<p>The transition period is critical for dairy cows, characterized by negative energy balance (NEB), excessive adipose mobilization, and metabolic challenges. This study investigated the effects of dietary omega-3 fatty acids (O3) and N-acetyl-tryptophan (NAT) on blood metabolites and adipose tissue gene expression in Holstein cows. Forty-eight multiparous cows were assigned to four groups (control, O3, NAT, O3+NAT)&#xa0;from -21 to +42 days relative to calving. Body weight (BW) and body condition score (BCS) were recorded, and plasma non-esterified fatty acids (NEFA), β-hydroxybutyrate (BHBA), insulin, and glucose were measured at -21, 0 (calving), +21, and +42 days. Adipose biopsies at +21 and +42 days postpartum were used to perform qPCR analysis of lipogenesis-related genes (Acetyl-CoA carboxylase alpha (ACACA), peroxisome proliferator-activated receptor gamma (PPARγ), lipoprotein lipase (LPL)), fatty acid oxidation (Acyl-CoA oxidase 1 (ACOX1)), lipolysis (hormone-sensitive lipase (LIPE), adipose triglyceride lipase (ATGL)), and adiponectin receptors (AdipoR1, AdipoR2).&#xa0;Statistical analysis used two-way ANOVA with repeated measures. Cows supplemented with O3+NAT maintained higher BW (p&lt;0.05) and BCS (p&lt;0.05), exhibited lower NEFA and BHBA (p&lt;0.05), and had increased insulin (p&lt;0.05) and tended to have higher glucose (p=0.08)&#xa0;compared with controls. PPARγ, LPL, and adiponectin receptors (AdipoR1, AdipoR2) were upregulated in all supplemented groups compared to controls (p&lt;0.05). ACOX1 was downregulated in O3, NAT, and O3+NAT groups compared to control (p&lt;0.05). Network analysis revealed strong positive correlations between insulin and AdipoR1/2 (r&gt;0.7) and positive correlations between NEFA/BHBA and LIPE/β2AR (r&gt;0.75) at d 21.&#xa0;These results demonstrate that O3 and NAT act via complementary mechanisms to attenuate lipolysis,&#xa0;promote lipid storage, and enhance metabolic homeostasis during the transition period.</p>

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Modulation of fat mobilization and adipose tissue gene expression in Holstein cows supplemented with omega-3 fatty acids and N-acetyl-tryptophan during the transition period

  • Mansoureh Ghorbanalinia,
  • Essa Dirandeh,
  • Zarbakht Ansari-Pirsaraei,
  • Hasan Sadri,
  • William W Thatcher

摘要

The transition period is critical for dairy cows, characterized by negative energy balance (NEB), excessive adipose mobilization, and metabolic challenges. This study investigated the effects of dietary omega-3 fatty acids (O3) and N-acetyl-tryptophan (NAT) on blood metabolites and adipose tissue gene expression in Holstein cows. Forty-eight multiparous cows were assigned to four groups (control, O3, NAT, O3+NAT) from -21 to +42 days relative to calving. Body weight (BW) and body condition score (BCS) were recorded, and plasma non-esterified fatty acids (NEFA), β-hydroxybutyrate (BHBA), insulin, and glucose were measured at -21, 0 (calving), +21, and +42 days. Adipose biopsies at +21 and +42 days postpartum were used to perform qPCR analysis of lipogenesis-related genes (Acetyl-CoA carboxylase alpha (ACACA), peroxisome proliferator-activated receptor gamma (PPARγ), lipoprotein lipase (LPL)), fatty acid oxidation (Acyl-CoA oxidase 1 (ACOX1)), lipolysis (hormone-sensitive lipase (LIPE), adipose triglyceride lipase (ATGL)), and adiponectin receptors (AdipoR1, AdipoR2). Statistical analysis used two-way ANOVA with repeated measures. Cows supplemented with O3+NAT maintained higher BW (p<0.05) and BCS (p<0.05), exhibited lower NEFA and BHBA (p<0.05), and had increased insulin (p<0.05) and tended to have higher glucose (p=0.08) compared with controls. PPARγ, LPL, and adiponectin receptors (AdipoR1, AdipoR2) were upregulated in all supplemented groups compared to controls (p<0.05). ACOX1 was downregulated in O3, NAT, and O3+NAT groups compared to control (p<0.05). Network analysis revealed strong positive correlations between insulin and AdipoR1/2 (r>0.7) and positive correlations between NEFA/BHBA and LIPE/β2AR (r>0.75) at d 21. These results demonstrate that O3 and NAT act via complementary mechanisms to attenuate lipolysis, promote lipid storage, and enhance metabolic homeostasis during the transition period.