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  • 1
    Electronic Resource
    Electronic Resource
    Insulin increases plasma leptin concentrations in normal subjects and patients with NIDDM (1996)
    Springer
    Diabetologia 39 (1996), S. 993-996 
    Details
    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
    URL: http://dx.doi.org/10.1007/BF00403921
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Insulin increases plasma leptin concentrations in normal subjects and patients with NIDDM (1996)
    Springer
    Diabetologia 39 (1996), S. 993-996 
    Details
    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
    URL: http://dx.doi.org/10.1007/BF00403921
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    Methodological aspects, dose-response characteristics and causes of interindividual variation in insulin stimulation of limb blood flow in normal subjects (1995)
    Springer
    Diabetologia 38 (1995), S. 555-564 
    Details
    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
    URL: http://dx.doi.org/10.1007/BF00400724
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    Paper (German National Licenses)
    Fulltext
  • 4
    Electronic Resource
    Electronic Resource
    Methodological aspects, dose-response characteristics and causes of interindividual variation in insulin stimulation of limb blood flow in normal subjects (1995)
    Springer
    Diabetologia 38 (1995), S. 555-564 
    Details
    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
    URL: http://dx.doi.org/10.1007/BF00400724
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    Paper (German National Licenses)
    Fulltext
  • 5
    Electronic Resource
    Electronic Resource
    Defective regulation of triglyceride metabolism by insulin in the liver in NIDDM (1997)
    Springer
    Diabetologia 40 (1997), S. 454-462 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Apolipoprotein B ; stable isotopes ; insulin resistance ; non-esterified fatty acids ; cholesterol.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Insulin administration to healthy subjects inhibits the production of very low density lipoprotein (VLDL)1 (Svedbergs flotation (Sf) rate 60–400) without affecting that of VLDL2 (Sf 20–60) subclass. This study was designed to test whether this hormonal action is impaired in non-insulin-dependent diabetes mellitus (NIDDM). We studied six men with NIDDM (age 53 ± 3 years, body mass index 27.0 ± 1.0 kg/m2, plasma triglycerides 1.89 ± 0.22 mmol/l) during an 8.5 h infusion of saline (control) and then in hyperinsulinaemic (serum insulin ∼ 540 pmol/l) conditions during 8.5 h infusions of glucose and insulin to give either hyper- and normoglycaemic conditions. [3-2H]-leucine was used as tracer and kinetic constants derived using a non-steady-state multicompartmental model. Compared to the control study, patients with NIDDM reduced VLDL1 apo B production by only 3 ± 8 % after 8.5 h of hyperinsulinaemia (701 ± 102 vs 672 ± 94 mg/day respectively, NS) in hyperglycaemic conditions and by 9 ± 21 % under normoglycaemic conditions (603 ± 145 mg/day). In contrast, in normal subjects insulin induced a 50 ± 15 % decrement in VLDL1 apo B production (p 〈 0.05). Direct synthesis of VLDL2 apo B in patients with NIDDM was not markedly affected by insulin. We conclude that a contributory factor to hypertriglyceridaemia in NIDDM is the inability of insulin to inhibit acutely the release of VLDL1 from the liver, despite efficient suppression of serum non-esterfied fatty acids. [Diabetologia (1997) 40: 454–462]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250050700
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    Paper (German National Licenses)
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  • 6
    Electronic Resource
    Electronic Resource
    Effects of the neuropeptide Y Y1 receptor antagonist SR 120107A on sympathetic vascular control in pigs in vivo (1996)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 354 (1996), S. 633-642 
    Details
    ISSN: 1432-1912
    Keywords: Key words Neuropeptide Y Y1 receptor antagonist ; SR 120107A ; Sympathetic vasoconstriction ; Pig
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  The possible involvement of neuropeptide Y in sympathetic vasoconstriction in various vascular beds in anesthetized pigs in vivo was studied using the neuropeptide Y Y1 receptor antagonist SR 120107A. Single impulse sympathetic nerve stimulation evoked rapid vasoconstrictor responses in hind limb and nasal mucosa which were not affected by SR 120107A (1.5 mg kg–1). Vascular responses to high frequency stimulation was measured in kidney, spleen (three 1 s bursts at 20 Hz or 300 impulses at 10 Hz), hind limb and nasal mucosa (three 1 s bursts at 20 Hz). High frequency stimulation evoked rapid vasoconstriction in all vascular beds studied. This was followed by a long-lasting phase of reduced blood flow in hind limb and nasal mucosa. SR 120107A (1.5 mg kg–1) attenuated the vasoconstriction evoked by the 20 Hz stimulation in the kidney, whereas a higher dose (a total of 6.0 mg kg–1) was required to reduce the vascular response in kidney to the 10 Hz stimulation. SR 120107A (1.5 mg kg–1) did not inhibit the vascular responses in spleen, hind limb or nasal mucosa to the 20 Hz stimulation or the vasoconstriction in spleen to the 10 Hz stimulation (a total of 6 mg kg–1). Subsequent addition of the adrenoceptor antagonists phenoxybenzamine (5 mg kg–1) plus timolol (2 mg kg–1) strongly reduced the vascular responses to single impulse stimulation and high frequency stimulation (20 Hz series) in all vascular beds. We conclude that endogenous neuropeptide Y acting on the neuropeptide Y Y1 receptor, as revealed by SR 120107A, is likely to account for part of the sympathetic vasoconstriction upon high frequency stimulation in the kidney.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00170839
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    Paper (German National Licenses)
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