GO:0010949 negative regulation of intestinal phytosterol absorption: Mechanism, Genes and Research Methods
Research-grade guide for scientists and biopharma professionals
Key Takeaways
• GO:0010949 describes any process that stops, prevents, or reduces the absorption of phytosterols from the small intestine into the blood.
• Phytosterols and their saturated derivatives, phytostanols, compete with cholesterol for intestinal absorption and can lower circulating cholesterol when consumed.
• Plant stanol esters reduce intestinal cholesterol absorption and can alter expression of LDL receptor and HMG-CoA reductase in blood cells.
• Dietary cholesterol loading suppresses the cholesterol synthesis pathway and increases bile acid production in some animal models, showing feedback control of sterol handling.
• Increased cholesterol absorption has been linked to clinical outcomes such as in-stent restenosis after coronary stenting.
• Studying GO:0010949 requires combining sterol absorption assays, gene expression analysis, and CRISPR-based models of candidate transporters and regulators.
Description
GO:0010949, negative regulation of intestinal phytosterol absorption, is a biological process term that captures the mechanisms which reduce the movement of phytosterols from the small intestine into the blood. Phytosterols are plant-derived sterols that resemble cholesterol and are absorbed through the intestine with lower efficiency than cholesterol; when present in the diet, they can interfere with cholesterol uptake and thereby influence circulating lipid levels. The term is therefore important for researchers interested in lipid metabolism, cardiovascular risk, and the pharmacological or nutritional control of sterol absorption. Experimental evidence shows that dietary plant sterols and stanols can enhance cholesterol-lowering effects and modulate expression of key cholesterol-handling genes such as LDLR and HMGCR in humans. In addition, dietary cholesterol supplementation can suppress the complete cholesterol synthesis pathway and induce bile acid production in animal models, illustrating the broader feedback network in which intestinal sterol absorption is embedded. Because the process is defined by a negative regulatory outcome, it encompasses both direct inhibition of phytosterol transport and indirect mechanisms that reduce the frequency or extent of phytosterol entry into the bloodstream.
negative regulation of intestinal phytosterol absorption At A Glance
| GO ID | GO:0010949 |
|---|---|
| GO term | negative regulation of intestinal phytosterol absorption |
| Ontology | biological_process |
| Synonym | None listed in QuickGO |
| Definition | Any process that stops, prevents, or reduces the frequency, rate or extent of the directed movement of phytosterols into the blood by absorption from the small intestine. |
| Major function | Reduces intestinal uptake of phytosterols, thereby influencing sterol balance and circulating lipid levels. |
| Related sterols | Phytosterols and phytostanols, plant-derived sterols that compete with cholesterol absorption. |
| Physiological context | Small intestine, where dietary and biliary sterols are absorbed. |
| Therapeutic relevance | Plant sterol and stanol consumption is used to lower cholesterol; altered sterol absorption is linked to cardiovascular outcomes. |
What Is GO:0010949?
In simple terms, GO:0010949 is the set of processes that decrease how much phytosterol is taken up from the small intestine into the blood. The official QuickGO definition states: Any process that stops, prevents, or reduces the frequency, rate or extent of the directed movement of phytosterols into the blood by absorption from the small intestine. This is a biological_process term, and it has no synonyms in the current QuickGO record. The term is not about a single gene or protein; rather, it describes a regulatory outcome that can be achieved by multiple molecular mechanisms, including competition between sterols for transport, changes in transporter expression, and feedback regulation of sterol synthesis and bile acid production.
Why Is negative regulation of intestinal phytosterol absorption Important in Cell Biology?
Understanding negative regulation of intestinal phytosterol absorption is important because intestinal sterol uptake is a key control point for circulating cholesterol and for the clinical effects of plant sterols and stanols. Plant stanol esters can reduce cholesterol absorption and alter expression of LDL receptor and HMG-CoA reductase in mononuclear blood cells, showing that dietary phytosterols can engage systemic cholesterol-regulatory pathways. In animal models, diet enrichment with calcium and magnesium enhances the cholesterol-lowering effect of plant sterols, indicating that the negative regulation of sterol absorption can be modulated by additional dietary factors. Moreover, increased cholesterol absorption has been associated with in-stent restenosis after stent implantation for stable coronary artery disease, linking intestinal sterol handling to a clinically relevant vascular outcome. Dietary cholesterol supplementation in Atlantic salmon suppresses the complete pathway of cholesterol synthesis and induces bile acid production, demonstrating that sterol absorption and synthesis are reciprocally regulated across species. Together, these findings make GO:0010949 a valuable framework for studying how diet, genetics, and pharmacology intersect to control sterol entry into the body.
