Impaired superficial femoral artery vasodilation and leg blood flow in young obese women following an oral glucose tolerance test

2012 ◽  
Vol 37 (1) ◽  
pp. 176-183 ◽  
Author(s):  
T.D. Olver ◽  
T.J. Hazell ◽  
C.D. Hamilton ◽  
J.K. Shoemaker ◽  
P.W.R. Lemon

This study was designed to test the hypothesis that glucose ingestion following an overnight fast increases leg vascular conductance (LVCd) and superficial femoral artery (SFA) vasodilation in lean but not obese young women. Obese (23.5 ± 4.0 years, 84.7 ± 14.7 kg, 37.2% ± 6.4% fat; mean ± SD, n = 8) and lean (23.8 ± 2.4 years, 60.6 ± 4.0 kg, 22.3% ± 2.8% fat; n = 8) women arrived in the laboratory at 0830 h after a 12-h overnight fast for body composition (densitometry) assessment. Then, capillary blood glucose (BGlu), plasma insulin, heart rate, cardiac output, mean arterial pressure, leg blood flow (Doppler ultrasound), and LVCd were measured (after 15 min in the supine position), and at 30-min intervals for 2 h following glucose ingestion (75 g glucose load, 12.5% solution). Fasting BGlu concentration was not different between groups (obese = 5.1 ± 0.47 vs. lean = 4.9 ± 0.37 mmol·L–1, p = 0.71) but 60, 90, and 120 min postingestion BGlu was elevated (p ≤ 0.03) in the obese women. Insulin differences were not significant. Fasting LVCd was not different between groups (lean = 0.72 ± 0.49 vs. obese = 0.70 ± 0.19 mL·min–1·mm Hg–1; p = 0.48); however, LVCd, as well as Δ in SFA diameter were significantly elevated (p ≤ 0.04) in the lean compared with the obese group at 60, 90, and 120 min postglucose ingestion (LVCd, peak lean = 1.4 ± 0.5 vs. peak obese = 0.8 ± 0.1 mL·min–1·mm Hg–1; Δ in SFA, peak lean = 0.51 ± 0.30 vs. peak obese = 0.09 ± 0.45 mm). The reduced LVCd following glucose ingestion could contribute to impaired glucose tolerance. Further, the lack of SFA dilation may be evidence of impaired vascular insulin responsiveness in these obese young women.

1998 ◽  
Vol 84 (4) ◽  
pp. 1365-1373 ◽  
Author(s):  
Paul J. Arciero ◽  
Denise L. Smith ◽  
Jorge Calles-Escandon

The purpose of this investigation was to examine the effects of 7–10 days of inactivity (IA) on glucose tolerance (GT), resting metabolic rate (RMR), thermic effect of a meal (TEM), and limb blood flow in endurance-trained men. Eight highly trained (peak O2 consumption 64 ± 2 ml ⋅ kg−1 ⋅ min−1) endurance athletes participated in this study involving two identical test days, one ∼24 h after a normal training bout (Tr) and the second after 7–10 days of IA. The following tests were conducted at each visit: 75-g oral glucose tolerance test (OGTT), RMR, and TEM and measurements of calf and forearm blood flow (BF) by using venous occlusive plethysmography. Body weight remained unchanged during this short period of IA (Tr, 78.5 ± 1 kg; IA, 78.7 ± 1 kg). The area under the glucose and insulin curves increased 65% (Tr, 3,375 ± 877 vs. IA, 5,559.4 ± 621 mg ⋅ dl−1 ⋅ 180 min−1) and 73% (Tr, 2,182.5 ± 270 vs. IA, 3,793.1 ± 739 μU ⋅ ml−1 ⋅ 180 min−1) after IA, respectively ( P < 0.01). RMR decreased significantly (4%; 1.5 ± 0.02 vs. 1.44 ± 0.02 kcal/min; P < 0.05) and respiratory exchange ratio during the OGTT increased (4%, 0.812 ± 0.011 vs. 0.842 ± 0.009; P < 0.05) after IA, whereas TEM increased similarly in the Tr and IA states. In the Tr state, mean calf BF increased by 22% (3.17 ± 0.22 vs. 3.87 ± 0.38 ml ⋅ 100 ml−1 ⋅ min−1; P < 0.05) during the OGTT but remained unchanged after IA, whereas no differences at rest or during OGTTs existed between the two conditions for forearm BF. Incremental insulin area above fasting during the OGTT was correlated with mean calf BF in the Tr ( r = 0.76, P < 0.05) and IA ( r = 0.72, P < 0.05) states. In conclusion, 7–10 days of IA results in a deterioration in GT and a reduction in RMR. After glucose ingestion, calf BF was elevated compared with resting levels in the Tr state but was unchanged in the IA state; however, limb BF was not related to GT or RMR. Thus our findings raise questions regarding the relative contribution of BF in modulating glucose tolerance and energy expenditure in endurance athletes in their habitual Tr or IA state.


