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  • 11
    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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  • 12
    Electronic Resource
    Electronic Resource
    Differences in HDL-cholesterol:apoA-I + apoA-II ratio and apoE phenotype with albuminuric status in Type I diabetic patients (2000)
    Springer
    Diabetologia 43 (2000), S. 1353-1359 
    Details
    ISSN: 1432-0428
    Keywords: Keywords HDL-cholesterol, apolipoprotein E phenotype, ɛ2 allele, apolipoproteins, albuminuria, Type I diabetes, apolipoprotein A-I, apolipoprotein A-II, diabetic nephropathy, progression.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Aims/hypothesis. To examine whether the HDL-cholesterol:apoA-I + apoA-II ratio and the ɛ2 allele are related to albuminuria at baseline and whether they are risk factors for progression of albuminuria in a cohort study of patients with Type I (insulin-dependent) diabetes mellitus.¶Methods. At baseline, the study cohort comprised 617 patients, aged 15–60 years, from seven European diabetic centres of the EURODIAB study. Albumin excretion rate, measured in a central laboratory, was categorised as normoalbuminuria at 20 μg/min or less, microalbuminuria between 20 and 200 μg/min or macroalbuminuria at 200 μg/min or over. Of the 250 patients who were normoalbuminuric at baseline and had follow-up albuminuria measurements, 34 patients were defined as early progressors.¶Results. At baseline, the mean HDL-cholesterol:apoA-I + apoA-II ratio was lower in macroalbuminuric patients (0.79, 95 % CI:0.74–0.83) compared with normoalbuminuric (0.88, 95 % CI:0.87–0.90) patients (p = 0.0002, adjusted for age and sex). At follow-up, 34 patients who progressed from normoalbuminuria to microalbuminuria or macroalbuminuria also had a slightly lower baseline ratio (0.85, 95 % CI:0.80–0.89) than those 216 who remained normoalbuminuric (0.89, 95 % CI:0.87–0.92) (adjusted p = 0.08). Neither of these relations were independent of LDL-cholesterol or fasting triglyceride. There was no association of the ɛ2 allele with albuminuria either at baseline (OR = 1.4, 95 % CI:0.7–2.8) or with progression of albuminuria (OR = 0.4, 95 % CI:0.1–3.5).¶Conclusion/interpretation. There is an inverse relation of HDL-cholesterol:apoA-I + apoA-II ratio with albuminuria at baseline. This lower ratio in microalbuminuric or macroalbuminuric patients could contribute to the increased risk of cardiovascular disease associated with nephropathy. There is weak evidence that HDL-composition is a risk factor for progression of albuminuria and no association of the ɛ2 allele with diabetic nephropathy. [Diabetologia 2000 43: 1353–1359]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250051538
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  • 13
    Electronic Resource
    Electronic Resource
    Lipoprotein lipase activity and serum lipoproteins in untreated Type 2 (insulin-independent) diabetes associated with obesity (1982)
    Springer
    Diabetologia 22 (1982), S. 46-50 
    Details
    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
    URL: http://dx.doi.org/10.1007/BF00253869
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  • 14
    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: 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. [Diabetologia (1996) 39: 453–461]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400677
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  • 15
    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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  • 16
    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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  • 17
    Electronic Resource
    Electronic Resource
    Lowering of triglycerides by gemfibrozil affects neither the glucoregulatory nor antilipolytic effect of insulin in Type 2 (non-insulin-dependent) diabetic patients (1993)
    Springer
    Diabetologia 36 (1993), S. 161-169 
    Details
    ISSN: 1432-0428
