Sterol regulatory element binding protein and dietary lipid regulation of fatty acid synthesis in the mammary epithelium
The lactating mammary gland synthesizes large amounts of triglyceride from fatty acids derived from the blood and from de novo lipogenesis. The latter is significantly increased at parturition and decreased when additional dietary fatty acids become available. To begin to understand the molecular re...
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Published in | American journal of physiology: endocrinology and metabolism Vol. 299; no. 6; pp. E918 - E927 |
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Main Authors | , , , , , , , , |
Format | Journal Article |
Language | English |
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United States
American Physiological Society
01.12.2010
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Abstract | The lactating mammary gland synthesizes large amounts of triglyceride from fatty acids derived from the blood and from de novo lipogenesis. The latter is significantly increased at parturition and decreased when additional dietary fatty acids become available. To begin to understand the molecular regulation of de novo lipogenesis, we tested the hypothesis that the transcription factor sterol regulatory element binding factor (SREBF)-1c is a primary regulator of this system. Expression of Srebf1c mRNA and six of its known target genes increased ≥2.5-fold at parturition. However, Srebf1c-null mice showed only minor deficiencies in lipid synthesis during lactation, possibly due to compensation by Srebf1a expression. To abrogate the function of both isoforms of Srebf1, we bred mice to obtain a mammary epithelial cell-specific deletion of SREBF cleavage-activating protein (SCAP), the SREBF escort protein. These dams showed a significant lactation deficiency, and expression of mRNA for fatty acid synthase (Fasn), insulin-induced gene 1 (Insig1), mitochondrial citrate transporter (Slc25a1), and stearoyl-CoA desaturase 2 (Scd2) was reduced threefold or more; however, the mRNA levels of acetyl-CoA carboxylase-1α (Acaca) and ATP citrate lyase (Acly) were unchanged. Furthermore, a 46% fat diet significantly decreased de novo fatty acid synthesis and reduced the protein levels of ACACA, ACLY, and FASN significantly, with no change in their mRNA levels. These data lead us to conclude that two modes of regulation exist to control fatty acid synthesis in the mammary gland of the lactating mouse: the well-known SREBF1 system and a novel mechanism that acts at the posttranscriptional level in the presence of SCAP deletion and high-fat feeding to alter enzyme protein. |
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AbstractList | The lactating mammary gland synthesizes large amounts of triglyceride from fatty acids derived from the blood and from de novo lipogenesis. The latter is significantly increased at parturition and decreased when additional dietary fatty acids become available. To begin to understand the molecular regulation of de novo lipogenesis, we tested the hypothesis that the transcription factor sterol regulatory element binding factor (SREBF)-1c is a primary regulator of this system. Expression of Srebf1c mRNA and six of its known target genes increased ≥2.5-fold at parturition. However, Srebf1c-null mice showed only minor deficiencies in lipid synthesis during lactation, possibly due to compensation by Srebf1a expression. To abrogate the function of both isoforms of Srebf1, we bred mice to obtain a mammary epithelial cell-specific deletion of SREBF cleavage-activating protein (SCAP), the SREBF escort protein. These dams showed a significant lactation deficiency, and expression of mRNA for fatty acid synthase ( Fasn), insulin-induced gene 1 ( Insig1), mitochondrial citrate transporter ( Slc25a1), and stearoyl-CoA desaturase 2 ( Scd2) was reduced threefold or more; however, the mRNA levels of acetyl-CoA carboxylase-1α ( Acaca) and ATP citrate lyase ( Acly) were unchanged. Furthermore, a 46% fat diet significantly decreased de novo fatty acid synthesis and reduced the protein levels of ACACA, ACLY, and FASN significantly, with no change in their mRNA levels. These data lead us to conclude that two modes of regulation exist to control fatty acid synthesis in the mammary gland of the lactating mouse: the well-known SREBF1 system and a novel mechanism that acts at the posttranscriptional level in the presence of SCAP deletion and high-fat feeding to alter enzyme protein. The lactating mammary gland synthesizes large amounts of triglyceride from fatty acids derived from the blood and from de novo lipogenesis. The latter is significantly increased at parturition and decreased when additional dietary fatty acids become available. To begin to understand the molecular regulation of de novo lipogenesis, we tested the hypothesis that the transcription factor sterol regulatory element binding factor (SREBF)-1c is a primary regulator of this system. Expression of Srebf1c mRNA and six of its known target genes increased ≥2.5-fold at parturition. However, Srebf1c -null mice showed only minor deficiencies in lipid synthesis