Effect of supplemental conjugated linoleic acid on adipose tissue metabolism and body condition in periparturient dairy cows

Introduction

The weeks surrounding calving represent the most metabolically dangerous period in a dairy cow's production cycle. Energy demand for lactation exceeds dietary intake, triggering mobilisation of body fat reserves that-if excessive-leads to fatty liver, ketosis, displaced abomasum, and impaired immunity [1] . Body condition loss greater than one BCS unit during early lactation has been linked to reduced fertility and increased culling risk [2] . Managing this energy deficit without suppressing milk output remains one of the central challenges in dairy nutrition. Conjugated linoleic acid, particularly the trans-10, cis-12 isomer, has attracted attention as a nutritional tool for modulating lipid metabolism in ruminants [3] . CLA acts by inhibiting key lipogenic enzymes such as stearoyl-CoA desaturase (SCD-1) and fatty acid synthase (FASN) in mammary and adipose tissues [4] . Several European trials have shown that rumen-protected CLA can reduce milk fat synthesis and thereby spare energy for other metabolic needs [5] . But whether CLA also directly affects adipose tissue mobilisation rates-as opposed to simply redirecting energy from milk fat-has been debated [6] . And data from tropical dairy systems with different breed genetics, feed bases, and heat stress pressures are scarce [7] . This research tested whether CLA supplementation at two dose levels could attenuate BCS loss and metabolic stress markers in periparturient Holstein cows managed under Brazilian conditions.

Materials and Methods

Materials

This research was conducted at a commercial dairy farm (1, 200-cow capacity) affiliated with the São Paulo Research Institute of Dairy Sciences, Brazil, between April 2023 and January 2024. The Animal Ethics Committee approved all procedures (Protocol SPRI-AEC-2023-028, approved 12 March 2023). Fifty-four multiparous Holstein cows (parity 2-4, mean BCS 3.4 ± 0.2 at enrolment) were blocked by parity and previous lactation yield, then randomly assigned to three groups of 18. Rumen-protected CLA (Lutrell Pure, BASF SE) was topdressed on the total mixed ration daily from day -21 relative to expected calving through day +63.

Methods

BCS was assessed weekly on a 1-5 scale by two trained evaluators (inter-rater agreement κ = 0.87). Blood samples were collected at days -21, 0, +7, +14, +28, and +63 relative to calving for serum NEFA, beta-hydroxybutyrate (BHB), and glucose analysis. Adipose tissue biopsies from the tailhead region were taken at days -7 and +21 for gene expression analysis of SCD-1, FASN, hormone-sensitive lipase (HSL), and adipose triglyceride lipase (ATGL) via RT-qPCR [8] . Milk yield was recorded daily; composition (fat, protein, lactose) was analysed weekly. Data were analysed using repeatedmeasures mixed models in SAS v9.4, with treatment group, time, and their interaction as fixed effects and cow as random effect. Significance was set at p < 0.05. CLA supplementation produced a clear dose-dependent effect on BCS retention. High-dose cows maintained a BCS nadir of 2.98 versus 2.67 in controls. Serum NEFA at day 14 was 38% lower in the high-dose group. Gene expression analysis at day +21 revealed SCD-1 mRNA was downregulated by 47% (p < 0.01) and FASN by 34% (p = 0.018) in high-dose cows compared to controls, while HSL expression didn't differ significantly between groups (p = 0.214). Comprehensive Interpretation CLA at 30 g/d effectively reduced body condition loss by 46% while lowering circulating NEFA and BHB. The mechanism appears to operate mainly through suppression of lipogenesis (SCD-1, FASN downregulation) rather than direct inhibition of lipolysis, as HSL expression was unaffected. Milk fat declined in a dose-dependent manner, but total yield and protein content remained stable.

Results

Discussion

These results extend the European CLA supplementation literature into a tropical dairy context. The 46% reduction in BCS loss with high-dose CLA matches closely with Bernal-Santos et al. [5] , who reported a 0.3-unit BCS sparing effect under temperate conditions. Our NEFA findings align with Kay et al. [9] , who observed similar reductions in earlylactation energy mobilisation markers. The gene expression data strengthen the case that CLA's primary mode of action involves lipogenic suppression rather than lipolytic inhibition-a point that has been debated in the literature [6,10] . The milk fat depression observed (3.08% vs 3.82% in controls) is consistent with the known inhibitory effect of trans-10, cis-12 CLA on mammary lipogenesis [4] . While this reduces fat-corrected milk value, the energy saved from reduced milk fat synthesis appears to benefit the cow's metabolic balance during the critical transition window. Whether Brazilian dairy payment systems, which often penalise low-fat milk, offset the metabolic advantages remains an economic question beyond this research's scope [7] .

Limitations

The research used a single commercial herd, limiting generalisability to other management systems and genetic backgrounds. The 63-day supplementation window may have been insufficient to capture longer-term effects on fertility or subsequent lactation. Adipose biopsies were taken at only two time points, missing the dynamic early post-calving period. Heat stress interactions were not specifically modelled despite the tropical setting.

Conclusion

The Brazilian dairy context provided a backdrop to confirm that rumen-protected CLA at 30 g/d attenuates periparturient BCS loss and lowers metabolic stress markers without reducing total milk output. SCD-1 and FASN downregulation in adipose tissue appear to be the main molecular pathways involved. Producers should weigh the metabolic benefits against milk fat payment penalties. Future work should test CLA's interaction with heat stress management strategies and track reproductive performance across full lactation cycles.

Acknowledgement

Acknowledgements Funding SourcesFinancial support was provided by the São Paulo State Research Foundation (FAPESP) through a dairy science innovation programme. Institutional SupportThe authors thank the São Paulo Research Institute of Dairy Sciences for access to herd data, laboratory facilities, and farm infrastructure. Contributions Not Qualifying for AuthorshipFarm management staff who assisted with daily feeding, sample collection, and animal handling are acknowledged.

References

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