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  • 1
    Electronic Resource
    Electronic Resource
    Response of adipose tissue lipoprotein lipase activity and serum lipoproteins to acute hyperinsulinaemia in man (1984)
    Springer
    Diabetologia 27 (1984), S. 364-369 
    Details
    ISSN: 1432-0428
    Keywords: Adipose tissue lipoprotein lipase ; insulin ; glucose ; insulin sensitivity ; lipoproteins
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In order to assess the short-term effects of hyperinsulinaemia and hyperglycaemia on adipose tissue lipoprotein lipase activity and on serum lipoproteins, we measured these variables in ten normal subjects during euglycaemic and hyperglycaemic hyperinsulinaemic clamps. The mean steady-state plasma glucose and insulin concentrations, respectively, were 4.7 mmol/l and 101 mU/l during euglycaemic moderate-insulin clamp, 4.9 mmol/l and 565 mU/l during euglycaemic high-insulin clamp, and 8.8 mmol/l and 148 mU/l during hyperglycaemic clamp. Saline infusion was used as control. The adipose tissue lipoprotein lipase activity rose significantly over 5 h during high-insulin clamp (p〈0.01) and during hyperglycaemic clamp (p〈0.05), but did not change during the moderate-insulin clamp. The magnitude of change of lipoprotein lipase activity from baseline (either rise or fall) was inversely related to the preclamp activity during euglycaemic moderate-insulin clamp (r= -0.67), during hyperglycaemic clamp (r= -0.68) and during infusion of saline (r= -0.75, p〈0.05). Total serum triglyceride concentration decreased significantly during all clamp studies compared with the control experiment. This change was mainly accounted for by a decrease of VLDL triglyceride. The LDL cholesterol level fell by an average of 5% (p〈0.05) during the high-insulin clamp and by 10% (p〈0.05) during the hyperglycaemic clamp. The HDL cholesterol level did not change significantly. It is concluded that adipose tissue lipoprotein lipase activity in man is increased by physiological insulin levels during hyperglycaemia and also by supraphysiological insulin levels during euglycaemia, but is not influenced by physiological hyperinsulinaemia without hyperglycaemia. Low basal lipoprotein lipase activity is more sensitive to insulin-glucose stimulation than primarily high lipoprotein lipase activity. Acute hyperinsulinaemia decreases VLDL triglyceride and LDL cholesterol concentrations.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00304851
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  • 2
    Electronic Resource
    Electronic Resource
    Modulation of hepatic glucose production by non-esterified fatty acids in Type 2 (non-insulin-dependent) diabetes mellitus (1991)
    Springer
    Diabetologia 34 (1991), S. 409-415 
    Details
    ISSN: 1432-0428
    Keywords: Type 2 (non-insulin-dependent) diabetes ; hepatic glucose production ; insulin resistance ; non-esterified fatty acids ; nicotinic acid derivative
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary To study the effect of changes in plasma non-esterified fatty acid concentration on suppression of hepatic glucose production by insulin eight Type 2 (non-insulin-dependent) diabetic patients participated in three euglycaemic, hyperinsulinaemic (108pmol · m2−1 · min−1) clamp studies combined with indirect calorimetry and infusion of [3-3H]-glucose and [1-14C]palmitate; (1) a control experiment with infusion of NaCl 154 mmol/l, (2) heparin was infused together with insulin, and (3) an antilipolytic agent, Acipimox, was administered at the beginning of the experiment. Six healthy volunteers participated in the control experiment. Plasma non-esterified fatty acid concentrations during the insulin clamp were in diabetic patients: (1) 151±36 μmol/1, (2) 949±178 μmol/l, and (3) 65±9 μmol/l; in healthy control subjects 93±13 μmol/l. Non-esterified fatty acid transport rate, oxidation and non-oxidative metabolism were significantly higher during the heparin than during the Acipimox experiment (p〈0.001). Suppression of hepatic glucose production by insulin was impaired in the diabetic compared to control subjects (255±42 vs 51±29 μmol/min, p〈0.01). Infusion of heparin did not affect the suppression of hepatic glucose production by insulin (231±49 μmol/min), whereas Acipimox significantly enhanced the suppression (21±53 μmol/min, p〈0.001 vs 154 mmol/l NaCl experiment). We conclude that insulin-mediated suppression of hepatic glucose production is not affected by increased non-esterified fatty acid availability. In contrast, decreased non-esterified fatty acid availability enhances the suppression of hepatic glucose production by insulin.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00403179
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  • 3
    Electronic Resource
    Electronic Resource
    Metabolism of HDL apolipoprotein A-I and A-II in Type 1 (insulin-dependent) diabetes mellitus (1992)
    Springer
    Diabetologia 35 (1992), S. 347-356 
    Details
    ISSN: 1432-0428