during lactation, possibly due to compensation by Srebf1a expression. To abrogate the function of both isoforms of Srebf1 , we bred mice to obtain a mammary epithelial cell-specific deletion of SREBF cleavage-activating protein (SCAP), the SREBF escort protein. These dams showed a significant lactation deficiency, and expression of mRNA for fatty acid synthase ( Fasn ), insulin-induced gene 1 ( Insig 1), mitochondrial citrate transporter ( Slc25a1 ), and stearoyl-CoA desaturase 2 ( Scd2 ) was reduced threefold or more; however, the mRNA levels of acetyl-CoA carboxylase-1α ( Acac a) and ATP citrate lyase ( Acly ) were unchanged. Furthermore, a 46% fat diet significantly decreased de novo fatty acid synthesis and reduced the protein levels of ACACA, ACLY, and FASN significantly, with no change in their mRNA levels. These data lead us to conclude that two modes of regulation exist to control fatty acid synthesis in the mammary gland of the lactating mouse: the well-known SREBF1 system and a novel mechanism that acts at the posttranscriptional level in the presence of SCAP deletion and high-fat feeding to alter enzyme protein. The lactating mammary gland synthesizes large amounts of triglyceride from fatty acids derived from the blood and from de novo lipogenesis. The latter is significantly increased at parturition and decreased when additional dietary fatty acids become available. To begin to understand the molecular regulation of de novo lipogenesis, we tested the hypothesis that the transcription factor sterol regulatory element binding factor (SREBF)-1c is a primary regulator of this system. Expression of Srebf1c mRNA and six of its known target genes increased ≥2.5-fold at parturition. However, Srebf1c-null mice showed only minor deficiencies in lipid synthesis during lactation, possibly due to compensation by Srebf1a expression. To abrogate the function of both isoforms of Srebf1, we bred mice to obtain a mammary epithelial cell-specific deletion of SREBF cleavage-activating protein (SCAP), the SREBF escort protein. These dams showed a significant lactation deficiency, and expression of mRNA for fatty acid synthase (Fasn), insulin-induced gene 1 (Insig1), mitochondrial citrate transporter (Slc25a1), and stearoyl-CoA desaturase 2 (Scd2) was reduced threefold or more; however, the mRNA levels of acetyl-CoA carboxylase-1α (Acaca) and ATP citrate lyase (Acly) were unchanged. Furthermore, a 46% fat diet significantly decreased de novo fatty acid synthesis and reduced the protein levels of ACACA, ACLY, and FASN significantly, with no change in their mRNA levels. These data lead us to conclude that two modes of regulation exist to control fatty acid synthesis in the mammary gland of the lactating mouse: the well-known SREBF1 system and a novel mechanism that acts at the posttranscriptional level in the presence of SCAP deletion and high-fat feeding to alter enzyme protein. [PUBLICATION ABSTRACT] |
Author | Foote, Monica R Anderson, Steven M Burns, Valerie Monks, Jenifer Neville, Margaret C Phistry, Meridee Marians, Russell Rudolph, Michael C Bauman, Dale E |
Author_xml | – sequence: 1 givenname: Michael C surname: Rudolph fullname: Rudolph, Michael C organization: 1Department of Physiology and Biophysics, University of Colorado Denver, Aurora, CO, USA – sequence: 2 givenname: Jenifer surname: Monks fullname: Monks, Jenifer – sequence: 3 givenname: Valerie surname: Burns fullname: Burns, Valerie – sequence: 4 givenname: Meridee surname: Phistry fullname: Phistry, Meridee – sequence: 5 givenname: Russell surname: Marians fullname: Marians, Russell – sequence: 6 givenname: Monica R surname: Foote fullname: Foote, Monica R – sequence: 7 givenname: Dale E surname: Bauman fullname: Bauman, Dale E – sequence: 8 givenname: Steven M surname: Anderson fullname: Anderson, Steven M – sequence: 9 givenname: Margaret C surname: Neville fullname: Neville, Margaret C |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/20739508$$D View this record in MEDLINE/PubMed |
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SubjectTerms | Alcohol Animals Binding sites Blotting, Western Breasts Cells Dietary Fats - metabolism Fatty acids Fatty Acids - analysis Fatty Acids - biosynthesis Female Gene Expression Immunohistochemistry Intracellular Signaling Peptides and Proteins - genetics Intracellular Signaling Peptides and Proteins - metabolism Lactation - metabolism Lipogenesis - genetics Mammary Glands, Animal - cytology Mammary Glands, Animal - metabolism Membrane Proteins - genetics Membrane Proteins - metabolism Mice Mice, Knockout Milk - chemistry Proteins Reverse Transcriptase Polymerase Chain Reaction Ribonucleic acid RNA Steroids Sterol Regulatory Element Binding Protein 1 - genetics Sterol Regulatory Element Binding Protein 1 - metabolism |
Title | Sterol regulatory element binding protein and dietary lipid regulation of fatty acid synthesis in the mammary epithelium |
URI | https://www.ncbi.nlm.nih.gov/pubmed/20739508 https://www.proquest.com/docview/816569793/abstract/ https://search.proquest.com/docview/815551528 https://pubmed.ncbi.nlm.nih.gov/PMC3006251 |
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