2003 ◽  
Vol 88 (10) ◽  
pp. 4559-4564 ◽  
Author(s):  
Soffia Gudbjörnsdóttir ◽  
Mikaela Sjöstrand ◽  
Lena Strindberg ◽  
John Wahren ◽  
Peter Lönnroth

Abstract To elucidate mechanisms regulating capillary transport of insulin and glucose, we directly calculated the permeability surface (PS) area product for glucose and insulin in muscle. Intramuscular microdialysis in combination with the forearm model and blood flow measurements was performed in healthy males, studied during an oral glucose tolerance test or during a one-step or two-step euglycemic hyperinsulinemic clamp. PS for glucose increased significantly from 0.29 ± 0.1 to 0.64 ± 0.2 ml/min·100 g after oral glucose tolerance test, and glucose uptake increased from 1.2 ± 0.4 to 2.6 ± 0.6 μmol/min·100 g (P &lt; 0.05). During one-step hyperinsulinemic clamp (plasma insulin, 1.962 pmol/liter), PS for glucose increased from 0.2 ± 0.1 to 2.3 ± 0.9 ml/min·100 g (P &lt; 0.05), and glucose uptake increased from 0.6 ± 0.2 to 5.0 ± 1.4 μmol/min·100 g (P &lt; 0.05). During the two-step clamp (plasma insulin, 1380 ± 408 and 3846 ± 348 pmol/liter), the arterial-interstitial difference and PS for insulin were constant. The PS for glucose tended to increase (P = not significant), whereas skeletal muscle blood flow increased from 4.4 ± 0.7 to 6.2 ± 0.8 ml/min·100 ml (P &lt; 0.05). The present data show that PS for glucose is markedly increased by oral glucose, whereas a further vasodilation exerted by high insulin concentrations may not be physiologically relevant for capillary delivery of either glucose or insulin in resting muscle.


2010 ◽  
Vol 24 (S1) ◽  
Author(s):  
Jean Lorraine Gutierrez ◽  
Matthew Cooke ◽  
Rafer Lutz ◽  
Bowden Rodney ◽  
Robert Kane ◽  
...  

2019 ◽  
Vol 104 (8) ◽  
pp. 3481-3490 ◽  
Author(s):  
Alfonso Galderisi ◽  
Cosimo Giannini ◽  
Michelle Van Name ◽  
Sonia Caprio

Abstract Context The consumption of high-fructose beverages is associated with a higher risk for obesity and diabetes. Fructose can stimulate glucagon-like peptide 1 (GLP-1) secretion in lean adults, in the absence of any anorexic effect. Objective We hypothesized that the ingestion of glucose and fructose may differentially stimulate GLP-1 and insulin response in lean adolescents and adolescents with obesity. Design We studied 14 lean adolescents [four females; 15.9 ± 1.6 years of age; body mass index (BMI), 21.8 ± 2.2 kg/m2] and 23 adolescents with obesity (five females; 15.1 ± 1.6 years of age; BMI, 34.5 ± 4.6 kg/m2). Participants underwent a baseline oral glucose tolerance test to determine their glucose tolerance and estimate insulin sensitivity and β-cell function [oral disposition index (oDIcpep)]. Eligible subjects received, in a double-blind, crossover design, 75 g of glucose or fructose. Plasma was obtained every 10 minutes for 60 minutes for the measures of glucose, insulin, and GLP-1 (radioimmunoassay) and glucose-dependent insulinotropic polypeptide (GIP; ELISA). Incremental glucose and hormone levels were compared between lean individuals and those with obesity by a linear mixed model. The relationship between GLP-1 increment and oDIcpep was evaluated by regression analysis. Results Following the fructose challenge, plasma glucose excursions were similar in both groups, yet the adolescents with obesity exhibited a greater insulin (P &lt; 0.001) and GLP-1 (P &lt; 0.001) increase than did their lean peers. Changes in GIP were similar in both groups. After glucose ingestion, the GLP-1 response (P &lt; 0.001) was higher in the lean group. The GLP-1 increment during 60 minutes from fructose drink was correlated with a lower oDIcpep (r2 = 0.22, P = 0.009). Conclusion Fructose, but not glucose, ingestion elicits a higher GLP-1 and insulin response in adolescents with obesity than in lean adolescents. Fructose consumption may contribute to the hyperinsulinemic phenotype of adolescent obesity through a GLP-1–mediated mechanism.