    Keywords: Triglycerides ; gemfibrozil ; insulin resistance ; Type 2 (non-insulin-dependent) diabetes mellitus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Hypertriglyceridaemia and insulin resistance are closely associated but it is unknown whether hypertriglyceridaemia per se contributes to insulin resistance. In the present study we examined whether gemfibrozil, by lowering triglyceride levels, improves the glucoregulatory and antilipolytic action of insulin in Type 2 (non-insulin-dependent) diabetes mellitus. Twenty patients were randomly allocated to receive either placebo or gemfibrozil 1200 mg daily for 12 weeks in a double-blind study. Very low density lipoprotein triglyceride levels decreased in the gemfibrozil group by 42±12% (p〈0.01). Gemfibrozil had no effect on the diurnal concentration of non-esterified fatty acids (NEFA). At the randomization HbA1c levels were comparable (7.6±0.3 vs 7.8±0.2%, NS) and increased slightly both in the gemfibrozil (8.2±0.4%, p〈0.05) and placebo groups (8.0±0.3%, NS). Pre- and post-treatment diurnal glucose and insulin concentrations remained unchanged. Basal pre- and post-treatment hepatic glucose production rates were comparable in both groups and similarly suppressed by insulin. Rate of whole body glucose disposal during a low-dose insulin infusion (serum insulin ∼90 pmol/l) (pre- vs post-gemfibrozil 11.9±1.1 vs 11.1±0.7, pre- vs post-placebo 9.9±1.1 vs 10.8±0.8 μmol·kg−1·min−1, NS for both) and a high-dose insulin infusion (serum insulin ∼500 pmol/l) (16.2+-1.7 vs 17.7±2.7, 17.1±4.2 vs 17.4±2.9 μmol·kg−1·min−1, respectively, NS for both) remained unchanged. Basal pre- and post-treatment NEFA turnover rates were comparable in both groups and similarly suppressed by insulin. Also rates of total lipid oxidation, plasma NEFA oxidation and non-oxidative NEFA metabolism remained unchanged in both groups. We conclude that gemfibrozil effectively lowers serum triglycerides but has no effect on insulin sensitivity of glucose and NEFA metabolism. The data suggest that hypertriglyceridaemia is a consequence rather than a cause of insulin resistance in Type 2 diabetic patients.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400699
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  • 18
    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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  • 19
    Electronic Resource
    Electronic Resource
    Changes of lipolytic enzymes cluster with insulin resistance syndrome (1995)
    Springer
    Diabetologia 38 (1995), S. 344-350 
    Details
    ISSN: 1432-0428
    Keywords: Insulin resistance ; lipase activities ; lipoproteins
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The activities of hepatic and lipoprotein lipase and the levels of lipo- and apoproteins were compared in two groups of normoglycaemic men representing the highest (n=18) and lowest (n=15) fasting insulin quintiles of first degree male relatives of non-insulin-dependent diabetic patients. The high insulin group representing insulin-resistant individuals had significantly lower post-heparin plasma lipoprotein lipase activity than the low insulin group (14.2±4.0 vs 20±5.8 Μmol NEFA·ml−1·h−1, p〈0.001); hepatic lipase activity did not differ between the two groups (24.2±11 vs 18.0±5.3 Μmol NEFA·ml−1·h−1, NS). The lipoprotein lipase/hepatic lipase ratio in the high insulin group was decreased by 66% as compared to the low insulin group (0.75±0.57 vs 1.25±0.65, p〈0.01). In the high insulin group both total and VLDL triglycerides were higher than in the low insulin group (1.61±0.57 vs 0.86±0.26 mmol/l, p〈 0.001 and 1.00±0.47 vs 0.36±0.16 mmol/l, p〈0.001, respectively) whereas HDL cholesterol and HDL2 cholesterol were lower (1.20±0.30 vs 1.43±0.22 mmol/l, p〈0.05 and 0.49±0.21 vs 0.71±0.17 mmol/l, p〈0.05, respectively). Total cholesterol, LDL cholesterol or HDL3 cholesterol did not differ between the two groups. The mean particle size of LDL was smaller in the high insulin group than in the low insulin group (258±7 vs 265±6 å, p〈0.05). We propose that the changes of lipoprotein lipase and lipoprotein lipase/hepatic lipase ratio cluster with insulin resistance and provide a possible mechanism to explain the lowering of HDL cholesterol and elevation of triglyceride concentrations observed in insulin-resistant subjects.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400640
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  • 20
    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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