Altered Renal Microvascular Function in Early Diabetes

Author(s):  
Pamela K. Carmines ◽  
Joseph P. Bast ◽  
Naohito Ishii
2011 ◽  
Vol 111 (5) ◽  
pp. 1361-1371 ◽  
Author(s):  
Jill M. Slade ◽  
Theodore F. Towse ◽  
Ved V. Gossain ◽  
Ronald A. Meyer

Long-term or untreated diabetes leads to micro- and macrovascular complications. However, there are few tests to evaluate microvascular function. A postcontraction blood oxygen level-dependent (BOLD) magnetic resonance imaging (MRI) technique was exploited to measure peripheral microvascular function in diabetics and healthy controls matched with respect to age, body mass index, and physical activity. Postcontraction BOLD microvascular response was measured following 1-s maximal isometric ankle dorsiflexion in individuals with diabetes mellitus type I [DMI, n = 15, age 33 ± 3 yr (means ± SE), median diabetes duration = 5.5 yr] and type II (DMII, n = 16, age 45 ± 2 yr, median duration = 2.4 yr); responses were compared with controls (CONI and CONII). Peripheral macrovascular function of the popliteal and tibial arteries was assessed during exercise hyperemia with phase contrast magnetic resonance angiography following repetitive exercise. There were no group differences as a result of diabetes in peripheral microvascular function (peak BOLD response: DMI = 2.04 ± 0.38% vs. CONI = 2.08 ± 0.48%; DMII = 0.93 ± 0.24% vs. CONII = 1.13 ± 0.24%; mean ± SE), but the BOLD response was significantly influenced by age (partial r = −0.384, P = 0.003), supporting its sensitivity as a measure of microvascular function. Eleven individuals had no microvascular BOLD response, including three diabetics with neuropathy and four controls with a family history of diabetes. There were no differences in peripheral macrovascular function between groups when assessing exercise hyperemia or the pulsitility and resistive indexes. Although the BOLD microvascular response was not impaired in early diabetes, these results encourage further investigation of muscle BOLD as it relates to peripheral microvascular health.


Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 2374-PUB
Author(s):  
SPIROS FOURLANOS ◽  
NICHOLAS D. MINGOS ◽  
LOIS M. ROWAN ◽  
RAHUL BARMANRAY ◽  
MERVYN KYI

Peptides ◽  
2021 ◽  
pp. 170491
Author(s):  
Livia Victorino Souza ◽  
Sandro Soares de Almeida ◽  
Franciele De Meneck ◽  
Fernanda Thomazini ◽  
Ronaldo Carvalho Araujo ◽  
...  

2021 ◽  
Author(s):  
Ida K. B. Rasmussen ◽  
Philip Hasbak ◽  
Bernt J. Scholten ◽  
Jens C. Laursen ◽  
Emilie H. Zobel ◽  
...  

Author(s):  
Rebecca E. Weiss ◽  
Nevert Badreldin ◽  
Kathleen Drexler ◽  
Charlotte Niznik ◽  
Lynn M. Yee

Objective The study aimed to evaluate perinatal outcomes associated with introduction of and adherence to early diabetes screening guidelines. Study Design Retrospective cohort study of all women who received prenatal care at a single, high-volume tertiary care center before (“preguidelines”) and after (“postguidelines”) American College of Obstetrics and Gynecology guidelines for early pregnancy diabetes screening for women at high risk for diabetes. Women with known pregestational diabetes, late entry to prenatal care, a fetus with a known anomaly, or multiple gestation were excluded. Multivariable linear and logistic regression models were constructed to compare maternal and neonatal outcomes between women in the preguidelines cohort to those in the postguidelines cohort. Similarly, adherence to screening guidelines was assessed, and among all women who were eligible for early diabetes screening, multivariable linear, and logistic models were created to compare outcomes between those women who were screened early to those who were not. Results Of the 2,069 women eligible for analysis, 64.6% (n = 1,337) were in the postguideline cohort. Women in the postguideline cohort were older, less likely to have a history of smoking, and more likely to be non-Hispanic white. On multivariable analysis, women in the postguideline cohort had significantly less gestational weight gain (aβ = −2.3; 95% confidence interval [CI]: −3.4 to −1.1), but a higher odds of 5-minute Apgar's score of <7 (adjusted odds ratio: 2.51; 95% CI: 1.11–5.66). Of 461 women who met ACOG early diabetes screening criteria, 58.7% (n = 270) were screened appropriately. Adherence to screening was associated with parity, race, insurance, and BMI. On multivariable analysis, there were no significant differences in neonatal outcomes between women meeting early screening criteria who were screened early and those who were not. Conclusion Introduction of early diabetes screening guidelines was associated with a significant decrease in gestational weight gain, but did not improve neonatal outcomes. Key Points


2019 ◽  
Vol 104 (7) ◽  
pp. 1136-1146 ◽  
Author(s):  
S. Tony Wolf ◽  
Craig W. Berry ◽  
Anna E. Stanhewicz ◽  
Lauren E. Kenney ◽  
Sara B. Ferguson ◽  
...  

2007 ◽  
Vol 293 (2) ◽  
pp. R707-R713 ◽  
Author(s):  
Sharyn M. Fitzgerald ◽  
Barbara K. Kemp-Harper ◽  
Helena C. Parkington ◽  
Geoffrey A. Head ◽  
Roger G. Evans

We determined whether nitric oxide (NO) counters the development of hypertension at the onset of diabetes in mice, whether this is dependent on endothelial NO synthase (eNOS), and whether non-NO endothelium-dependent vasodilator mechanisms are altered in diabetes in mice. Male mice were instrumented for chronic measurement of mean arterial pressure (MAP). In wild-type mice, MAP was greater after 5 wk of Nω-nitro-l-arginine methyl ester (l-NAME; 100 mg·kg−1·day−1 in drinking water; 97 ± 3 mmHg) than after vehicle treatment (88 ± 3 mmHg). MAP was also elevated in eNOS null mice (113 ± 4 mmHg). Seven days after streptozotocin treatment (200 mg/kg iv) MAP was further increased in l-NAME-treated mice (108 ± 5 mmHg) but not in vehicle-treated mice (88 ± 3 mmHg) nor eNOS null mice (104 ± 3 mmHg). In wild-type mice, maximal vasorelaxation of mesenteric arteries to acetylcholine was not altered by chronic l-NAME or induction of diabetes but was reduced by 42 ± 6% in l-NAME-treated diabetic mice. Furthermore, the relative roles of NO and endothelium-derived hyperpolarizing factor (EDHF) in acetylcholine-induced vasorelaxation were altered; the EDHF component was enhanced by l-NAME and blunted by diabetes. These data suggest that NO protects against the development of hypertension during early-stage diabetes in mice, even in the absence of eNOS. Furthermore, in mesenteric arteries, diabetes is associated with reduced EDHF function, with an apparent compensatory increase in NO function. Thus, prior inhibition of NOS results in endothelial dysfunction in early diabetes, since the diabetes-induced reduction in EDHF function cannot be compensated by increases in NO production.


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