Correction: Preserved endothelial function in young adults with type 1 diabetes.
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ABSTRACT:
SUBMITTER: PLOS ONE Staff
PROVIDER: S-EPMC6281262 | biostudies-literature | 2018
REPOSITORIES: biostudies-literature
Publications
Correction: Preserved endothelial function in young adults with type 1 diabetes.
PloS one 20181205 12
[This corrects the article DOI: 10.1371/journal.pone.0206523.]. ...[more]
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Project description:Background and aimEndothelial dysfunction is involved in the pathogenesis of atherosclerosis and is typically present in older adults with type 1 diabetes (T1D). In young adults, we aimed to assess the impact of T1D on endothelial function as detected by digital peripheral arterial tonometry (PAT) and its relationship with cardiovascular risk factors and long term glycemic control.Materials and methodsReactive hyperemia index (RHI) as a measure of endothelial function was assessed by PAT in 46 T1D patients and 32 healthy controls. All were participants in the "Atherosclerosis and Childhood Diabetes" study, with baseline values registered five years previously. Annual measurements of HbA1c for assessment of glycemic burden were provided by the Norwegian Childhood Diabetes Registry.ResultsThe diabetes patients had a mean age of 20.8 years, a median duration of diabetes of 10.0 years and a mean HbA1c of 8.7%. RHI was not significantly decreased in the diabetes group, mean 2.00 (SD = 0.59) vs. 2.21 (SD = 0.56), p = .116. There was no gender difference or any associations with traditional risk factors. Furthermore, there was no significant association between RHI and either HbA1c or long term glycemic burden.ConclusionsRHI as a measure of endothelial function was preserved in young adults with T1D compared with healthy controls.
| S-EPMC6201945 | biostudies-literature
Project description:Data indicate endothelium-dependent dilation (EDD) may be preserved in the skeletal muscle microcirculation of young, obese adults. Preserved EDD might be mediated by compensatory mechanisms, impeding insight into preclinical vascular dysfunction. We aimed to determine the functional roles of nitric oxide synthase (NOS) and cyclooxygenase (COX) toward EDD in younger obese adults. We first hypothesized EDD would be preserved in young, obese adults. Further, we hypothesized a reduced contribution of NOS in young, obese adults would be replaced by increased COX signaling. Microvascular EDD was assessed with Doppler ultrasound and brachial artery infusion of acetylcholine (ACh) in younger (27 ± 1 year) obese (n = 29) and lean (n = 46) humans. Individual and combined contributions of NOS and COX were examined with intra-arterial infusions of l-NMMA and ketorolac, respectively. Vasodilation was quantified as an increase in forearm vascular conductance (ΔFVC). Arterial endothelial cell biopsies were analyzed for protein expression of endothelial nitric oxide synthase (eNOS). ΔFVC to ACh was similar between groups. After l-NMMA, ΔFVC to ACh was greater in obese adults (p < 0.05). There were no group differences in ΔFVC to ACh with ketorolac. With combined NOS-COX inhibition, ΔFVC was greater in obese adults at the intermediate dose of ACh. Surprisingly, arterial endothelial cell eNOS and phosphorylated eNOS were similar between groups. Younger obese adults exhibit preserved EDD and eNOS expression despite functional dissociation of NOS-mediated vasodilation and similar COX signaling. Compensatory NOS- and COX-independent vasodilatory mechanisms conceal reduced NOS contributions in otherwise healthy obese adults early in life, which may contribute to vascular dysfunction.