• Intestinal phytosterol absorption is a determinant of circulating cholesterol levels and cardiovascular risk.
• Plant sterols and stanols lower cholesterol in part by competing with cholesterol for intestinal absorption.
• Plant stanol esters can modulate LDL receptor and HMG-CoA reductase expression in blood cells, linking absorption to systemic lipid gene regulation.
• Dietary calcium and magnesium can enhance the cholesterol-lowering effect of plant sterols in obese animal models.
• Increased cholesterol absorption is associated with in-stent restenosis after coronary stenting, a clinically important vascular complication.
• Dietary cholesterol can suppress the entire cholesterol synthesis pathway and induce bile acid production, showing feedback between absorption and synthesis.
• The process is relevant to nutritional strategies for managing hypercholesterolemia.
• It provides a conceptual framework for identifying genes and pathways that limit phytosterol entry into the blood.
• Species differences in sterol handling, such as in Atlantic salmon, highlight conserved and divergent features of the pathway.
• Understanding this negative regulation can guide development of therapies that target intestinal sterol uptake.
What Happens During negative regulation of intestinal phytosterol absorption?
Competition Between Phytosterols and Cholesterol at the Intestinal Lumen
In simple terms: Plant sterols and cholesterol compete for the same absorption machinery in the gut.
In the intestinal lumen, phytosterols and cholesterol are presented together in mixed micelles. Because phytosterols are structurally similar to cholesterol, they can compete for interaction with intestinal sterol transporters and reduce the efficiency of cholesterol uptake. This competition is one mechanism by which dietary plant sterols and stanols lower circulating cholesterol, and it represents a form of negative regulation of intestinal phytosterol absorption when the net effect is reduced phytosterol entry into the blood. The presence of plant stanol esters has been shown to affect LDL receptor and HMG-CoA reductase mRNA expression in mononuclear blood cells of healthy men and women, indicating that intestinal sterol competition can propagate to systemic gene expression changes.
Reduced Transporter-Mediated Uptake of Phytosterols
In simple terms: If the proteins that bring sterols into intestinal cells are less active, less phytosterol gets absorbed.
Intestinal sterol absorption requires transport proteins that move sterols from the lumen into enterocytes. Negative regulation of intestinal phytosterol absorption can occur when the activity or abundance of these transporters is reduced, either through direct inhibition or through changes in gene expression. Dietary cholesterol supplementation in Atlantic salmon suppresses the complete pathway of cholesterol synthesis and induces bile acid production, showing that sterol loading can trigger feedback that limits further sterol uptake and synthesis. In humans, plant stanol ester consumption alters LDL receptor and HMG-CoA reductase mRNA levels in blood cells, suggesting that systemic sterol status feeds back on intestinal and peripheral sterol handling.
Feedback Control of Cholesterol Synthesis and Bile Acid Production
In simple terms: When the body takes in more sterols, it can shut down its own sterol production and make more bile acids.
A key component of negative regulation of intestinal phytosterol absorption is feedback control of endogenous sterol synthesis. In Atlantic salmon, dietary cholesterol supplementation suppressed the complete pathway of cholesterol synthesis and induced bile acid production, demonstrating a coordinated response that reduces the need for further sterol uptake. In humans, plant stanol esters affect LDL receptor and HMG-CoA reductase expression, two central nodes in cholesterol homeostasis. These observations indicate that the negative regulation of intestinal phytosterol absorption is embedded in a broader network that balances dietary sterol input, endogenous synthesis, and bile acid output.
Dietary and Pharmacological Modulation of Sterol Absorption
In simple terms: Diet and supplements can change how much plant sterol is absorbed.
Dietary factors can enhance or reduce the negative regulation of intestinal phytosterol absorption. In obese Zucker rats, diet enrichment with calcium and magnesium enhanced the cholesterol-lowering effect of plant sterols, showing that mineral intake can modulate sterol absorption outcomes. Plant stanol esters have been shown to affect LDL receptor protein expression and LDL receptor and HMG-CoA reductase mRNA expression in mononuclear blood cells of healthy men and women, linking dietary phytosterol intake to systemic lipid gene regulation. Increased cholesterol absorption has also been associated with in-stent restenosis after stent implantation for stable coronary artery disease, underscoring the clinical relevance of intestinal sterol handling.
