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  • 1
    ISSN: 1432-0428
    Keywords: Hyperinsulinaemic clamp ; muscle ; blood flow ; venous occlusion plethysmography ; Doppler ultrasound ; blood pressure
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary To resolve some of the controversy regarding insulin regulation of blood flow, we performed in 20 normal subjects a) a reproducibility study of plethysmographic, Doppler ultrasound and laser Doppler blood flow measurements (n=7), b) a sequential insulin dose-response study with measurement of forearm (plethysmography), leg (Doppler ultrasound) and skin (laser Doppler) blood flow (n=12), and c) a sequential insulin dose-response study with comparison of forearm (plethysmography) and calf (plethysmography) blood flow (n=8). We also searched for factors which might explain the interindividual variation in the blood flow response to insulin. During sequential insulin infusions (2 h each, 61±2, 139±6, 462±15 mU/l), forearm blood flow increased by 17±6, 50±14 and 113±17% (p〈0.05 or less between steps), respectively. The increase at the 61±2 mU/l insulin concentration barely exceeded methodological variation (13±2%). In contrast to the continuous increase in blood flow, the glucose arterio venous difference reached its maximum (1.7±0.2 mmol/l) at the lowest 61±2 mU/l insulin concentration and remained constant thereafter. Forearm and calf blood flow responses to insulin were virtually identical when determined with plethysmography. In contrast, only a 27% increase was detected in femoral flow index as determined by Doppler ultrasound. Forearm blood flow (per forearm volume) was highly correlated with the relative forearm muscle content (mean 59±5%, range 24–81%) both basally (r=0.86, p〈0.001, n=12) and at all insulin concentrations (r=0.85–0.92, p〈0.001) indicating that the percent of forearm that is muscle explains 70–85% of interindividual variation in blood flow. In conclusion 1) physiological insulin concentrations stimulate glucose uptake mainly by increasing glucose extraction while supraphysiological insulin concentrations increase forearm glucose uptake predominantly via increases in blood flow. 2) The dose-response characteristics of insulin stimulation of forearm and calf blood flow are similar when determined with strain-gauge plethysmography. 3) Relative forearm muscle content is a key factor in determining both basal forearm blood flow and the interindividual variation in its response to insulin in normal subjects.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-0428
    Keywords: Keywords Insulin sensitivity ; obesity ; fat ; non-insulin-dependent diabetes mellitus.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Insulin is known to increase expression of the ob gene product leptin in adipose tissue of rodents. We determined whether insulin increases circulating leptin concentrations in humans, and whether this effect might be altered in patients with non-insulin-dependent diabetes mellitus (NIDDM). Plasma leptin concentrations were determined during an 8.5-h hyperinsulinaemic clamp (serum free insulin approximately 480 pmol/l) and during an 8.5-h infusion of physiological NaCl solution (saline) in eight normal subjects (age 51 ± 3 years, BMI 26.3 ± 0.6 kg/m2, fasting plasma glucose 5.6 ± 0.2 mmol/l) and seven patients with NIDDM (age 54 ± 2 years, 27.0 ± 0.9 kg/m2, 11.1 ± 0.8 mmol/l). Fasting serum insulin level correlated with plasma leptin (r = 0.72, p 〈 0.005), even after adjusting for the percentage of body fat (p 〈 0.005). During the insulin infusion, a significant increase in the plasma leptin concentration was observed after 6 h (37 ± 14 %; 5.2 ± 0.8 vs 3.9 ± 0.6 ng/ml, 6 vs 0 h, p 〈 0.05) in the normal subjects and after 8.5 h (38 ± 11 %; 7.1 ± 1.0 vs 5.5 ± 0.9 ng/ml, 8.5 vs 0 h, p 〈 0.05) in the patients with NIDDM. During the saline infusion, plasma leptin concentrations decreased significantly in the normal subjects by 11 ± 1 % (p 〈 0.005) and in the patients with NIDDM by 14 ± 1 % (p 〈 0.01) after 2 h. During the infusion of insulin as compared to saline, plasma leptin concentrations were 32 ± 13 (p 〈 0.05), 53 ± 14 (p 〈 0.001), 106 ± 15 (p 〈 0.001) and 165 ± 21 (p 〈 0.001) % higher at 2, 4, 6 and 8.5 h in the normal subjects, and 11 ± 9 (p 〈 0.05), 27 ± 10 (p 〈 0.05), 58 ± 7 (p 〈 0.001) and 106 ± 13 (p 〈 0.001) % higher in the patients with NIDDM, respectively. No differences were observed in plasma leptin concentrations between the normal subjects and patients with NIDDM, under any conditions. We conclude that prolonged exposure to insulin increases plasma leptin concentrations in humans implying a role for insulin in chronic but not acute regulation of plasma leptin concentrations. The decrease in plasma leptin concentrations during saline infusion was greater than that expected on the basis of change in serum insulin concentrations, suggesting that factors other than insulin also contribute to regulation of plasma leptin concentrations. [Diabetologia (1996) 39, 993–996]
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-0428