| S-EPMC4686588 | biostudies-literature
Project description:ObjectiveImpaired insulin sensitivity is associated with hyperfiltration (i.e., elevated glomerular filtration rate [GFR]) in adolescents with type 2 diabetes (T2D) and adults with prediabetes. Yet, these relationships are based on studies that relied on estimated GFR (eGFR), estimates of insulin sensitivity, or both. We aimed to verify the relationship between insulin sensitivity and renal hemodynamic function by gold standard methods in adults with T2D.Research design and methodsInsulin sensitivity was assessed by hyperinsulinemic-euglycemic clamp (M value) (glucose infusion rate in mg/kglean/min) and renal hemodynamic function by urinary inulin (GFR) and para-aminohippuric acid (effective renal plasma flow [ERPF]) clearances in participants with T2D without overt kidney disease. Filtration fraction (FF) (GFR/ERPF) was calculated. Relationships between insulin sensitivity and renal hemodynamic parameters were examined by multivariable linear regression. Renal hemodynamic parameters were examined across tertiles of M values.ResultsWe tested 44 adults with T2D, of whom 77% were male, with mean ± SD age 63 ± 7 years, BMI 31.2 ± 4.0 kg/m2, and HbA1c 7.4 ± 0.6%. Average GFR was 110 ± 26 mL/min, with an FF of 22.1 ± 2.8% and median 24-h urinary albumin excretion of 11.3 mg (interquartile range 5.8-17.0). Average M value was 5.6 ± 2.9 mg/kglean/min. Insulin sensitivity inversely correlated with GFR (r = -0.44, P < 0.01) and FF (r = -0.40, P < 0.01), and these associations remained significant after multivariable adjustments for age, sex, renin-angiotensin system inhibitor use, and HbA1c. In addition, GFR, FF, and urinary albumin excretion were highest in the participants in the lowest M value tertile.ConclusionsFor the first time, we demonstrate that impaired insulin sensitivity is associated with intrarenal hemodynamic dysfunction by gold standard techniques in adults with T2D treated with metformin monotherapy.
| S-EPMC7118247 | biostudies-literature
Project description:In type 1 diabetes (T1D), impaired insulin sensitivity may contribute to the development of diabetic kidney disease (DKD) through alterations in kidney oxidative metabolism. Young adults with T1D and healthy controls underwent single-cell RNA sequencing, and spatial metabolomics to assess this relationship.
2024-11-11 | GSE279086 | GEO
Project description:IntroductionClinician-led diabetes education is a fundamental component of care to assist people with Type 1 diabetes (T1D) self-manage their disease. Recent initiatives to incorporate a more patient-centered approach to diabetes education have included recommendations to make such education more individualized. Yet there is a dearth of research that identifies patients' perceptions of clinician-led diabetes education. We aimed to describe the experience of diabetes education from the perspective of young adults with T1D.MethodsWe designed a self-reported survey for Australian adults, aged 18-35 years, with T1D. Participants (n = 150) were recruited by advertisements through diabetes consumer-organizations. Respondents were asked to rate aspects of clinician-led diabetes education and identify sources of self-education. To expand on the results of the survey we interviewed 33 respondents in focus groups.ResultsSurveyThe majority of respondents (56.0%) were satisfied with the amount of continuing clinician-led diabetes education; 96.7% sought further self-education; 73.3% sourced more diabetes education themselves than that provided by their clinicians; 80.7% referred to diabetes organization websites for further education; and 30.0% used online chat-rooms and blogs for education. Focus groups: The three key themes that emerged from the interview data were deficiencies related to the pedagogy of diabetes education; knowledge deficiencies arising from the gap between theoretical diabetes education and practical reality; and the need for and problems associated with autonomous and peer-led diabetes education.ConclusionOur findings indicate that there are opportunities to improve clinician led-diabetes education to improve patient outcomes by enhancing autonomous health-literacy skills and to incorporate peer-led diabetes education and support with clinician-led education. The results provide evidence for the potential value of patient engagement in quality improvement and health-service redesign.