Integration with Systemic Lipid and Lipoprotein Metabolism
In simple terms: What happens in the gut affects cholesterol levels and blood vessel health throughout the body.
Negative regulation of intestinal phytosterol absorption is not an isolated intestinal event; it is integrated with systemic lipid and lipoprotein metabolism. Plant stanol ester consumption alters LDL receptor and HMG-CoA reductase expression in circulating mononuclear cells, indicating that intestinal sterol absorption signals are transmitted to peripheral tissues. Increased cholesterol absorption is associated with in-stent restenosis after coronary stenting, providing a direct link between intestinal sterol uptake and a vascular clinical outcome. In Atlantic salmon, dietary cholesterol suppresses the cholesterol synthesis pathway and induces bile acid production, illustrating conserved feedback between absorption and synthesis across vertebrates. These findings support the view that GO:0010949 is a node in a multi-tissue regulatory network.
Key Genes Involved in GO:0010949 negative regulation of intestinal phytosterol absorption
The following genes and proteins have been experimentally linked to intestinal sterol absorption, cholesterol homeostasis, or the systemic response to plant sterols and stanols in the cited literature.
| Gene | Major Role | Research Relevance |
|---|---|---|
| LDLR | LDL receptor; mediates uptake of LDL cholesterol from circulation | Plant stanol esters alter LDLR mRNA and protein expression in mononuclear blood cells |
| HMGCR | Rate-limiting enzyme of cholesterol synthesis | Plant stanol esters alter HMGCR mRNA expression in blood cells |
| CYP7A1 | Cholesterol 7-alpha-hydroxylase; initiates bile acid synthesis | Dietary cholesterol induces bile acid production in Atlantic salmon |
| ABCG5 | Sterol efflux transporter in intestine and liver | General sterol absorption pathway component; relevant to phytosterol handling |
| ABCG8 | Sterol efflux transporter partnering with ABCG5 | General sterol absorption pathway component; relevant to phytosterol handling |
| NPC1L1 | Intestinal cholesterol and phytosterol uptake transporter | Central to intestinal sterol absorption; target of negative regulation |
| SREBF2 | Sterol regulatory element-binding transcription factor 2 | Master regulator of cholesterol synthesis genes; feedback-controlled by sterol status |
| INSIG1 | Insulin-induced gene 1; regulates SREBP processing | Part of sterol-sensing feedback control of synthesis |
| INSIG2 | Insulin-induced gene 2; regulates SREBP processing | Part of sterol-sensing feedback control of synthesis |
| HMGCS1 | HMG-CoA synthase 1; cholesterol synthesis enzyme | Suppressed by dietary cholesterol in Atlantic salmon |
| MVK | Mevalonate kinase; cholesterol synthesis enzyme | Part of the complete cholesterol synthesis pathway suppressed by dietary cholesterol |
| PMVK | Phosphomevalonate kinase; cholesterol synthesis enzyme | Part of the complete cholesterol synthesis pathway suppressed by dietary cholesterol |
| MVD | Mevalonate diphosphate decarboxylase; cholesterol synthesis enzyme | Part of the complete cholesterol synthesis pathway suppressed by dietary cholesterol |
| FDPS | Farnesyl diphosphate synthase; cholesterol synthesis enzyme | Part of the complete cholesterol synthesis pathway suppressed by dietary cholesterol |
| SQLE | Squalene epoxidase; cholesterol synthesis enzyme | Part of the complete cholesterol synthesis pathway suppressed by dietary cholesterol |
| LSS | Lanosterol synthase; cholesterol synthesis enzyme | Part of the complete cholesterol synthesis pathway suppressed by dietary cholesterol |
| DHCR7 | 7-dehydrocholesterol reductase; final cholesterol synthesis enzyme | Part of the complete cholesterol synthesis pathway suppressed by dietary cholesterol |
How Is negative regulation of intestinal phytosterol absorption Regulated?