    Keywords: Key words Hyperinsulinaemic clamp ; muscle ; blood flow ; venous occlusion plethysmography ; Doppler ultrasound ; blood pressure.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary To resolve some of the controversy regarding insulin regulation of blood flow, we performed in 20 normal subjects a) a reproducibility study of plethysmographic, Doppler ultrasound and laser Doppler blood flow measurements (n = 7), b) a sequential insulin dose-response study with measurement of forearm (plethysmography), leg (Doppler ultrasound) and skin (laser Doppler) blood flow (n = 12), and c) a sequential insulin dose-response study with comparison of forearm (plethysmography) and calf (plethysmography) blood flow (n = 8). We also searched for factors which might explain the interindividual variation in the blood flow response to insulin. During sequential insulin infusions (2 h each, 61 ± 2, 139 ± 6, 462 ± 15 mU/l), forearm blood flow increased by 17 ± 6, 50 ± 14 and 113 ± 17 % (p 〈 0.05 or less between steps), respectively. The increase at the 61 ± 2 mU/l insulin concentration barely exceeded methodological variation (13 ± 2 %). In contrast to the continuous increase in blood flow, the glucose arterio venous difference reached its maximum (1.7 ± 0.2 mmol/l) at the lowest 61 ± 2 mU/l insulin concentration and remained constant thereafter. Forearm and calf blood flow responses to insulin were virtually identical when determined with plethysmography. In contrast, only a 27 % increase was detected in femoral flow index as determined by Doppler ultrasound. Forearm blood flow (per forearm volume) was highly correlated with the relative forearm muscle content (mean 59 ± 5 %, range 24–81 %) both basally (r = 0.86, p 〈 0.001, n = 12) and at all insulin concentrations (r = 0.85–0.92, p 〈 0.001) indicating that the percent of forearm that is muscle explains 70–85 % of interindividual variation in blood flow. In conclusion 1) physiological insulin concentrations stimulate glucose uptake mainly by increasing glucose extraction while supraphysiological insulin concentrations increase forearm glucose uptake predominantly via increases in blood flow. 2) The dose-response characteristics of insulin stimulation of forearm and calf blood flow are similar when determined with strain-gauge plethysmography. 3) Relative forearm muscle content is a key factor in determining both basal forearm blood flow and the interindividual variation in its response to insulin in normal subjects. [Diabetologia (1995) 38: 555–564]
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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  • 4
    ISSN: 1432-0428
    Keywords: Insulin sensitivity ; obesity ; fat ; non-insulin-dependent diabetes mellitus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Insulin is known to increase expression of the ob gene product leptin in adipose tissue of rodents. We determined whether insulin increases circulating leptin concentrations in humans, and whether this effect might be altered in patients with non-insulin-dependent diabetes mellitus (NIDDM). Plasma leptin concentrations were determined during an 8.5-h hyperinsulinaemic clamp (serum free insulin approximately 480 pmol/l) and during an 8.5-h infusion of physiological NaCl solution (saline) in eight normal subjects (age 51±3 years, BMI 26.3±0.6 kg/ m2, fasting plasma glucose 5.6±0.2 mmol/l) and seven patients with NIDDM (age 54±2 years, 27.0±0.9 kg/m2, 11.1±0.8 mmol/l). Fasting serum insulin level correlated with plasma leptin (r=0.72, p〈0.005), even after adjusting for the percentage of body fat (p〈0.005). During the insulin infusion, a significant increase in the plasma leptin concentration was observed after 6 h (37±14%; 5.2±0.8 vs 3.9±0.6 ng/ml, 6 vs 0 h, p〈0.05) in the normal subjects and after 8.5 h (38±11%; 7.1±1.0 vs 5.5±0.9 ng/ml, 8.5 vs 0 h, p〈0.05) in the patients with NIDDM. During the saline infusion, plasma leptin concentrations decreased significantly in the normal subjects by 11±1% (p〈0.005) and in the patients with NIDDM by 14±1% (p〈0.01) after 2 h. During the infusion of insulin as compared to saline, plasma leptin concentrations were 32±13 (p〈0.05), 53±14 (p〈0.001), 106±15 (p〈0.001) and 165±21 (p〈0.001)% higher at 2, 4, 6 and 8.5 h in the normal subjects, and 11±9 (p〈0.05), 27±10 (p〈0.05), 58±7 (p〈0.001) and 106±13 (p〈0.001)% higher in the patients with NIDDM, respectively. No differences were observed in plasma leptin concentrations between the normal subjects and patients with NIDDM, under any conditions. We conclude that prolonged exposure to insulin increases plasma leptin concentrations in humans implying a role for insulin in chronic but not acute regulation of plasma leptin concentrations. The decrease in plasma leptin concentrations during saline infusion was greater than that expected on the basis of change in serum insulin concentrations, suggesting that factors other than insulin also contribute to regulation of plasma leptin concentrations.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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