| S-EPMC4065294 | biostudies-literature
Project description:Preclinical models of type 1 diabetes mellitus exhibit marked declines in skeletal muscle health including significant impairments in muscle repair. The present study investigated, for the first time, whether muscle repair was altered in young adults with uncomplicated type 1 diabetes (T1D) following damaging exercise.In this cohort study, eighteen physically-active young adults (M=22.1, SEM=0.9 years) with T1D (n, male/female=4/5; MHbA1c= 58, SEMHbA1c=5.9 mmol/mol) and without T1D (n, male/female=4/5) performed 300 unilateral eccentric contractions (90°s-1) of the knee extensors. Prior to exercise, at 48-hours and at 96-hours after exercise, participants gave a venous blood sample and vastus lateralis biopsy and performed a maximal voluntary isometric knee extension. Skeletal muscle extracellular matrix content, and satellite cell content/proliferation were assessed by immunofluorescence. Transmission electron microscopy was used to quantify ultrastructural damage.Maximal isometric strength was comparable between T1D and their sex-matched control group prior to exercise for both sexes. Immediately following damaging exercise, strength was decreased in both groups but there was a moderate effect size for lower strength during recovery in the T1D group at both 48-hours and 96-hours. Serum creatine kinase, an indicator of muscle damage, was moderately higher in T1D participants compared to controls at rest, and exhibited a small elevation 96-hours after exercise. Immunofluorescence analyses showed satellite cell content was lower at all timepoints in those with type 1 diabetes. T1D participants demonstrated a moderate delay in satellite cell proliferation (as assessed by Pax7+/Ki67+ nuclei counts) after exercise, reaching peak levels of proliferation 48-hours after control participants. Despite these differences, those with T1D did not exhibit greater ultrastructural muscle damage than controls as assessed by electron microscopy. Finally, a transcriptomic investigation of T1D muscle revealed several networks of dysregulated genes involving RNA translation as well as mitochondrial respiration function, providing potential explanations for previous observations of mitochondrial dysfunction in similar T1D cohorts. Our novel findings indicate that skeletal muscle from physically active, young adults with moderately controlled T1D may have a reduced ability to handle, and repair from, damaging exercise. While larger cohort studies are clearly needed, these results suggest that those with T1D may require longer recovery times following damaging exercise.
2021-10-29 | GSE182494 | GEO
Project description:Background: Recent studies highlight racial-ethnic disparities in insulin pump and continuous glucose monitor (CGM) use in people with type 1 diabetes (T1D), but drivers of disparities remain poorly understood beyond socioeconomic status (SES). Methods: We recruited a diverse sample of young adults (YA) with T1D from six diabetes centers across the United States, enrolling equal numbers of non-Hispanic (NH) White, NH Black, and Hispanic YA. We used multivariate logistic regression to examine to what extent SES, demographics, health care factors (care setting, clinic attendance), and diabetes self-management (diabetes numeracy, self-monitoring of blood glucose, and Self-Care Inventory score) explained insulin pump and CGM use in each racial-ethnic group. Results: We recruited 300 YA with T1D, aged 18-28 years. Fifty-two percent were publicly insured, and the mean hemoglobin A1c was 9.5%. Large racial-ethnic disparities in insulin pump and CGM use existed: 72% and 71% for NH White, 40% and 37% for Hispanic, and 18% and 28% for NH Black, respectively. After multiple adjustment, insulin pump and CGM use remained disparate: 61% and 53% for NH White, 49% and 58% for Hispanic, and 20 and 31% for NH Black, respectively. Conclusions: Insulin pump and CGM use was the lowest in NH Black, intermediate in Hispanic, and highest in NH White YA with T1D. SES was not the sole driver of disparities nor did additional demographic, health care, or diabetes-specific factors fully explain disparities, especially between NH Black and White YA. Future work should examine how minority YA preferences, provider implicit bias, systemic racism, and mistrust of medical systems help to explain disparities in diabetes technology use.
| S-EPMC7994432 | biostudies-literature
Project description:BackgroundThe transition of young adults with type 1 diabetes (T1D) from pediatric to adult care is challenging and frequently accompanied by worsening of diabetes-related health. To date, there are no reports which prospectively assess the effects of theory-based psycho-behavioral interventions during the transition period neither on glycemic control nor on psychosocial factors that contribute to poor glycemic control. Therefore, the overall aim of this study was to develop and pilot test an integrative group intervention based on the underlying principles of self-determination theory (SDT), in young adults with T1D.MethodsFifty-one young adults with T1D participated in an education and case management-based transition program, of which 9 took part in the Diabetes Empowerment Council (DEC), a 12-week holistic, multimodality facilitated group intervention consisting of "council" process based on indigenous community practices, stress-reduction guided imagery, narrative medicine modalities, simple ritual, and other integrative modalities. Feasibility, acceptability, potential mechanism of effects, and bio-behavioral outcomes were determined using mixed qualitative and quantitative methods.ResultsThe intervention was highly acceptable to participants, though presented significant feasibility challenges. Participants in DEC showed significant reductions in perceived stress and depression, and increases in general well-being relative to other control participants. Reduction in perceived stress, independent of intervention group, was associated with reductions in hemoglobin A1C. A theoretical model explaining the effects of the intervention included the promotion of relatedness and autonomy support, 2 important aspects of SDT.ConclusionsThe DEC is a promising group intervention for young adults with T1D going through transition to adult care. Future investigations will be necessary to resolve feasibility issues, optimize the multimodality intervention, determine full intervention effects, and fully test the role of the underlying theoretical model of action.ClinicalTrials.gov Registration Number NCT02807155; Registration date: June 15, 2016 (retrospectively registered).
