Effect of Metformin on Postprandial Lipemia in Patients With Fairly to Poorly Controlled NIDDM

Jeppesen, Jørgen; Zhou, Mingyue; Chen, Y-D. Ida; Reaven, Gerald M.

doi:10.2337/diacare.17.10.1093

Cited by 116 publications

(76 citation statements)

References 22 publications

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“…First of all, metformin lowers blood glucose levels [20]. Next, it improves lipid profiles in type 2 diabetic patients, whether it is used with a sulphonylurea or not [20,21,22,23,24,25]. In fact, in the present study, HbA 1 c levels in the glibenclamide plus metformin group significantly improved during the observation period.…”

Section: Discussionsupporting

confidence: 45%

Metformin or gliclazide, rather than glibenclamide, attenuate progression of carotid intima-media thickness in subjects with type 2 diabetes

et al. 2004

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Aim/hypothesis. Metformin is a well-known oral hypoglycaemic agent and has been commonly used, in combination with sulphonylurea, to treat type 2 diabetes. However, the advantageous effect of metformin plus sulphonylurea on diabetic macroangiopathy has yet to be clarified. To evaluate whether sulphonylurea or sulphonylurea plus metformin prevent diabetic macroangiopathy, we examined the progression of carotid artery intima-media thickness (IMT) as a surrogate end point. Methods. Subjects with type 2 diabetes were divided into three groups, receiving the following treatments: (i) glibenclamide (n=59); (ii) gliclazide (n=30); and (iii) glibenclamide + metformin (n=29). Maximum IMT and average IMT (the greatest value among 6 average values of each 3 points including greatest thickness) were measured at the beginning and end of the observation period. Results. For the follow-up period of 3 years, the annual change in average IMT of the glibenclamide plus metformin group (0.003±0.048 mm) was smaller than that of the glibenclamide group (0.064±0.045 mm) and gliclazide group (0.032±0.036 mm) (p<0.0001 and p=0.043 respectively). In the gliclazide group, average IMT increased during the follow-up period, but annual change in average IMT was significantly smaller than that of the glibenclamide group (p=0.005). Glibenclamide + metformin or gliclazide also attenuated the progression of maximum IMT, compared with that of glibenclamide (0.041±0.105, 0.044±0.106, 0.114±0.131 mm/year respectively, p=0.029 and p=0.035 respectively). Multivariable regression analysis implied that administration of metformin or gliclazide significantly and independently (p<0.05) reduces the progression of average IMT, compared with glibenclamide monotherapy. Conclusions/interpretation. These data indicate that metformin or gliclazide, rather than glibenclamide, have a potent anti-atherogenic effect in type 2 diabetes.

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Section: Discussionsupporting

confidence: 45%

Metformin or gliclazide, rather than glibenclamide, attenuate progression of carotid intima-media thickness in subjects with type 2 diabetes

et al. 2004

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“…Thiazolidinediones have been reported to exert beneficial effects on postprandial TG metabolism [17][18][19][20], but these are unlikely to be mediated by reduced NEFA flux to the liver, a mechanism that is largely independent of improved glycaemia. Both metformin [21,22] and glipizide [23] can improve postprandial lipaemia in poorly controlled patients with type 2 diabetes. This may be secondary to improved glycaemic control and reduced insulin resistance.…”

Section: Discussionmentioning

confidence: 99%

Vildagliptin therapy reduces postprandial intestinal triglyceride-rich lipoprotein particles in patients with type 2 diabetes

et al. 2006

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Aims/hypothesis We assessed the effects of vildagliptin, a novel dipeptidyl peptidase IV inhibitor, on postprandial lipid and lipoprotein metabolism in patients with type 2 diabetes. Subjects, materials and methods This was a single-centre, randomised, double-blind study in drug-naive patients with type 2 diabetes. Patients received vildagliptin (50 mg twice daily, n=15) or placebo (n=16) for 4 weeks. Triglyceride, cholesterol, lipoprotein, glucose, insulin, glucagon and glucagon-like peptide-1 (GLP-1) responses to a fat-rich mixed meal were determined for 8 h postprandially before and after 4 weeks of treatment. Results Relative to placebo, 4 weeks of treatment with vildagliptin decreased the AUC 0-8h for total trigyceride by 22±11% (p=0.037), the incremental AUC 0-8h for total triglyceride by 85±47% (p=0.065), the AUC 0-8h for chylomicron triglyceride by 65±19% (p=0.001) and the IAUC 0-8h for chylomicron triglyceride by 91±28% (p=0.002). This was associated with a decrease in chylomicron apolipoprotein B-48 (AUC 0-8h , −1.0±0.5 mg l −1 h, p=0.037) and chylomicron cholesterol (AUC 0-8h , −0.14± 0.07 mmol l −1 h, p=0.046). Consistent with previous studies, 4 weeks of treatment with vildagliptin also increased intact GLP-1, suppressed inappropriate glucagon secretion, decreased fasting and postprandial glucose, and decreased HbA 1c from a baseline of 6.7% (change, −0.4±0.1%, p<0.001), all relative to placebo. Conclusions/interpretation Treatment with vildagliptin for 4 weeks improves postprandial plasma triglyceride and apolipoprotein B-48-containing triglyceride-rich lipoprotein particle metabolism after a fat-rich meal. The mechanisms underlying the effects of this dipeptidyl peptidase IV inhibitor on postprandial lipid metabolism remain to be explored.

