The Role of TCA Cycle Anaplerosis in Ketosis and Fatty Liver in Periparturient Dairy Cows

White, H.M.

doi:10.3390/ani5030384

Cited by 94 publications

(90 citation statements)

References 47 publications

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“…In the present study, the hepatic mRNA levels of FABP1 and ACSL1 were significantly increased in the cows with CK or SCK, which promoted the intracellular transport and activation of fatty acids in the liver; this may be because the metabolic adaptations occurred in the liver to further use overloaded fatty acids in ketotic cows. More importantly, enhanced intracellular metabolism of fatty acids (increased activation of fatty acids to acyl-CoA, increased protein-mediated transport of fatty acids, and increased metabolism through both anabolic and catabolic pathways) increases fatty acid uptake (Mashek and Coleman, 2006), which coincides with the study of White (2015), who showed that fatty acid uptake from plasma by the liver is increased in ketotic cows. Li et al, (2012a) also reported that the expression level of ACSL1 was significantly increased in SCK cows, which further supported our study.…”

Section: Discussionsupporting

confidence: 73%

“…Fatty acids are energy-rich molecules and play important roles in the induction of hepatic lipid metabolic disorder of dairy cows during the transition period (Li et al, 2013). Ex-cessive fatty acids absorbed by liver from plasma can be metabolized into ketones in hepatocytes, thereby inducing subclinical ketosis (SCK) or clinical ketosis (CK; Ospina et al, 2010;White, 2015). Subclinical ketosis was defined as BHB concentration <3.0 and ≥1.2 mM in the absence of clinical sighs, whereas CK was defined as BHB concentration ≥3.0 mM (McArt et al, 2011;Du et al, 2018).…”

Section: Introductionmentioning

confidence: 99%

“…It is clear that the disturbances of fatty acid uptake, transport, activation, oxidation, synthesis, and esterification play promoting roles in the onset and progression of the ketosis (White, 2015). The expression of hepatic lipid metabolic genes involved in the above processes were mainly regulated by 2 transcription factors, peroxisome proliferator-activated receptor α (PPARα) and sterol regulatory element-binding protein 1c (SREBP-1c; Li et al, 2015;Kersten and Stienstra, 2017).…”

Section: Introductionmentioning

confidence: 99%

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Expression patterns of hepatic genes involved in lipid metabolism in cows with subclinical or clinical ketosis

Zhu¹,

Liu²,

et al. 2019

Journal of Dairy Science

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Section: Discussionsupporting

confidence: 73%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Expression patterns of hepatic genes involved in lipid metabolism in cows with subclinical or clinical ketosis

Zhu¹,

Liu²,

et al. 2019

Journal of Dairy Science

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“…Body fat mobilization due to negative energy balance in early lactation results in increased plasma concentrations of nonesterified fatty acids (NEFA) in dairy cows (Gross et al, 2013). Excessive NEFA absorbed by liver from plasma are metabolized into ketone bodies (acetoacetate, BHB, and acetone) in hepatocytes, thereby inducing ketosis (White, 2015). High concentrations of circulating NEFA in ketotic cows are a significant contributor to milk fat synthesis in the mammary gland (Adewuyi et al, 2005;Palmquist et al, 2006).…”

Section: Introductionmentioning

confidence: 99%

High expression of cell death-inducing DFFA-like effector a (CIDEA) promotes milk fat content in dairy cows with clinical ketosis

