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Diabetes and Vascular Disease Research
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Improvement of postprandial lipid handling and glucose tolerance in a non-diabetic population by the dual PPAR{alpha}/{gamma} agonist, tesaglitazar

Bjorn Fagerberg

Wallenberg Laboratory for Cardiovascular Research, Sahlgrenska University Hospital, 41345 Göteborg, Sweden.

Herbert Schuster

Humboldt University, Berlin, Germany.

Grethe Støa Birketvedt

University Hospital, Tromso, Norway.

Serena Tonstad

Ullevål University Hospital, Oslo, Norway.

Karl Peter Öhman

AstraZeneca, Wilmington, DE, US.

Ingrid Gause-Nilsson

AstraZeneca R&D, Mölndal, Sweden.

This study examined the effect of tesaglitazar (GALIDATM), a dual peroxisome proliferator-activated receptor (PPAR){alpha}/{gamma} agonist, on postprandial metabolism.

This investigation was part of the Study in Insulin Resistance (SIR) (SH-SBT-0001), a randomised, double-blind, placebo-controlled study that reported improvements in fasting lipid and glucose values with tesaglitazar (0.1, 0.25, 0.5 or 1 mg once daily for 12 weeks) in hypertriglyceridaemic, abdominally obese, non-diabetic patients. A subgroup of 222 patients underwent postprandial lipid and glucose testing at baseline and treatment end.

Tesaglitazar 0.25, 0.5 and 1 mg reduced postprandial area under the curve (AUC) for triglycerides by 20% (p=0.003), 30% (p<0.0001) and 41% (p<0.0001), respectively. Free fatty acid (FFA) levels were reduced by 17% with tesaglitazar 0.5 mg (p=0.002) and by 29% with tesaglitazar 1 mg (p<0.0001). Tesaglitazar significantly improved glucose tolerance and increased the proportion of patients with normal glucose tolerance as measured by the oral glucose tolerance test (OGTT).

To conclude, postprandial dyslipidaemia and hyper-glycaemia, indicators of increased vascular risk, were significantly improved by tesaglitazar treatment in these non-diabetic, hypertriglyceridaemic, abdominally obese subjects.

Key Words: dyslipidaemia • insulin resistance • peroxisome proliferator-activated receptor • postprandial • tesaglitazar

Diabetes and Vascular Disease Research, Vol. 4, No. 3, 174-180 (2007)
DOI: 10.3132/dvdr.2007.038


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