Abstract

To determine whether insulin exerts an effect on milk fat yield through the direct regulation of milk fat synthesis in the mammary gland, the hyperinsulinemic-euglycemic clamp procedure was performed in lactating goats in the present study. The effects of the hyperinsulinemic-euglycemic clamp on milk yield, milk composition, milk fatty acid yield and the expression levels of mRNAs of milk fat synthesis-related genes were examined. The results revealed that the hyperinsulinemiceuglycemic clamp had no significant effect on the milk yield, the milk protein yield, the yield and content of lactose or the yield and content of solids-not-fat (SNF) (P > 0.05). In contrast, the milk fat percentage and milk fat yield were decreased by 35.3% and 33.6%, respectively (P C16) and 5 fatty acids synthesized de novo in the mammary gland ( 0.05), including acetyl-coenzyme A carboxylase (ACC), fatty acid synthase (FAS), fatty acidbinding protein (FABP), lipoprotein lipase (LPL), stearoyl-CoA desaturase (SCD) and glycerol-3-phosphate acyltransferase (GPAT). However, the expression level of the SCD gene was significantly reduced during the post-procedure period (P

Highlights

  • Milk fat depression (MFD) refers to the diet-induced inhibition of milk fat synthesis in ruminants

  • An abomasal infusion study has demonstrated that the critical level of t10c12CLA for the inhibition of milk fat synthesis is 0.045 g/kg of body weight (BW), at which the milk fat yield can be reduced by 45%

  • The hyperinsulinemic-euglycemic clamp procedure results in a 5% - 15% reduction in milk fat yield in mid-lactation and late-lactation dairy cows. These results suggest that insulin inhibits milk fat synthesis primarily through the suppression of body fat mobilization

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Summary

Introduction

Milk fat depression (MFD) refers to the diet-induced inhibition of milk fat synthesis in ruminants. The BH theory states that under certain dietary conditions, the BH of polyunsaturated fatty acids by ruminal microorganisms results in increased yields of a number of intermediate metabolites. Once accumulated in the mammary gland to a certain critical level, the intermediate metabolites inhibit milk fat synthesis. An abomasal infusion study has demonstrated that the critical level of t10c12CLA for the inhibition of milk fat synthesis is 0.045 g/kg of body weight (BW), at which the milk fat yield can be reduced by 45%. T10c12CLA upregulates the expression of fat synthesis-related genes in body tissues, while in mammary gland tissues, this fatty acid downregulates the expression of fat synthesis-related genes [5]-[7] At 2 - 3 d after the termination of infusion, the milk fat yield returns to normal [4]. t10c12CLA upregulates the expression of fat synthesis-related genes in body tissues, while in mammary gland tissues, this fatty acid downregulates the expression of fat synthesis-related genes [5]-[7]

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