Very low density lipoprotein subfraction abnormalities in IDDM patients: any effect of blood glucose control?

Patti, L.; Marino, L.; Maffettone, Ada; Romano, G.; Annuzzi, Giovanni; Riccardi, Gabriele; Rivellese, Angela Albarosa

doi:10.1007/bf00400602

Cited by 14 publications

(13 citation statements)

References 28 publications

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“…Furthermore, insulin therapy induces a significant reduction of HL activity. The relative enrichment in small VLDL and decrease in HL activity observed in NIDDM during insulin treatment closely resembles the metabolic picture described in IDDM patients (18,25), thus supporting the hypothesis that the abnormal VLDL subfraction distribution in IDDM patients is an effect of subcutaneous insulin administration mediated by a reduced activity of HL.…”

Section: Discussionsupporting

confidence: 52%

“…In fact, in these conditions, there is no increase in the absolute lipid concentration of these particles. However, if an optimal blood glucose control is not reached with insulin therapy, an increase in the absolute amount of small VLDL accompanies their percentage increase, as shown in IDDM patients with unsatisfactory blood glucose control (25). Of course, the absolute increase in small VLDL could have clinical relevance, especially as a possible atherogenic risk factor.…”

Section: Discussionmentioning

confidence: 96%

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Insulin and Sulfonylurea Therapy in NIDDM Patients: Are the Effects on Lipoprotein Metabolism Different Even With Similar Blood Glucose Control?

et al. 1997

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This study evaluates the effects of insulin versus glibenclamide on lipoprotein metabolism at comparable levels of blood glucose control, in particular on the concentration and distribution of VLDL subfractions and lipolytic enzyme activities in nine NIDDM men (aged 56 +/- 3 years, BMI 26.5 +/- 0.9 kg/m2) (means +/- SE) participating in a crossover study. After a 3-week washout period, patients were randomly assigned to 2-month treatment periods (insulin or glibenclamide); thereafter, each patient crossed to the other treatment. At the end of each period, mean daily blood glucose (MDBG), HbA1e, plasma lipids, lipoproteins (VLDL, LDL, HDL), lipoprotein subfractions (VLDL1, 2, 3; HDL2, HDL3), and post-heparin lipase activities (lipoprotein lipase [LPL], hepatic lipase [HL]) were evaluated. Although glucose control was similar at the end of both periods (MDBG 8.3 +/- 0.3 vs. 7.9 +/- 0.3 mmol/l; HbA1c 7.4 +/- 0.3 vs. 7.0 +/- 0.2%, insulin versus glibenclamide), insulin compared with glibenclamide induced a significant reduction in plasma triglycerides (0.9 +/- 0.1 vs. 1.1 +/- 0.1 mmol/l, P < 0.05), VLDL triglycerides (50.1 +/- 12.2 vs. 63.6 +/- 12.3 mg/dl, P < 0.02), VLDL1 lipid concentration (24.9 +/- 7.5 vs. 39.9 +/- 9.5 mg/dl, P < 0.006), and increased HDL2 cholesterol (25.2 +/- 1.6 vs. 20.3 +/- 1.3 mg/dl, P < 0.03). In terms of VLDL percentage subfraction distribution, with insulin, there was a decrease in the larger subfractions (VLDL1 26.5 +/- 3.0 vs. 37.8 +/- 3.4%, P < 0.02) and an increase in the smallest (VLDL3 47.3 +/- 3.8 vs. 37.3 +/- 3.3%, P < 0.05). Moreover, HL activity was significantly lower after insulin than after glibenclamide (HL 247.2 +/- 22.3 vs. 263.5 +/- 22.6 mU/ml, P < 0.05). In conclusion, compared with glibenclamide, insulin treatment (independent of variations in glucose control) is able to decrease significantly plasma triglycerides, to increase HDL2 cholesterol, and to reduce only the concentration of the larger VLDL subfractions, with a consequent redistribution of their profile.

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Section: Discussionsupporting

confidence: 52%

Section: Discussionmentioning

confidence: 96%

Insulin and Sulfonylurea Therapy in NIDDM Patients: Are the Effects on Lipoprotein Metabolism Different Even With Similar Blood Glucose Control?

et al. 1997

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“…The differences were most apparent between patients with intermediate and poor glycaemic control. Earlier studies in patients with normal AER have been limited by rather small numbers of patients and have only reported effects of glycaemic control on HDL-and VLDL-cholesterol [25]. Total cholesterol, LDL-and HDL-cholesterol, triacylglycerol and ApoB were independently associated with HbA 1c in studies including patients with various degrees of kidney disease [26,27].…”

