NUTRITION ▶▶▶
Avoiding milk fat drop during heat stress
BY ILKYU YOON, PHD, DIRECTOR, RUMINANT RESEARCH & TECHNICAL SUPPORT, DIAMOND V
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ilk fat synthesis depends on fatty acids from two sources. Long-chain fatty acids (greater than 16 carbon atoms per molecule) derive from the uptake of circulating preformed fatty
acids, dietary fat absorbed from the digestive tract, and non-esterified fatty acids (NEFA) from the mobilisation of body fat reserves. Short-chain (4 to 8 carbons) and medi- um-chain (10 to 14 carbons) fatty acids originate in the mam- mary gland from de novo synthesis (fatty acids created ‘anew’ in the mammary from smaller molecules). The 16-carbon fat- ty acids can originate from both sources. For a well-fed cow, an estimated 4% to 8% of milk fatty acids originate from the breakdown of body fat (such as NEFA). However, the propor- tion of fatty acids from this source could increase progressive- ly as the cow’s net energy balance decreases (Bauman and Griinari, 2001). Under heat stress, there are two potential mechanisms for milk fat depression (MFD). The first one is ru- men fatty acid biohydrogenation – inhibiting de novo milk fat synthesis. The second one is rumen lipopolysaccharide – limiting substrate supply and de novo milk fat synthesis.
Altered fatty acid biohydrogenation According to the well-accepted ‘biohydrogenation theory’ (Bauman and Griinari, 2001), MFD results from changes in ru- men biohydrogenation of unsaturated fatty acids and the passage of specific intermediates of biohydrogenation out of the rumen (such as trans-10, cis-12 CLA). These biohydro- genation intermediates subsequently interfere with the ex- pression of genes involved in fat synthesis thereby reducing milk fat synthesis in the mammary gland. Furthermore, the in- creased rate of feedstuffs outflow from the rumen may in- crease the likelihood of biohydrogenation intermediates pass- ing through the rumen. So the theory identifies how certain feedstuffs can represent risk factors for MFD (Figure 1). Dairy nutritionists sometimes suggest feeding supplemental fat to maintain the cow’s energy intake during heat stress. However, it is important that the source of fat is rumen inert. Otherwise, low rumen pH, which occurs in heat stressed cows, could gen- erate more intermediates of biohydrogenation and increase the risk of MFD.
Heat stressed dairy cows often suffer milk fat depression, which can be costly to producers in the current challenging dairy market. However, ongoing research suggests that optimising rumen function can help sustain milk fat concentrations in cows under heat stress.
Altered rumen LPS production The other potential mechanism for MFD during heat stress in- volves the concentration of rumen lipopolysaccharide (LPS), which comes from Gram-negative bacteria when they die. Research shows that when rumen pH decreases, the rumen concentration of LPS increases. Also, as rumen LPS concentra- tion increases, milk fat concentration decreases. Zebeli and Ametaj (2009) showed greater concentrations of rumen LPS as the proportion of grain in the diet increased. As rumen LPS increased, milk fat content decreased (Figure 2). This correla- tion could be due to the ability of LPS to induce insulin pro- duction in the pancreas (Waldron et al., 2006). Increased cir- culating insulin and increased insulin sensitivity of heat stressed cows could reduce body fat mobilisation. This condi- tion could occur even though heat stressed cows are under negative energy balance due to reduced feed intake and in- creased maintenance demands (Baumgard and Rhoads,
Figure 1 - Dietary components can impact the risk of milk fat depression in 3 ways through the rumen biohydrogenation (BH) pathway. Adapted from Lock and Bauman (2007).
1. Increase the amount of unsaturated fat
Linoleic acid (cis-9, cis-12 18:2) Rumenic acid (cis-9, trans-11 CLA)
Vaccenic acid (trans-11, 18:1)
3. Inhibit final step / alter rates of BH
Stearic acid (18:0)
Stearic acid (18:0)
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2. Alter rumen environment - pH
- Starch fermentability
trans-10, cis-12 CLA
trans-10, 18:1
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