    Keywords: Type 1 (insulin-dependent) diabetes mellitus ; HDL cholesterol ; apolipoprotein A-I ; apolipoprotein A-II ; kinetic analyses ; VLDL triglyceride ; lipolytic enzymes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Concentrations of HDL cholesterol and apolipoprotein A-I are commonly increased in Type 1 (insul-independent) diabetes mellitus but the mechanisms whereby diabetes influences HDL metabolism have not been studied. We investigated the metabolism of HDL apoproteins A-I and II in normolipidaemic Type 1 diabetic men (n=17, HbA1 6.4–11.9%) without microalbuminuria but with a wide range of HDL cholesterol (0.85–2.10 mmol/l) and in nondiabetic men (n=18) matched for body mass index and the range of HDL cholesterol. Input rates and fractional catabolic rates for apolipoproteins A-I and II were determined following injection of 125I-apolipoprotein A-I and 131I-apolipoprotein A-II tracers. Additional multicompartmental analysis was performed using a model to describe the kinetics of HDL particles containing only apolipoprotein A-I (Lp A-I) and apolipoprotein A-I and apolipoprotein A-II (Lp A-I/ A-II). No gross differences from normal subjects were observed in the mean levels of lipids, lipoproteins, apoproteins and the lipolytic enzymes in the diabetic men as a result of the selection process. Furthermore, the relationship between apolipoprotein A kinetics and plasma HDL cholesterol levels appeared to be preserved in the diabetic group. However, some normal interrelationships were disrupted in the diabetic men. Firstly, the rate of apolipoprotein A-II synthesis was 22% lower than in control subjects (p〈0.05). Modelling indicated that this was due to decreased input of Lp A-I/A-II particles whereas the input of Lp A-I particles was similar in the two groups. Secondly, there was no correlation between VLDL triglyceride and HDL cholesterol or VLDL triglyceride and the fractional catabolic rate of apolipoproteins A-I and A-II in diabetic men in contrast to that seen in control subjects. We conclude that there is a disruption in the normal association between VLDL and HDL metabolism in Type 1 diabetic men and postulate that the observed differences may be due to the therapeutic use of exogenous insulin.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00401202
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  • 4
    Electronic Resource
    Electronic Resource
    LDL subclasses in IDDM patients: relation to diabetic nephropathy (1994)
    Springer
    Diabetologia 37 (1994), S. 681-688 
    Details
    ISSN: 1432-0428
    Keywords: Key words IDDM, diabetic nephropathy, microalbuminuria, proteinuria, lipid metabolism, small dense LDL
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary To answer the question whether the elevation of LDL-cholesterol in IDDM patients with incipient and established diabetic nephropathy is accompanied by changes in LDL size or composition, we studied distribution of LDL particles in 57 normoalbuminuric [AER 7 (1–19) µg/min, median and range], in 46 microalbuminuric [AER 50 (20–192) µg/min] and in 33 proteinuric [AER 422 (233–1756) µg/min] IDDM patients as well as in 49 non-diabetic control subjects with normoalbuminuria. The three diabetic groups were matched for duration of diabetes and glycaemic control. The mean particle diameter of the major LDL peak was determined by nondenaturing gradient gel electrophoresis. Composition and density distribution of LDL were determined in the subgroups of each patient group by density gradient ultracentrifugation. Normoalbuminuric IDDM patients had larger LDL particles than non-diabetic control subjects (260 Å vs 254 Å, p 〈0.05). LDL particle diameter was inversely correlated with serum triglycerides in all groups (p 〈0.05 for normoalbuminuric and p 〈0.001 for other groups). Triglyceride content of LDL was higher in three IDDM groups compared to control group (p 〈0.05). The elevation of LDL mass in microalbuminuric and proteinuric IDDM groups compared to normoalbuminuric IDDM group (p 〈0.05 for both) was mainly due to the increment of light LDL (density 1.0212–1.0343 g/ml). There were no significant changes in the density distribution or composition of LDL between the three diabetic groups. In conclusion the increase of LDL mass without major compositional changes suggests that the elevation of LDL in incipient and established diabetic nephropathy is primarily due to the increased number of LDL particles. The prevalence of atherogenic small dense LDL particles in IDDM patients with microalbuminuria and proteinuria is closely dependent on plasma triglyceride concentration. [Diabetologia (1994) 37: 681–688]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00417692
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  • 5
    Electronic Resource
    Electronic Resource
    Regulation of low-density lipoprotein particle size distribution in NIDDM and coronary disease: importance of serum triglycerides (1996)
    Springer
    Diabetologia 39 (1996), S. 453-461 
    Details
    ISSN: 1432-0428
