Abstract
Dairy cows are often fed a high-concentrate (HC) diet to meet lactation demands; however, long-term concentrate feeding is unhealthy and decreases milk fat. Therefore, we investigated the effects of liver lipid metabolism on milk fat synthesis. Ten lactating Holstein cows were assigned randomly into HC and LC (low-concentrate) diet groups. After 20 weeks of feeding, milk fat declined, and lipopolysaccharide levels in the jugular, portal, and hepatic veins increased in the HC group. Liver consumption and release of nonesterified fatty acid (NEFA) into the bloodstream also decreased. AMP-activated protein kinase alpha (AMPKα) was up-regulated significantly in the livers of the HC-fed cows. The HC diet also up-regulated the expression of the transcription factor peroxisome proliferator-activated receptor α (PPARα) and its downstream targets involved in fatty acid oxidation, including carnitine palmitoyltransferase-1,2 (CPT-1, CPT-2), liver-fatty acid-binding protein (L-FABP), and acyl-CoA oxidase (ACO). The HC diet increased blood glucagon (GC) levels, and liver glucagon receptor (GCGR) expression was elevated. Cumulatively, a long-term HC diet decreased plasma concentrations of NEFA via the GC/GCGR-AMPK-PPARα signalling pathway and reduced their synthesis in the liver. The decreased NEFA concentration in the blood during HC feeding may explain the decline in the milk fat of lactating cows.
Highlights
Several studies have noted that an HC diet leads to a decrease in milk fat
We found that the mRNA expression levels of peroxisome proliferator-activated receptor α (PPARα), carnitine palmitoyltransferase-1 (CPT-1), liver-fatty acid-binding protein (L-FABP) and acyl-CoA oxidase (ACO) were significantly increased in the HC cows compared with the LC cows (p < 0.05)
The results suggested that more nonesterified fatty acid (NEFA) and TG were consumed from the livers of HC diet cows compared with cows fed a LC diet
Summary
Several studies have noted that an HC diet leads to a decrease in milk fat. Our previous study showed that the expression profiles of genes involved in the inflammatory response and lipid metabolism in the liver were altered significantly in ruminants after feeding with an HC diet[12]. The mechanism of the relationship between liver lipid metabolism and milk fat depression is largely unknown in ruminants fed HC diets for long periods of time. The objective of this study was to investigate the potential mechanisms in the liver that contribute to the input of substrate precursors to the mammary gland after feeding an HC diet to lactating cows
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