Key result
Pioglitazone lowers fasting and postprandial triglycerides compared to rosiglitazone despite similar glycemic control.
Why the study?
Postprandial metabolism is impaired in patients with type 2 diabetes, and pioglitazone and rosiglitazone differ in their effects on fasting lipids, but their comparative effects on postprandial metabolism were unclear.
Does pioglitazone improve postprandial glucose and lipid metabolism compared to rosiglitazone in patients with type 2 diabetes mellitus?
RCT (n=17)
Crossover
Does pioglitazone improve postprandial glucose and lipid metabolism compared to rosiglitazone in patients with type 2 diabetes mellitus?
Absolute Event Rate: -0.35% vs 0.44%
p-value: p=<0.04
While pioglitazone and rosiglitazone have similar effects on glycemic control, pioglitazone demonstrates a more favorable effect on fasting and postprandial lipid metabolism, particularly in reducing triglycerides.
Supports preferring pioglitazone to rosiglitazone for postprandial lipid control in T2DM; extends class differences in TZD metabolic effects.
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.
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Chappuis et al. (2007) conducted an RCT in Type 2 diabetes mellitus (n=17). Pioglitazone vs. Rosiglitazone was evaluated on Change in fasting triglyceride levels (mmol/L) (p=<0.04). Pioglitazone significantly lowered fasting triglycerides (-0.35 vs 0.44 mmol/L; P<0.04) and postprandial AUC-TG compared to rosiglitazone, despite similar improvements in glycemic control.
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