2011 ◽  
Vol 57 (5) ◽  
pp. 490-500 ◽  
Author(s):  
J. Sokolovska ◽  
J. Rumaks ◽  
N. Karajeva ◽  
D. Grinvalde ◽  
J. Sharipova ◽  
...  

Streptozotocin (STZ) was used to induce the diabetic rat model. STZ rats were treated with mildronate (100 mg/kg daily, per os or intraperitoneally for 6 weeks). Body weight, blood glucose, triglyceride, ketone body concentrations, glycated hemoglobin percent (HbA1c%), glucose tolerance, and the development of neuropathic pain were monitored throughout the experiment. In the STZ + mildronate group, mildronate treatment caused a significant decrease in mean blood glucose (on week 4) and triglyceride concentrations (on weeks 3-6), significantly slowed the increase in HbA1c% (on week 6) and improved glucose tolerance 120 minutes after glucose ingestion during oral glucose tolerance test versus the STZ group. Mildronate completely protected development of STZ-induced neuropathic pain from the first administration week up to end of the experiment. The obtained data indicate clinical usefulness of the drug for the treatment of diabetes mellitus and its complications.


2012 ◽  
Vol 2012 ◽  
pp. 1-5 ◽  
Author(s):  
Serdar Farhan ◽  
Ammon Handisurya ◽  
Jelena Todoric ◽  
Andrea Tura ◽  
Giovanni Pacini ◽  
...  

Objective. Fetuin-A has been associated with gestational diabetes mellitus (GDM). We investigated fetuin-A levels during and after pregnancy in women with GDM. Fetuin-A measurements were performed in 10 women with GDM and 10 age and body mass index (BMI) matched healthy pregnant women. All women underwent an oral glucose tolerance test (OGTT) in and 3 months after gestation.Results. Fasting fetuin-A correlated with BMI in women with former GDM (r=0.90,P<0.0001) but showed no association with parameters of glucose tolerance in women with GDM or post-GDM. GDM featured significantly lower insulin sensitivity and higher insulin and C-peptide secretion profiles compared to NGT during pregnancy (P<0.05). Fasting and postprandial fetuin-A did not differ between groups, neither during nor after pregnancy.Conclusion. Fetuin-A is not influenced by glucose tolerance during or after pregnancy or acute glucose elevations following glucose ingestion in young women, but closely relates to BMI early postpartum.


2005 ◽  
Vol 31 (3) ◽  
pp. 213-218 ◽  
Author(s):  
Mehtap Cakir ◽  
Ramazan Sari ◽  
Ozgur Tosun ◽  
Umit Karayalcin

2010 ◽  
Vol 42 ◽  
pp. 325-326
Author(s):  
Jean L. Gutierrez ◽  
Matthew B. Cooke ◽  
Rodney G. Bowden ◽  
Rafer Lutz ◽  
Robert R. Kane ◽  
...  

1992 ◽  
Vol 126 (2) ◽  
pp. 132-136 ◽  
Author(s):  
Per Olav Dale ◽  
Tom Tanbo ◽  
Ole Djøseland ◽  
Jak Jervell ◽  
Thomas Åbyholm

To investigate the effect of long-term androgen suppression on insulin sensitivity, obese and non-obese women with the polycystic ovary syndrome and obese and non-obese ovulatory women were given an oral glucose tolerance test before and after treatment with a gonadotropin-releasing hormone agonist. The women with polycystic ovary syndrome showed higher basal luteinizing hormone and androgen levels than the ovulatory women. All women with the polycystic ovary syndrome responded non-diabetically to the glucose tolerance test. However, compared with controls, the obese women with the polycystic ovary syndrome showed a hyperinsulinemic response to the glucose tolerance test, indicating insulin resistance. During the 3-h glucose tolerance test there was no concomitant change in androgen levels in the hyperinsulinemic women with the polycystic ovary syndrome. The insulin response to an oral glucose tolerance test remained unchanged in all women, although a hypogonadotropic hypogonadal state was maintained for several weeks. This study therefore suggests that endogenous androgens do not play a role in sustaining insulin resistance in women with the polycystic ovary syndrome.


Sign in / Sign up

Export Citation Format

Share Document