The negative regulation of intestinal phytosterol absorption is controlled by feedback loops that sense sterol status and adjust synthesis, uptake, and bile acid production. In Atlantic salmon, dietary cholesterol supplementation suppressed the complete pathway of cholesterol synthesis and induced bile acid production, demonstrating that sterol input can shut down endogenous synthesis and increase sterol elimination. In humans, plant stanol esters alter LDL receptor and HMG-CoA reductase mRNA and protein expression in mononuclear blood cells, indicating that dietary phytosterols can modulate systemic cholesterol-regulatory genes. Dietary calcium and magnesium enhance the cholesterol-lowering effect of plant sterols in obese Zucker rats, showing that additional nutritional factors can tune the negative regulation of sterol absorption. Increased cholesterol absorption has been associated with in-stent restenosis after coronary stenting, suggesting that dysregulation of these feedback mechanisms may have clinical consequences.
negative regulation of intestinal phytosterol absorption and Human Disease
| Gene | Disease / Biology | Potential Experimental Model |
|---|---|---|
| LDLR | Hypercholesterolemia; LDL clearance | Hepatic or intestinal cell line with LDLR knockout or overexpression |
| HMGCR | Cholesterol synthesis; statin response | Cell line with HMGCR point mutation or knockout |
| CYP7A1 | Bile acid synthesis; cholesterol elimination | Hepatocyte model with CYP7A1 knockout or overexpression |
| ABCG5/ABCG8 | Sitosterolemia; phytosterol accumulation | Intestinal organoid or cell line with ABCG5/ABCG8 knockout |
| NPC1L1 | Intestinal cholesterol and phytosterol uptake | Enterocyte-like cell line with NPC1L1 knockout or knockdown |
Cardiovascular Disease and In-Stent Restenosis
Intestinal sterol absorption is clinically relevant to cardiovascular disease. Increased cholesterol absorption is associated with in-stent restenosis after stent implantation for stable coronary artery disease, linking the efficiency of intestinal sterol uptake to a vascular complication. Plant sterols and stanols lower cholesterol in part by competing with cholesterol for absorption, and plant stanol esters alter LDL receptor and HMG-CoA reductase expression in blood cells. These findings suggest that the negative regulation of intestinal phytosterol absorption is a modifiable process with potential impact on cardiovascular outcomes.
Hypercholesterolemia and Lipid Management
The negative regulation of intestinal phytosterol absorption is directly relevant to hypercholesterolemia management. Diet enrichment with calcium and magnesium enhances the cholesterol-lowering effect of plant sterols in obese Zucker rats, indicating that nutritional modulation of sterol absorption can improve lipid profiles. Plant stanol esters affect LDL receptor protein expression and LDL receptor and HMG-CoA reductase mRNA expression in healthy men and women, showing that dietary phytosterols engage the same pathways targeted by lipid-lowering strategies. Dietary cholesterol supplementation suppresses the complete cholesterol synthesis pathway and induces bile acid production in Atlantic salmon, illustrating the feedback plasticity of sterol handling.
Metabolic and Nutritional Disorders
Altered sterol absorption is relevant to metabolic and nutritional disorders. In obese Zucker rats, the cholesterol-lowering effect of plant sterols is enhanced by dietary calcium and magnesium, suggesting that mineral status interacts with sterol absorption in obesity. Dietary cholesterol supplementation in Atlantic salmon suppresses the complete pathway of cholesterol synthesis and induces bile acid production, demonstrating that sterol absorption and synthesis are reciprocally regulated in response to nutritional input. These observations support the study of GO:0010949 in the context of metabolic syndrome and diet-responsive lipid disorders.
From negative regulation of intestinal phytosterol absorption-Related Genes to Experimental Models
| Research Question | Suitable Model |
|---|---|
| Does loss of a candidate transporter increase phytosterol absorption? | Knockout cell model (e.g., NPC1L1, ABCG5, or ABCG8 knockout) |
| Does a specific point mutation alter sterol transport activity? | Point-mutation knock-in cell model in a sterol transporter gene |
| Can a regulatory element be tagged to track sterol-responsive gene expression? | Tagged knock-in of a cholesterol synthesis gene such as HMGCR |
| Does overexpression of a candidate gene reduce phytosterol uptake? | Overexpression cell model for LDLR, ABCG5, or ABCG8 |
| Which genes mediate the cholesterol-lowering effect of plant stanols? | CRISPR library screening in intestinal or hepatic cell models |
| How does dietary cholesterol feedback affect the entire synthesis pathway? | RNA-seq or targeted expression panel in a cell or animal model |
How to Study the negative regulation of intestinal phytosterol absorption Process
| Method | What It Measures | Typical Application |
|---|---|---|
| Sterol uptake assay | Amount of phytosterol or cholesterol absorbed by cells | Testing candidate genes in intestinal cell models |
| RNA-seq | Transcriptome-wide gene expression changes | Mapping feedback suppression of cholesterol synthesis genes |
| qPCR | Expression of specific sterol genes | Measuring LDLR and HMGCR mRNA after plant stanol treatment |
| Western blot | Protein abundance of sterol transporters or receptors | Validating LDLR protein changes in blood cells |
| CRISPR knockout | Loss-of-function effect on sterol absorption | Testing NPC1L1, ABCG5, or ABCG8 function |
| CRISPR overexpression | Gain-of-function effect on sterol absorption | Testing whether LDLR overexpression reduces uptake |
| CRISPR library screening | Genome-wide identification of regulators | Discovering new negative regulators of phytosterol absorption |
| Lipid profiling | Circulating or cellular sterol levels | Linking absorption to clinical outcomes such as restenosis |
Sterol Absorption Assays
Measuring intestinal phytosterol absorption is central to studying GO:0010949. Experimental systems can use labeled sterols or plant stanol esters to quantify uptake across intestinal cell monolayers or in animal models. Plant stanol ester studies in humans have used blood cell gene expression as a readout of systemic sterol handling, providing a bridge between intestinal absorption and peripheral markers. In animal models, diet enrichment with calcium and magnesium has been used to test whether the cholesterol-lowering effect of plant sterols can be enhanced, offering a template for absorption-focused experiments.
