Comparative effects of rosiglitazone and pioglitazone on fasting and postprandial low-density lipoprotein size and subclasses in patients with Type 2 diabetes.

OBJECTIVE: To assess the effects of pioglitazone and rosiglitazone on fasting and postprandial low-density lipoprotein (LDL) size and subclasses in patients with Type 2 diabetes. RESEARCH DESIGN AND METHODS: Nine Type 2 diabetic patients (age 61 +/- 10 years, body mass index 30 +/- 5 kg/m(2), glycosylated hemoglobin [HbA1c] 7.5 +/- 0.5%) were randomized in a crossover trial to rosiglitazone 4 mg b.i.d. or pioglitazone 45 mg/day for 12 weeks with an 8-week wash-out period. LDL size and subclasses were determined by non-denaturing polyacrylamide gradient gel electrophoresis. A standardized breakfast was served and variables were assessed after 3 and 6 h. RESULTS: HbA1c, insulin sensitivity (as assessed by the homeostasis model assessment) and LDL size and subclasses did not differ before treatments. Rosiglitazone and pioglitazone resulted in a similar improvement in HbA1c and insulin sensitivity. Fasting total cholesterol increased more after rosiglitazone compared with pioglitazone (p = 0.04), whereas triglycerides decreased after pioglitazone and increased after rosiglitazone (p = 0.004). Fasting LDL size similarly increased after both treatments, mainly due to increased LDL-I particles. Pioglitazone resulted in a more prominent LDL-IIA subfraction compared with rosiglitazone (p = 0.03). After 3 h, pioglitazone lead to increased LDL-IIB (p = 0.01) and decreased LDL-IVB (p = 0.05), however, after 6 h no significant changes were found. CONCLUSIONS: Pioglitazone was more effective than rosiglitazone in increasing larger LDL concentrations (in both fasting and postprandial status) as well as in reducing levels of atherogenic small, dense particles (in postprandial status only). Whether or not these findings differentially affect the atherogenic process and the clinical endpoints such as cardiovascular events remains to be determined.

Differential effect of pioglitazone (PGZ) and rosiglitazone (RGZ) on postprandial glucose and lipid metabolism in patients with type 2 diabetes mellitus: a prospective, randomized crossover study.

BACKGROUND: Postprandial metabolism is impaired in patients with type 2 diabetes (T2Dm). Two thiazolidinediones pioglitazone (PGZ) and rosiglitazone (RGZ) have similar effects on glycaemic control but differ in their effects on fasting lipids. This study investigated the effects of RGZ and PGZ on postprandial metabolism in a prospective, randomized crossover trial. METHODS: Seventeen patients with T2Dm were randomized to RGZ or PGZ for 12 weeks, with an 8-week wash-out period. Fasting blood samples were taken for glucose (FPG), insulin, HbA(1c), lipids, apolipoproteins (apo), lipoprotein (LPL) and hepatic lipase (HL), and cholesterol ester transfer protein (CETP) activity. A standardized breakfast was served and postprandial glucose, insulin, and lipid subfraction profiles were determined. RESULTS: RGZ and PGZ treatment resulted in a similar improvement in FPG, HbA(1c) and homeostasis model assessment. Fasting and postprandial triglyceride (TG) levels were significantly lower following PGZ therapy (fasting: -0.35 vs 0.44 mmol/L; p < 0.04; postprandial AUC-TG: -195.6 vs 127.9 mmol/L/min; p < 0.02) associated with changes in VLDL-2-TG (-0.10 vs 0.21 mmol/L; p = 0.23) and VLDL-3-TG (0.0 vs 0.34 mmol/L; p < 0.04). Fasting cholesterol increased with RGZ compared to PGZ (0.06 vs 0.59 mmol/L; p < 0.04), particularly in VLDL-2-C (-0.30 vs 0.59 mmol/L; p < 0.03) and VLDL-3-C (-0.85 vs 2.11 mmol/L; p < 0.02). Postprandial VLDL lipid and protein content increased after RGZ and decreased after PGZ. Fasting apoB, apoA-I, apoC-II/C-III-ratio, and LPL activity did not differ. CETP activity decreased after RGZ and increased after PGZ (-6.2 vs 4.2 p/mol/mL/min; p < 0.002). CONCLUSIONS: Both the glitazones had similar effects on glucose metabolism. The additional beneficial effect of PGZ on lipid metabolism may be related to its effects on insulin-independent VLDL production and CETP activity.

Mansonella perstans causing symptomatic hypereosinophilia in a missionary family.

Mansonella perstans is rarely pathogenic. The rare reports of symptomatic cases, however, include severe complications. Three cases of symptomatic hypereosinophilia with multi-organ involvement are described in a missionary family returning from tropical Africa. Pathogenicity may be related to the induction of hypereosinophilia rather than direct host-parasite interactions.