    Keywords: Non-insulin-dependent diabetes mellitus ; coronary artery disease ; LDL composition ; small dense LDL ; electrophoresis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary An increase of low-density lipoprotein triglycerides (LDL-Tg) was found to be an independent coronary artery disease (CAD) risk factor for non-insulin-dependent diabetic (NIDDM) patients in a recent prospective study. We examined the composition and size of LDL particles in 50 NIDDM men with angiographically verified CAD (NIDDM+ CAD+) and in 50 NIDDM men without CAD (NIDDM+ CAD−) as compared to 50 non-diabetic men with CAD (NIDDM− CAD+) and 31 non-diabetic men without CAD (NIDDM− CAD−). The groups had similar ranges of age and BMI LDL particle size was determined by gradient gel electrophoresis, and LDL was isolated by sequential ultracentrifugation for compositional analyses. Serum Tg was increased in NIDDM patients as compared to non-diabetic subjects (p〈0.05), and in patients with CAD as compared to subjects without the disease (p〈0.05). LDL cholesterol was lower in NIDDM patients than in non-diabetic subjects (p〈0.001). Mean diameter of LDL particles was less than 255 å, but closely comparable in all groups. The presence of NIDDM was associated with increases of Tg and protein but lowering of free cholesterol in LDL (p〈0.005 for all). In multivariate regression analyses neither NIDDM nor CAD were associated with LDL particle size, but serum Tg was the major determinant of LDL size in both NIDDM and non-diabetic subjects (p〈0.001). When the patients were divided into quartiles according to fasting serum Tg levels, the LDL particle size and free cholesterol content decreased, but Tg and protein contents of LDL particles increased from the lowest to the highest Tg quartile (analysis of variance p〈0.001 for all). When the subjects were categorized into two groups according to the median of VLDL-Tg (1.10 mmol/l) LDL size was associated with VLDL-Tg in the high but not in the low VLDL-Tg group. We conclude that in NIDDM patients with or without CAD serum Tg is the major determinant of the properties of LDL particles. The clinical implication is that in NIDDM serum Tg should be as low as possible to prevent atherogenic changes in LDL.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400677
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  • 6
    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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  • 7
    Electronic Resource
    Electronic Resource
    Scandinavian society for the study of diabetes Abstracts Seventh Meeting (1971)
    Springer
    Diabetologia 7 (1971), S. 395-404 
    Details
    ISSN: 1432-0428
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01219478
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  • 8
    Electronic Resource
    Electronic Resource
    Insulin resistance and abnormal albumin excretion in non-diabetic first-degree relatives of patients with NIDDM (1995)
    Springer
    Diabetologia 38 (1995), S. 363-369 
    Details
    ISSN: 1432-0428
    Keywords: Key words Microalbuminuria ; insulin resistance syndrome ; insulin sensitivity ; euglycaemic hyperinsulinaemic clamp.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Microalbuminuria has recently been associated with insulin resistance in both insulin-dependent and non-insulin-dependent (NIDDM) diabetes mellitus. To establish whether microalbuminuria in non-diabetic subjects as well is associated with insulin resistance and associated abnormalities in glucose and lipid metabolism, oral glucose tolerance tests were performed with measurement of urinary albumin excretion rate, lipids and lipoproteins in 582 male non-diabetic first-degree relatives of patients with NIDDM. In addition, insulin sensitivity was assessed in 20 of these subjects with the euglycaemic hyperinsulinaemic clamp technique. Abnormal albumin excretion rate (AER), defined as AER 15–200 μg/min, was associated with higher systolic blood pressure (p 〈 0.05), higher fasting glucose values (p 〈 0.05), lower HDL-cholesterol (p 〈 0.05) and lower apolipoprotein A-I (p 〈 0.05) concentrations than observed in subjects with normal AER. The rate of glucose metabolism was lower in subjects with abnormal compared to subjects with normal albumin excretion rate (38.0 ± 2.8 vs 47.3 ± 2.4 μmol · kg lean body mass–1· min–1; p = 0.028). This difference was almost completely accounted for by a reduction in non-oxidative glucose metabolism (17.7 ± 1.9 vs 27.4 ± 2.7 μmol · kg lean body mass–1· min–1; p = 0.010), which correlated inversely with the AER (r = –0.543; p = 0.013). These results suggest that in non-diabetic individuals genetically predisposed to NIDDM, abnormal AER is associated with insulin resistance and abnormalities in glucose and lipid metabolism. [Diabetologia (1995) 38: 363 –369]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400643
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  • 9
    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
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  • 10
    Electronic Resource
    Electronic Resource
    Fourth meeting of the Scandinavian Society for the Study of Diabetes Stockholm, February 1–3, 1968 Abstracts (1968)
    Springer
    Diabetologia 4 (1968), S. 309-315 
    Details
    ISSN: 1432-0428
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01309907
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