Gene Expression Analysis
RNA-level analysis of cholesterol synthesis and uptake genes is a key method for studying the negative regulation of intestinal phytosterol absorption. Plant stanol esters alter LDL receptor and HMG-CoA reductase mRNA expression in mononuclear blood cells of healthy men and women, demonstrating the utility of expression profiling in this field. In Atlantic salmon, dietary cholesterol supplementation suppressed the complete pathway of cholesterol synthesis and induced bile acid production, an effect that can be mapped by transcriptomic analysis of synthesis and bile acid genes. These approaches allow researchers to connect intestinal sterol exposure to downstream gene regulatory networks.
Protein and Lipid Profiling
Protein-level and lipid-level measurements complement gene expression studies of GO:0010949. Plant stanol esters affect LDL receptor protein expression in mononuclear blood cells, showing that protein quantification is needed to capture functional changes. Cholesterol absorption efficiency has been associated with clinical outcomes such as in-stent restenosis, indicating that lipid profiling and clinical endpoints can be integrated into mechanistic studies. In animal models, bile acid production can be measured as a functional output of sterol feedback regulation.
CRISPR-Based Functional Genomics
CRISPR-based perturbation is a powerful approach to identify genes that negatively regulate intestinal phytosterol absorption. Knockout of candidate transporters such as NPC1L1, ABCG5, or ABCG8 can test their role in sterol uptake. Overexpression of LDLR or other sterol-responsive genes can test whether increased expression reduces phytosterol absorption. CRISPR library screening in intestinal or hepatic cell models can uncover novel regulators of the pathway, and bioinformatic analysis can prioritize hits for follow-up.
How CRISPR Can Be Used to Study GO:0010949 negative regulation of intestinal phytosterol absorption
Knockout
CRISPR knockout of candidate sterol transporters such as NPC1L1, ABCG5, or ABCG8 can test whether loss of function increases or decreases intestinal phytosterol absorption. Knockout models are useful for establishing causality between a gene and the negative regulation of phytosterol uptake. In the context of cholesterol synthesis, knockout of genes in the mevalonate pathway can reveal how loss of endogenous synthesis affects sterol absorption feedback.
Point Mutation
Point-mutation knock-in models can dissect the specific residues or regulatory sites required for sterol transporter function or for feedback control of cholesterol synthesis genes. For example, mutations in transporter genes can distinguish transport-defective alleles from regulatory variants. Point mutations in HMGCR or LDLR can also model clinically relevant variants that affect sterol handling.
Knock-in
Knock-in of tagged or reporter alleles allows tracking of sterol-responsive gene expression and protein localization in intestinal cells. Tagged knock-in of LDLR or HMGCR can be used to monitor protein levels and turnover in response to plant stanols or cholesterol loading. Knock-in of regulatory elements can help map the feedback response to dietary sterols.
Overexpression
Overexpression of candidate genes such as LDLR, ABCG5, or ABCG8 can test whether increased activity reduces intestinal phytosterol absorption. Overexpression models are particularly useful for gain-of-function studies where the goal is to enhance the negative regulation of sterol uptake. Combining overexpression with sterol uptake assays provides a direct readout of the pathway.
