• The origin of milk fat depression induced by fish oil and plant oils remains unclear. • This condition was expected to be alleviated by 2-hydroxy-4-(methylthio) butanoate. • Supplementation with sea buckthorn oil was hypothesized to aggravate the syndrome. • Neither strategy was able to regulate the extent of milk fat depression in sheep. • The complex mechanisms involved in milk fat depression have not been unraveled yet. Milk fat depression ( MFD ) caused by diet supplementation with a combination of marine lipids and plant oils represents a complex condition that could be specifically explained by the interplay of two mechanisms: inhibition of mammary de novo fatty acid ( FA ) synthesis (mainly as a consequence of the trans -10 shift in biohydrogenation, linked to plant oil intake) and inhibition of preformed FA uptake (hypothetically due to direct antilipogenic effects of unsaturated FA from fish oil, such as cis -9 16:1 and cis -11 18:1). Therefore, this study was conducted with the aim of examining the ability of 2-hydroxy-4-methylthiobutanoate ( HMTBa ; a potential mitigating agent of trans -10 shift) and sea buckthorn oil ( SBO ; a rich source of cis -9 16:1 and cis -11 18:1) as regulators of fish oil-induced MFD in dairy sheep. Our initial hypotheses were that HMTBa would partially alleviate MFD and that SBO would aggravate this condition in sheep. The trial followed a replicated 3 × 3 Latin square design (n = 12 ewes) with 3 periods of 25 days each and 3 experimental diets: a total mixed ration including 1.5% DM fish oil to induce MFD (Control), and the same diet supplemented with 0.1% DM of HMTBa or with 1.5% DM of SBO. Animal performance, milk and ruminal digesta FA profiles, and ruminal fermentation characteristics were examined at the end of each period. Contrary to expectation, HMTBa did not alleviate MFD, nor did it cause changes in trans -10 FA concentrations in rumen and milk or in mammary de novo FA synthesis. Moreover, HMTBa had only subtle effects on FA indicative of other biohydrogenation pathways or steps, and did not cause changes in lipids used as microbial biomarkers (odd- and branched-chain FA and dimethyl acetals). Possible reasons for this behaviour may include HMTBa dosage or extent of the trans -10 shift. In the SBO treatment, the milk concentrations of cis -9 16:1 and cis -11 18:1 were sufficiently high (2.12 and 1.59% of total FA, respectively) to expect an effect on mammary lipogenesis. However, SBO supplementation did not affect preformed FA uptake or MFD extent. In conclusion, at the studied levels, neither HMTBa nor SBO regulated MFD in dairy sheep. The involvement of cis -9 16:1 and cis -11 18:1 in marine lipid-induced MFD is therefore challenged and the previously described relationship would not be causative, but probably a confounding effect. Further research is still required to unravel the complex mechanisms underlying MFD and to develop mitigation strategies.
Barrio et al. (Sun,) studied this question.