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  • 1
    ISSN: 1432-0428
    Keywords: Cholesterol ; triglyceride ; VLDL ; LDL ; HDL ; lipoprotein lipase ; adipose tissue ; skeletal muscle ; obesity ; Type 2 (insulin-independent) diabetes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Serum lipoproteins and the heparin-releasable lipoprotein lipase (LPL) activity of adipose tissue and skeletal muscle were measured in 36 untreated obese patients with Type 2 (insulin-independent) diabetes and the values were compared with those of non-diabetic subjects of similar age, sex and relative body weight. In diabetic men, the LPL activity of adipose tissue was significantly reduced when expressed per tissue weight or per fat cell (p〈0.01). Diabetic females had slightly but not significantly lower LPL activity in adipose tissue than the non-diabetic females. The muscle LPL activity was similar in diabetic and non-diabetic subjects of both sexes. When the diabetic men were classified according to fasting blood glucose, the patients with high glucose levels had lower adipose tissue LPL activity than those with moderate hyperglycaemia. In both diabetic and non-diabetic subjects, there was a significant positive correlation between HDL cholesterol concentrations and adipose tissue LPL activity. It is concluded that Type 2 diabetes influences adipose tissue LPL activity and plasma lipoprotein concentrations and that this effect is superimposed on the similar changes produced by obesity alone.
    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: 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
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