The PPARα/γ Agonist, Tesaglitazar, Improves Insulin Mediated Switching of Tissue Glucose and Free Fatty Acid Utilization In Vivo in the Obese Zucker Rat

Table 3

Insulin infusion rates, steady state plasma insulin and glucose levels, and GIRs needed to maintain isoglycemia during the clamps used in Study 2.

Group	Insulin infusion	Insulin	Glucose	GIR
Body weight (g)	(pmol/kglbm/min)	(nM)	(mM)	(µmol/min/kg)
Lean 396±13
Basal	0	0.3±0.1	6.7±0.3	0
ClampL	30	1.1±0.1	6.5±0.4	77.3±6.8
ClampH	300	22.3±3.2	6.5±0.2	152.7±10.9
Obese 583±21^∗∗∗
Basal	0	6.2±1.1^∗∗∗	9.8±0.4^∗∗∗	0
ClampL	120	11.4±1.2^∗∗∗	10.0±0.3^∗∗∗	28.3±5.7^∗∗∗
ClampH	1200	125±24^∗∗	9.7±1.8	41.2±13.9^∗∗∗
Tesaglitazar 654±13^†
Basal	0	0.6±0.1^†††	8.8±0.4	0
ClampL	60	2.1±0.1^†††	8.7±0.4^†	105.4±5.8^†††
ClampM	210	10.0±0.8	9.5±0.6	142.6±9.6^†††
ClampH	600	47.1±9.1^††	9.8±1.1	150.5±10.9^†††

ClampL performed at a physiological (postprandial) level of hyperinsulinemia, ClampH at supraphysiological insulin levels, ClampM (Tesaglitazar group only) designed to achieve plateau insulin levels corresponding to those in Obese ClampL group. Results are expressed as mean ± SE (𝑛 = 5–7). ^∗∗𝑃<0.01, and ^∗∗∗𝑃<0.001 versus corresponding state of Lean. ^†𝑃<0.05, ^††𝑃<0.01, and ^†††𝑃<0.001 versus corresponding state of Obese.