The peroxisome proliferator-activated receptor gamma (PPARγ) agonist thiazolidinedione (TZD) does not overcome trans-10, cis-12 conjugated linoleic acid (CLA) inhibition of milk fat synthesis in lactating dairy ewes

Abstract Text: Peroxisome proliferator-activated receptor gamma (PPARγ) is regulated by ligand activation and regulates lipid synthesis pathways, but a functional role for PPARγ in diet-induced MFD in vivo has not been established. This study evaluated the effect of PPARγ agonist thiazolidinedione (TZD) on milk fat synthesis and its interaction with trans-10, cis-12 CLA. Twenty-four lactating ewes (60 ± 0.45 kg of BW) were randomly assigned one of the four treatments (n=6/treatment) for 7 d: Control (100 mL/d of saline); TZD (IV 4 mg of TZD/kg of BW per d in 100 mL of saline); CLA (oral dose of 27 g/d of rumen-unprotected CLA (oil mixture: 29.9% trans-10, cis-12), and TZD+CLA(TZD infusion initiated one day before CLA dosing). Milk was sampled and analyzed for fat, protein and lactose concentration. Compared to control, fat content was 22.3% lower in CLA (6.14 vs. 4.77%, P = 0.05), tended to be 20.7% lower in TZD+CLA (6.14 vs. 4.87, P = 0.06), and did not differ between control and TZD (6.14 vs. 6.70%, P = 0.39). Compared to TZD, fat content was 28.8% lower in CLA (6.70 vs. 4.77%, P = 0.008) and 27.3% in TZD+CLA (6.70 vs. 4.87%, P = 0.01). Fat content did not differ between TZD+CLA and CLA (4.87 vs. 4.77%, P = 0.87). Treatments did not affect the concentration of milk protein and lactose (P > 0.05). In conclusion, TZD did not stimulate milk fat synthesis and was not able to overcome CLA inhibition of milk fat synthesis, indicating that PPARγ does not mediate CLA-induced MFD

Keywords: Milk fat depression, lipid synthesis pathway, peroxisome proliferator-activated receptor gamma