| S-EPMC5846920 | biostudies-literature
Project description:OBJECTIVE:With rising obesity, it is becoming increasingly difficult to distinguish between type 1 diabetes (T1D) and type 2 diabetes (T2D) in young adults. There has been substantial recent progress in identifying the contribution of common genetic variants to T1D and T2D. We aimed to determine whether a score generated from common genetic variants could be used to discriminate between T1D and T2D and also to predict severe insulin deficiency in young adults with diabetes. RESEARCH DESIGN AND METHODS:We developed genetic risk scores (GRSs) from published T1D- and T2D-associated variants. We first tested whether the scores could distinguish clinically defined T1D and T2D from the Wellcome Trust Case Control Consortium (WTCCC) (n = 3,887). We then assessed whether the T1D GRS correctly classified young adults (diagnosed at 20-40 years of age, the age-group with the most diagnostic difficulty in clinical practice; n = 223) who progressed to severe insulin deficiency <3 years from diagnosis. RESULTS:In the WTCCC, the T1D GRS, based on 30 T1D-associated risk variants, was highly discriminative of T1D and T2D (area under the curve [AUC] 0.88 [95% CI 0.87-0.89]; P < 0.0001), and the T2D GRS added little discrimination (AUC 0.89). A T1D GRS >0.280 (>50th centile in those with T1D) is indicative of T1D (50% sensitivity, 95% specificity). A low T1D GRS (<0.234, <5th centile T1D) is indicative of T2D (53% sensitivity, 95% specificity). Most discriminative ability was obtained from just nine single nucleotide polymorphisms (AUC 0.87). In young adults with diabetes, T1D GRS alone predicted progression to insulin deficiency (AUC 0.87 [95% CI 0.82-0.92]; P < 0.0001). T1D GRS, autoantibody status, and clinical features were independent and additive predictors of severe insulin deficiency (combined AUC 0.96 [95% CI 0.94-0.99]; P < 0.0001). CONCLUSIONS:A T1D GRS can accurately identify young adults with diabetes who will require insulin treatment. This will be an important addition to correctly classifying individuals with diabetes when clinical features and autoimmune markers are equivocal.
| S-EPMC5642867 | biostudies-literature
Project description:AimsCopeptin, a surrogate of vasopressin, is elevated in type 1 diabetes (T1D) and predicts kidney disease and cardiovascular mortality. Given the cardiorenal protective effects of SGLT2 inhibition (SGLT2i), our aim was to examine: 1) the relationship between serum copeptin, metabolic, renal and systemic hemodynamic parameters in adults with T1D; and 2) serum copeptin after SGLT2i with empagliflozin.Materials and methodsIn this post-hoc, exploratory analysis, serum copeptin, glomerular filtration rate (GFRInulin), effective renal plasma flow (ERPFPAH), plasma renin angiotensin aldosterone system markers, HbA1c, 24-hour urine volume and sodium excretion were measured in 40 participants with T1D (24.3±5.1 years) during eu- and hyperglycaemia before and after 8 weeks of 25mg of daily empagliflozin.ResultsHigher baseline copeptin correlated with higher HbA1c, lower 24-hour urine volume and sodium excretion, after correcting for age, sex, systolic blood pressure, and HbA1c. Copeptin concentrations increased in response to empagliflozin under euglycaemia (4.1±2.1 to 5.1±2.8pmol/L, P=0.0053) and hyperglycaemia (3.3±1.4 to 5.6±2.8pmol/L, P<0.0001). The rise in copeptin in response to empagliflozin correlated with change in 24-hour urine volume, but was independent of changes in fractional excretion of sodium and haematocrit.ConclusionsElevated serum copeptin was associated with worse glycaemic control and lower diuresis and natriuresis. SGLT2i increased serum copeptin in adults with T1D, and the rise correlated with change in diuresis, but not natriuresis and hemo-concentration. Further work is required to evaluate the clinical implications of elevated copeptin with SGLT2i, including whether it is simply a marker of diuresis or may contribute to cardiorenal disease long-term.
| S-EPMC7253338 | biostudies-literature