion in South Asian AYAs may precede insulin deficiency, reported in adults.

This study examined the association of consult modality (i.e., electronic consultation [e-consult], synchronous telemedicine, or in person) with 6-month HbA1c improvement to <8% (64 mmol/mol) among adults with uncontrolled type 2 diabetes. The impact of factors that affect diabetes management complexity on this association was also explored. This retrospective cohort study included adults with type 2 diabetes and HbA1c ≥ 8% seen for initial outpatient endocrinology consultation from 31 January 2021 to 1 April 2023 within the Veterans Health Administration. We used mixed-effects logistic regression to assess the association of consultation modality with 6-month HbA1c < 8%, adjusted for relevant patient-level variables. In total, 21,847 patients were included: 93.1% were men; mean age was 64 years; 54.7% were White; 5,180 received e-consults; 4,377 participated in synchronous telemedicine; and 12,290 had in-person visits. Almost half (49.5%) achieved 6-month HbA1c <8%. Compared with in-person care, patients who received e-consults (adjusted odds ratio [aOR] 0.77; 95% CI 0.71-0.83) and synchronous telemedicine (aOR 0.86; 95% CI 0.80-0.93) were less likely to have 6-month HbA1c < 8%. In sensitivity analysis, audio-only telemedicine was associated with lower odds of 6-month HbA1c < 8% (aOR 0.78; 95% CI 0.71-0.86), whereas video-based telemedicine was not (aOR 0.98; 95% CI 0.88-1.09). There were no significant differences in the associations of patient-level characteristics with glycemic outcomes across care modalities. e-Consult and audio-only telemedicine for initial endocrinology consultations were associated with inferior 6-month glycemic outcomes compared with in-person care among adults with uncontrolled type 2 diabetes, and video telemedicine had similar glycemic outcomes. e-Consult and audio-only telemedicine care protocols may need to incorporate additional support for patients to achieve glycemic outcomes equivalent to in-person consultation.

Body weight variability is linked to cardiometabolic outcomes, but its renal impact in type 2 diabetes remains uncertain. We tested whether the magnitude of seasonal BMI fluctuation is independently associated with kidney function decline. We analyzed a nationwide, multicenter Japanese cohort (2014-2020). Monthly BMI was modeled using seasonal-trend locally estimated scatterplot smoothing to quantify each participant's within-year peak-to-trough difference. The primary outcome was ≥40% decline in estimated glomerular filtration rate (eGFR). Secondary outcomes were ≥30% eGFR decline, creatinine doubling, incident chronic kidney disease (CKD) stage ≥3, and kidney failure. Associations were estimated using multivariable Cox models with clinic as a random effect. Among 6,700 outpatients (median follow-up: 6.8 years), 779 reached the primary end point. Each 1-SD increase in BMI fluctuation was associated with higher risk of ≥40% eGFR decline (hazard ratio [HR] 1.23, 95% CI 1.16-1.31). The highest versus lowest tertile showed a 1.7-fold increased risk (HR 1.72, 95% CI 1.42-2.09). Patterns were consistent for ≥30% eGFR decline (HR 1.18, 95% CI 1.13-1.23), creatinine doubling (HR 1.30, 95% CI 1.17-1.45), and incident CKD stage ≥3 (HR 1.11, 95% CI 1.07-1.16). Longitudinal analyses showed steeper eGFR decline in the highest-fluctuation group. Results were robust across sensitivity analyses, including models for time-varying medication exposure. In type 2 diabetes, larger intra-annual BMI fluctuations were independently and dose-dependently associated with kidney function decline. Seasonal BMI amplitude may identify higher-risk individuals; whether reducing seasonal BMI fluctuations improves kidney outcomes warrants prospective evaluation.

Obesity, kidney disease, and coronary artery disease (CAD) are interconnected. Here, the relationship between central obesity and CAD across albuminuria categories in type 1 diabetes was investigated. Data on 4,349 individuals without prior CAD from the Finnish Diabetic Nephropathy Study were analyzed. Central obesity was defined as waist-to-height ratio (WHtR) ≥0.5. Outcomes included acute myocardial infarction, coronary revascularizations, and CAD-related death. Associations were assessed with Cox regression adjusted for baseline covariates. Over a median 19-year follow-up, 664 CAD events (15.3%) occurred. The 10- and 20-year cumulative CAD incidences were 11.6% and 25.3%, respectively, in those with central obesity versus 4.4% and 9.9% without, respectively. In multivariable analysis, the hazard ratio for CAD per 0.1-unit WHtR increase was 1.21 (95% CI, 1.06-1.38); P = 0.006) overall and 1.26 (95% CI, 1.02-1.56; P = 0.03) among those without albuminuria. In conclusion, WHtR is associated with increased CAD risk in type 1 diabetes, particularly among those without albuminuria.