This research paper addresses the hypothesis that dietary pioglitazone (PGT), as synthetic and specific ligand for PPAR-γ or walnut meal (WM) as a natural ligand for PPAR-γ, affect plasma metabolites and reduce the oxidative status in high body condition score (BCS) dairy cows (≥4 BCS). Total of 36 multiparous Holstein cows were randomly assigned to one of the dietary treatments: 1- Control (basal diet; CTR), 2- Walnut meal (9·45% walnut meal of DMI; WM), and 3- Pioglitazone (6 mg/kg BW; PGT). The experimental diets were fed from parturition time to 21 d postpartum. Results showed that the PGT supplementation increased dry matter intake (DMI) (22·95 kg/d) compared to the CTR (21·45 kg/d) and WM (21·78 kg/d) groups. Results showed that milk yield and milk composition were not affected by the experimental diets. Body condition score losses tended to be higher in the CTR group compared to the PGT and WM cows. The PGT group had higher plasma insulin compared to the CTR group (11·84 vs. 10·68 mIU/l), and WM cows had intermediate plasma insulin. The PGT cows had lower plasma non esterified fatty acid (NEFA) and tended to have lower β-hydroxy butyric acid (BHBA) than the CTR group. Feeding pioglitazone decreased plasma malondialdehyde (MDA) and increased plasma total antioxidant capacity (TAC) and superoxide dismutase (SOD) compared to the CTR and WM groups. It was concluded that dietary pioglitazone had positive effects on DMI, BCS change, blood metabolites and oxidative status in fresh dairy cows with high pre-calving BCS. The anti-oxidant effects of walnut meal were not supported by the present data.

The trans-10, cis-12 conjugated linoleic acid (CLA) causes milk fat depression by downregulating expression of genes and transcription factors involved in lipogenesis and it has been proposed that peroxisome proliferator-activated receptor gamma (PPARγ) can be inhibited by trans-10, cis-12 CLA. The PPARγ is a nuclear receptor activated by natural or synthetic ligands and promotes expression of lipogenic genes and its effect on mammary lipogenesis and the interaction with trans-10, cis-12 CLA in lactating ewes was evaluated using thiazolidinedione (TZD), a chemical PPARγ agonist. A total of 24 lactating ewes were randomly assigned to one of the following treatments for 7 days: (1) Control (5 ml/day of saline solution); (2) TZD (4 mg/kg of BW/day in 5 ml of saline solution); (3) CLA (27 g/day with 29.9% of trans-10, cis-12); (4) TZD+CLA. Compared with Control, milk fat content was not changed by TZD, but was decreased 22.3% and 20.5% by CLA and TZD+CLA treatments. In the mammary gland, TZD increased PPARγ gene expression by 174.8% and 207.8% compared with Control and TZD+CLA treatments, respectively. Conjugated linoleic acid reduced sterol regulatory element-binding transcription protein 1 (SREBP1) gene expression 89.2% and 75.3% compared with Control and TZD+CLA, respectively, demonstrating that TZD fails to overcome CLA inhibition of SREBP1 signaling. In adipose tissue, the expression of SREBP1 and stearoyl CoA desaturase 1 (SCD1) genes were increased by the TZD+CLA treatment, compared with the other treatments. Conjugated linoleic acid decreased milk fat concentration and expression of lipogenic genes, while TZD had no effect on milk fat concentration, expression of lipogenic enzymes or regulators in the mammary gland and failed to overcome the inhibition of these by CLA. Therefore, CLA inhibition of milk fat synthesis was independent of the PPARγ pathway in lactating dairy ewes.

Bitter melon (Momordica charantia; BM) has been shown to ameliorate diet-induced obesity and insulin resistance. To examine the effect of BM supplementation on cell size and lipid metabolism in adipose tissues, three groups of rats were respectively fed a high-fat diet supplemented without (HF group) or with 5 % lyophilised BM powder (HFB group), or with 0·01 % thiazolidinedione (TZD) (HFT group). A group of rats fed a low-fat diet was also included as a normal control. Hyperinsulinaemia and glucose intolerance were observed in the HF group but not in HFT and HFB groups. Although the number of large adipocytes (>180 μm) of both the HFB and HFT groups was significantly lower than that of the HF group, the adipose tissue mass, TAG content and glycerol-3-phosphate dehydrogenase activity of the HFB group were significantly lower than those of the HFT group, implying that BM might reduce lipogenesis in adipose tissue. Experiment 2 was then conducted to examine the expression of lipogenic genes in adipose tissues of rats fed low-fat, HF or HFB diets. The HFB group showed significantly lower mRNA levels of fatty acid synthase, acetyl-CoA carboxylase-1, lipoprotein lipase and adipocyte fatty acid-binding protein than the HF group (P < 0·05). These results indicate BM can reduce insulin resistance as effective as the anti-diabetic drug TZD. Furthermore, BM can suppress the visceral fat accumulation and inhibit adipocyte hypertrophy, which may be associated with markedly down regulated expressions of lipogenic genes in the adipose.