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“…Venous blood was used for measurement of plasma cholesterol, triglyceride, and HDL cholesterol concentrations. 10 Plasma glucose 11 and insulin 12 concentrations were determined before and 30, 60, 90, 120, and 180 minutes after oral administration of 75 g glucose. The total integrated area of the plasma concentrations during this 180-minute period was used to quantify plasma glucose and insulin responses.…”

Section: Methodsmentioning

confidence: 99%

Relationship Between Insulin Resistance and Partially Oxidized LDL Particles in Healthy, Nondiabetic Volunteers

Carantoni

Abbasi

Warmerdam

et al. 1998

ATVB

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Abstract-This study was performed in 36 healthy volunteers to define the relationship between plasma concentrations of partially oxidized low density lipoprotein (poxLDL), plasma glucose and insulin responses to oral glucose, and steady-state plasma glucose (SSPG) concentrations after a 180-minute infusion of somatostatin, insulin, and glucose. The concentration of poxLDL was estimated by determining the amount of conjugated dienes formed during in vitro LDL oxidation in the presence or absence of alanine. Under these conditions, the greater the in vitro antioxidant effect of alanine, the lower the amount of poxLDL that was present in plasma. Key Words: oxidized LDL Ⅲ insulin resistance Ⅲ cardiovascular disease risk factors P revious reports from our laboratory have emphasized the potential link between insulin resistance, a cluster of associated abnormalities, and atherosclerosis in nondiabetic subjects.1,2 An important component of the metabolic abnormalities associated with insulin resistance is a change in LDL particle diameter, leading to the presence of smaller and denser LDL particles.3 Given the fact that such particles are more easily oxidized, 4 it seemed to be of great interest to know whether there were any associations between insulin resistance and the oxidative states of circulating LDL. Approaching this problem is complicated by the fact that oxLDL has been detected in the arterial wall, but not in the circulation.5 LDL oxidation has usually been assessed by determining the formation of thiobarbituric acid-reactive compounds or by the lag time for conjugated-diene formation during copper oxidation-methods that do not permit determination of the oxidized state of LDL present in the circulation. 6 In an effort to overcome this problem, Picard et al 7 have described a sensitive and reproducible method to quantify the oxidized state of LDL present in the circulation on the basis of the antioxidant properties of alanine. This effect of alanine depends on the amount of peroxides present in LDL and the fact that the greater the amount of peroxides in LDL, the less the antioxidant effect of alanine. Thus, by quantifying the antioxidant effect of alanine on isolated LDL, it is possible to gain an estimate of the amount of poxLDL that is present in the circulation. Picard et al 7 used this method to show that LDL oxidation was increased in patients with type 2 diabetes who had evidence of atherosclerosis but absent in diabetic subjects with no apparent vascular disease. Since there is increasing evidence 1,2,8 that insulin resistance or compensatory hyperinsulinemia is associated with a variety of CHD risk factors, we initiated the current study to see whether there was any relationship between the resistance of insulinmediated glucose disposal or the metabolic variables associated with insulin resistance and the amount of poxLDL in nondiabetic volunteers, all of whom were in general good health. MethodsThe study population consisted of 36 healthy volunteers, 14 men and 22 women, who responded to a newspap...

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Effect of Metformin on Postprandial Lipemia in Patients With Fairly to Poorly Controlled NIDDM

Cited by 116 publications

References 22 publications

Metformin or gliclazide, rather than glibenclamide, attenuate progression of carotid intima-media thickness in subjects with type 2 diabetes

Metformin or gliclazide, rather than glibenclamide, attenuate progression of carotid intima-media thickness in subjects with type 2 diabetes

Vildagliptin therapy reduces postprandial intestinal triglyceride-rich lipoprotein particles in patients with type 2 diabetes

Relationship Between Insulin Resistance and Partially Oxidized LDL Particles in Healthy, Nondiabetic Volunteers

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