Sun

Wang

Loor

et al. 2019

Journal of Dairy Science

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High blood concentrations of nonesterified fatty acids (NEFA) during ketosis represent a source of fatty acids for milk fat synthesis and explain the increase in milk fat content in ketotic cows. Cell death-inducing DFFA-like effector a (CIDEA) is a lipid droplet coat protein with important roles in the regulation of milk fat synthesis and secretion in mice. Whether ketosis alters the expression of CIDEA in mammary gland tissue and the extent to which it may contribute to regulation of milk fat synthesis and secretion are unknown. Mammary gland tissue and blood samples were collected from healthy (n = 15) and clinically ketotic (n = 15) cows. Mammary epithelial cells isolated from cows were infected with CIDEA overexpression adenovirus for 48 h, treated with 0, 0.3, 0.6, or 1.2 mM NEFA for 24 h, or infected with CIDEA-silencing adenovirus for 48 h and treated with 1.2 mM NEFA for 24 h. Serum concentrations of NEFA and β-hydroxybutyrate were greater in cows with clinical ketosis, and milk production and dry matter intake were lower in cows with clinical ketosis. However, compared with healthy cows, the content of milk fat of cows with clinical ketosis was greater. Compared with healthy cows, abundance of mRNA and protein of CIDEA, fatty acid synthase (FASN), acetyl-coA carboxylase 1 (ACACA), butyrophilin (BTN1A1), and xanthine dehydrogenase (XDH) was greater in mammary tissue of cows with clinical ketosis. Overexpression of CIDEA in cultured mammary epithelial cells increased the abundance of FASN, ACACA, XDH, and BTN1A1, and increased triacylglycerol (TAG) content in mammary epithelial cells. Exogenous NEFA increased the abundance of CIDEA, FASN, ACACA, XDH, and BTN1A1, and increased TAG content in mammary epithelial cells. Importantly, knockdown of CIDEA reversed the upregulation of FASN, ACACA, XDH, and BTN1A1 abundance and TAG content induced by NEFA treatment. Overall, these data suggest that high levels of NEFA stimulate the expression of CIDEA and enhance de novo fatty acid synthesis and milk fat secretion. As such, these mechanisms explain in part the elevation of milk fat content in dairy cows with clinical ketosis.

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“…NEFAs are oxidised by the liver to acetyl-CoA. Acetyl-CoA can undergo complete oxidation through the tricarboxylic acid cycle (TCA), converted to very-low density lipoprotein (VLDL) and exported, or converted to triglycerides (TAG) and stored by the liver (White 2015). The liver has a limited capacity to metabolise acetyl-CoA and if complete oxidation is not possible then acetyl-CoA is converted to ketone bodies that are exported as acetone, acetoacetate and betahydroxybutyrate (Aschenbach et al 2010).…”

Section: Introductionmentioning

confidence: 99%

Metabolic health, the metabolome and reproduction in female cattle: a review

D’Occhio

Baruselli

Campanile

2019

Italian Journal of Animal Science

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Studies over the past 30 years have confirmed the important role of metabolic hormones and metabolic substrates in reproductive function in female cattle. The emergence of metabolomics is providing a deeper understanding of the role of specific metabolites, and clusters of metabolites, in reproduction and also health and disease. Dairy cows undergo major fluctuations in metabolic health and metabolomics is helping to better understand the changes in metabolite profiles associated with negative energy balance and ketosis. New knowledge that emerges from this work should lead to improved nutritional management of dairy cows. In reproduction, it is now possible to gain a metabolomic signature of ovarian follicular fluid and of developing embryos. This should likewise lead to improvements in both natural and assisted reproduction in cattle. Systems biology integrates genomics, transcriptomics, proteomics and metabolomics, and contributes to gaining an understanding of complex biological networks. HIGHLIGHTSMetabolic hormones and metabolic substrates have a major influence on reproduction in female cattle. Negative energy balance and ketosis are associated with changes in the systemic and liver metabolome in dairy cows. The metabolome of ovarian follicular fluid influences oocyte quality and embryo development. Systems biology integrates genomics, transcriptomics, proteomics and metabolomics, and provides a deeper understanding of complex biological networks. ARTICLE HISTORY

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The Role of TCA Cycle Anaplerosis in Ketosis and Fatty Liver in Periparturient Dairy Cows

Cited by 94 publications

References 47 publications

Expression patterns of hepatic genes involved in lipid metabolism in cows with subclinical or clinical ketosis

Expression patterns of hepatic genes involved in lipid metabolism in cows with subclinical or clinical ketosis

High expression of cell death-inducing DFFA-like effector a (CIDEA) promotes milk fat content in dairy cows with clinical ketosis

Metabolic health, the metabolome and reproduction in female cattle: a review

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