Activation of AMP-activated protein kinase (AMPK) inhibits fatty acid synthesis in bovine mammary epithelial cells

McFadden, J.W.; Corl, Benjamin A.

doi:10.1016/j.bbrc.2009.09.017

Cited by 73 publications

(64 citation statements)

References 27 publications

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“…al. showed that direct AMPK activation suppressed de novo lipid synthesis and triglyceride formation in mammary epithelial cells [55]. Although our data support the conclusion that elevated AMPK activity is associated with impaired de novo lipogenesis in mammary epithelium of obese mice, additional functional studies, using pharmacological and/or genetic approaches to disrupt mammary gland AMPK activity, are required to demonstrate a direct relationship between these two observations and validate the physiological importance of AMPK in regulating de novo lipid synthesis in the lactating mammary gland.…”

Section: Discussionmentioning

confidence: 99%

Maternal Obesity Reduces Milk Lipid Production in Lactating Mice by Inhibiting Acetyl-CoA Carboxylase and Impairing Fatty Acid Synthesis

et al. 2014

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Maternal metabolic and nutrient trafficking adaptations to lactation differ among lean and obese mice fed a high fat (HF) diet. Obesity is thought to impair milk lipid production, in part, by decreasing trafficking of dietary and de novo synthesized lipids to the mammary gland. Here, we report that de novo lipogenesis regulatory mechanisms are disrupted in mammary glands of lactating HF-fed obese (HF-Ob) mice. HF feeding decreased the total levels of acetyl-CoA carboxylase-1 (ACC), and this effect was exacerbated in obese mice. The relative levels of phosphorylated (inactive) ACC, were elevated in the epithelium, and decreased in the adipose stroma, of mammary tissue from HF-Ob mice compared to those of HF-fed lean (HF-Ln) mice. Mammary gland levels of AMP-activated protein kinase (AMPK), which catalyzes formation of inactive ACC, were also selectively elevated in mammary glands of HF-Ob relative to HF-Ln dams or to low fat fed dams. These responses correlated with evidence of increased lipid retention in mammary adipose, and decreased lipid levels in mammary epithelial cells, of HF-Ob dams. Collectively, our data suggests that maternal obesity impairs milk lipid production, in part, by disrupting the balance of de novo lipid synthesis in the epithelial and adipose stromal compartments of mammary tissue through processes that appear to be related to increased mammary gland AMPK activity, ACC inhibition, and decreased fatty acid synthesis.

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Section: Discussionmentioning

confidence: 99%

Maternal Obesity Reduces Milk Lipid Production in Lactating Mice by Inhibiting Acetyl-CoA Carboxylase and Impairing Fatty Acid Synthesis

et al. 2014

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“…Upon activation, AMPK stimulates catabolic (ATP-generating) pathways and inhibits anabolic (ATP-consuming) pathways (Sriwijitkamol et al, 2006). AMPK prevents fatty acid accumulation by phosphorylating and inhibiting several key enzymes involved in fatty acid biosynthetic pathways, such as acetyl-CoA carboxylase (ACC) (Ramnanan et al, 2010), fatty acid synthase (Cool et al, 2006), glycerol-3-phosphate acyltransferase (McFadden and Corl, 2009), and HMG-CoA reductase (Lopez et al, 2010). An increasing body of evidence has shown that many metabolic disorders are commonly associated with the dysregulation of AMPK (Luo et al, 2005;Zhang et al, 2009).…”

Section: Introductionmentioning

confidence: 99%

The adenosine derivative 2′,3′,5′-tri-O-acetyl-N6-(3-hydroxylaniline) adenosine activates AMPK and regulates lipid metabolism in vitro and in vivo

et al. 2012

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“…Milk protein, fat content and milk fatty acids (FA) composition are the important indicators for milk quality measurement. Cow’s milk fat is the most variable component of milk and primarily composed of triacylglycerol (McFadden and Corl, 2009). Bovine milk contains about 3.5% to 5% total lipids, which about 95% to 98% or more of the lipid is triacylglycerol and the rest is made up of cholesterol, cholesteryl ester, 1,2-diacylglycerol, free fatty acids, monoacylglycerol and phospholipid (Jensen et al, 1991; German and Dillard, 2006).…”

Section: Introductionmentioning

confidence: 99%

Rapamycin Inhibits Expression of Elongation of Very-long-chain Fatty Acids 1 and Synthesis of Docosahexaenoic Acid in Bovine Mammary Epithelial Cells

Guo

Wang

Feng

et al. 2016

Asian Australas. J. Anim. Sci

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Mammalian target of rapamycin complex 1 (mTORC1) is a central regulator of cell growth and metabolism and is sufficient to induce specific metabolic processes, including de novo lipid biosynthesis. Elongation of very-long-chain fatty acids 1 (ELOVL1) is a ubiquitously expressed gene and the product of which was thought to be associated with elongation of carbon (C) chain in fatty acids. In the present study, we examined the effects of rapamycin, a specific inhibitor of mTORC1, on ELOVL1 expression and docosahexaenoic acid (DHA, C22:6 n-3) synthesis in bovine mammary epithelial cells (BMECs). We found that rapamycin decreased the relative abundance of ELOVL1 mRNA, ELOVL1 expression and the level of DHA in a time-dependent manner. These data indicate that ELOVL1 expression and DHA synthesis are regulated by mTORC1 in BMECs.

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Activation of AMP-activated protein kinase (AMPK) inhibits fatty acid synthesis in bovine mammary epithelial cells

Cited by 73 publications

References 27 publications

Maternal Obesity Reduces Milk Lipid Production in Lactating Mice by Inhibiting Acetyl-CoA Carboxylase and Impairing Fatty Acid Synthesis

Maternal Obesity Reduces Milk Lipid Production in Lactating Mice by Inhibiting Acetyl-CoA Carboxylase and Impairing Fatty Acid Synthesis

The adenosine derivative 2′,3′,5′-tri-O-acetyl-N6-(3-hydroxylaniline) adenosine activates AMPK and regulates lipid metabolism in vitro and in vivo

Rapamycin Inhibits Expression of Elongation of Very-long-chain Fatty Acids 1 and Synthesis of Docosahexaenoic Acid in Bovine Mammary Epithelial Cells

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