Section: Discussionmentioning

confidence: 99%

Relationship between lipid profiles and kidney function in patients with type 1 diabetes

et al. 2007

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Aims/hypothesis We studied the relationship between the lipid profile, estimated GFR (eGFR) and AER in patients with type 1 diabetes. We also assessed the association between the lipid profile and glycaemic control, obesity and hypertension in an environment free of manifest renal disease, as well as exploring how well the patients would have achieved the targets set in international guidelines. Methods A total of 2,927 adult patients who had type 1 diabetes and for whom lipid profiles were available were included from people participating in the nationwide, multicentre Finnish Diabetic Nephropathy Study (FinnDiane). eGFR was determined using the Cockcroft-Gault formula adjusted for body surface area. Results Patients with impaired renal function (eGFR <60 ml min −1 1.73 m −2 ) had higher total cholesterol, triacylglycerol and apolipoprotein B, and lower HDLcholesterol concentrations than patients with normal renal function (eGFR >90 ml min −1 1.73 m −2 ) or mildly impaired renal function (eGFR 60-90 ml min −1

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“…This suggests that other mechanisms could be involved in the way dietary cholesterol affects cardiovascular mortality, such as alterations in the concentration of lipoprotein subclasses or in their composition. Results from animal studies support this suggestion: in rabbits, for instance, dietary cholesterol has been shown to increase small very low density lipoprotein (VLDL) particles [11,12], which are considered to be more atherogenic than large VLDL particles [13] and which are already increased in IDDM patients (even normolipidaemic) [14,15]. The awareness of the effects of dietary cholesterol on lipid metabolism in IDDM patients ± who are also characterized by other subtle abnormalities [16] ± is important if proper dietary advice is to be given to them, especially considering that the aspect of cholesterol intake is generally neglected in clinical practice.…”

Section: ó Springer-verlag 1998mentioning

confidence: 97%

Effects of dietary cholesterol on plasma lipoproteins and their subclasses in IDDM patients

et al. 1998

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Clinical studies have shown that a high cholesterol intake increases the levels of plasma and low density lipoprotein (LDL) cholesterol, even when dietary fat is kept constant [1]. The elevation of LDL cholesterol level is highly variable (4±58 %) [1,2] and this may depend on different factors, such as the type of fat utilized in the diet, dietary cholesterol absorption efficiency, ability to reduce endogenous cholesterol synthesis, regulation of the synthesis of bile acids, amount of intracellular cholesterol, genetic background [1±6].Despite the large number of studies on healthy or hyperlipidaemic individuals [1±7], no data is available Diabetologia (1998) Summary To compare the effects of dietary cholesterol supplementation in insulin-dependent diabetic (IDDM) patients and normal subjects, 10 male IDDM patients in good glycaemic control (HbA 1 c 7.3 ± 0.9 %) (mean ± SD) and normal plasma lipid levels, and 11 control male subjects of similar age, body mass index and lipid plasma levels underwent a double blind, cross-over, sequential study. Cholesterol supplementation of 800 mg/day or placebo were given for consecutive periods of 3 weeks. The concentration of plasma total cholesterol increased significantly with the dietary cholesterol supplementation compared to placebo in IDDM patients by 6 % (p < 0.05) and in control subjects by 9 % (p < 0.05). No changes were observed in the concentration of plasma triglycerides in either group. The LDL cholesterol level increased by 12 % (p < 0.01) in patients and by 7 % (p < 0.05) in control subjects. In patients plasma HDL cholesterol concentration remained the same, while in control subjects it tended to increase after cholesterol supplementation (from 1.14 ± 0.26 to 1.23 ± 0.27 mmol/l, p = 0.06). During the cholesterol intake period the mean concentration of LDL1, LDL2 and LDL3 subclasses in patients showed a significant increase by 21.0 (p < 0.05), 20.4 (p < 0.001) and 11.1 % (p < 0.05), respectively, resulting in an 18.0 % increase in mean total LDL mass (p < 0.001) without major changes in LDL composition. In the control subjects the changes in the concentrations of LDL subclasses during cholesterol intake were less and not significant. In the IDDM patients the cholesterol intake did not affect the concentration or composition of HDL subclasses or total HDL mass. In contrast, in control subjects cholesterol intake increased the mean concentration of HDL2 a by 12.2.% (p < 0.05) and this increase was significantly different if compared to changes obtained in the patients. In conclusion, compared to normal subjects, in IDDM patients, dietary cholesterol intake increased the LDL particle mass significantly and had no positive effect on HDL. [Diabetologia (1998)

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Very low density lipoprotein subfraction abnormalities in IDDM patients: any effect of blood glucose control?

Cited by 14 publications

References 28 publications

Insulin and Sulfonylurea Therapy in NIDDM Patients: Are the Effects on Lipoprotein Metabolism Different Even With Similar Blood Glucose Control?

Insulin and Sulfonylurea Therapy in NIDDM Patients: Are the Effects on Lipoprotein Metabolism Different Even With Similar Blood Glucose Control?

Relationship between lipid profiles and kidney function in patients with type 1 diabetes

Effects of dietary cholesterol on plasma lipoproteins and their subclasses in IDDM patients

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