How EDITGENE Supports negative regulation of intestinal phytosterol absorption Research
Researchers studying negative regulation of intestinal phytosterol absorption-related genes often need to determine whether a candidate gene is causally involved in limiting phytosterol uptake, whether a specific variant alters transporter function, or whether overexpression of a protective gene reduces sterol absorption. Answering these questions requires precise, reproducible cell models that can be perturbed at the genomic level and interrogated with functional assays.
Contact EDITGENE today to design your custom CRISPR model for negative regulation of intestinal phytosterol absorption research.
Frequently Asked Questions About negative regulation of intestinal phytosterol absorption
What is GO:0010949?
GO:0010949 is the Gene Ontology biological process term for negative regulation of intestinal phytosterol absorption, defined as any process that stops, prevents, or reduces the frequency, rate or extent of phytosterol movement into the blood by absorption from the small intestine.
What does negative regulation of intestinal phytosterol absorption mean in simple terms?
It means the body has ways to reduce how much plant sterol is taken up from the gut into the bloodstream, often through competition with cholesterol or feedback control of sterol genes.
What genes are involved in intestinal phytosterol absorption?
Genes experimentally linked to this process include LDLR, HMGCR, CYP7A1, ABCG5, ABCG8, NPC1L1, and cholesterol synthesis genes such as HMGCS1, MVK, PMVK, MVD, FDPS, SQLE, LSS, and DHCR7.
How do plant sterols and stanols lower cholesterol?
Plant sterols and stanols compete with cholesterol for intestinal absorption and can alter expression of LDL receptor and HMG-CoA reductase, thereby reducing circulating cholesterol.
Is increased cholesterol absorption linked to heart disease?
Yes, increased cholesterol absorption has been associated with in-stent restenosis after stent implantation for stable coronary artery disease.
How does dietary cholesterol affect cholesterol synthesis?
In Atlantic salmon, dietary cholesterol supplementation suppressed the complete pathway of cholesterol synthesis and induced bile acid production, showing feedback regulation.
Can diet enhance the cholesterol-lowering effect of plant sterols?
In obese Zucker rats, diet enrichment with calcium and magnesium enhanced the cholesterol-lowering effect of plant sterols.
What research methods are used to study GO:0010949?
Common methods include sterol uptake assays, RNA-seq, qPCR, Western blot, CRISPR knockout, overexpression, CRISPR library screening, and lipid profiling.
What CRISPR models are useful for studying phytosterol absorption?
Knockout, point-mutation, knock-in, and overexpression models of genes such as NPC1L1, ABCG5, ABCG8, LDLR, and HMGCR are useful for testing causal roles in sterol absorption.
Why is GO:0010949 important for drug discovery?
It identifies the biological processes that limit intestinal phytosterol uptake, which can be targeted to lower cholesterol and potentially reduce cardiovascular complications such as restenosis.
Conclusion
GO:0010949, negative regulation of intestinal phytosterol absorption, provides a precise framework for studying how the body limits the entry of plant sterols into the bloodstream. Experimental evidence shows that this process involves competition between phytosterols and cholesterol, feedback control of cholesterol synthesis and bile acid production, and modulation of genes such as LDLR and HMGCR. Clinically, increased cholesterol absorption has been linked to in-stent restenosis, and dietary plant stanols can alter systemic lipid gene expression, underscoring the translational relevance of this pathway. By combining functional assays with CRISPR-based models, researchers can identify and validate the genes that negatively regulate intestinal phytosterol absorption, opening new avenues for nutritional and therapeutic intervention.
References
- 1. Otto S et al.. 2022. Increased cholesterol absorption is associated with In-stent-restenosis after stent implantation for stable coronary artery disease.. Steroids 187:109079 PMID: 35835203
- 2. Kortner TM et al.. 2014. Dietary cholesterol supplementation to a plant-based diet suppresses the complete pathway of cholesterol synthesis and induces bile acid production in Atlantic salmon (Salmo salar L.).. Br J Nutr 111(12):2089-103 PMID: 24635969
- 3. Vaskonen T et al.. 2001. Diet enrichment with calcium and magnesium enhances the cholesterol-lowering effect of plant sterols in obese Zucker rats.. Nutr Metab Cardiovasc Dis 11(3):158-67 PMID: 11590991
- 4. Plat J et al.. 2002. Effects of plant stanol esters on LDL receptor protein expression and on LDL receptor and HMG-CoA reductase mRNA expression in mononuclear blood cells of healthy men and women.. FASEB J 16(2):258-60 PMID: 11772951
