Summary of PPARA
PPAR alpha is a very important protein for metabolizing fat and glucose, which helps with weight loss. It alters the expression of a large number of genes. It's important for energy production.
Mice lacking PPAR-alpha have an impaired response to fasting, including low levels of ketone bodies, hypoglycemia, and fatty liver. PPAR-alpha increases bile synthesis/secretion (R).
PPAR alpha inhibits inflammation and animal models of autoimmune conditions such as Multiple Sclerosis (R). PPAR-a can help increase IGF-1, which will help you build muscle (R).
PPAR-alpha is a protein (transcription factor) that increases fat breakdown in the liver and elsewhere. Good metabolism is important for energy production.
PPAR-alpha alters the expression of a large number of genes. PPAR-alpha is activated under conditions of calorie restriction and is necessary for the process of ketogenesis, a key adaptive response to prolonged fasting .
PPAR-alpha is mainly found in the liver and brown fat, followed by the heart and kidney. Lower PPAR-alpha expression levels are found in the small and large intestine, muscle and adrenal gland.
Activation of PPAR-alpha promotes uptake, utilization, and breakdown of fatty acids by increasing genes involved in fatty acid transport, binding, activation, and oxidation.
Mice lacking PPAR-alpha have an impaired response to fasting, characterized by major metabolic disturbances including low levels of ketone bodies, hypoglycemia, and fatty liver. PPAR-alpha is at the core of fat utilization, as well glucose production and bile synthesis/secretion (R).
PPAR alpha inhibits animal models of autoimmune conditions such as MS (R). PPAR alpha is protective against heart disease by inhibiting macrophage inflammation and increasing cholesterol efflux (via LXR and ABCA1) (R).
Read: About PPAR Alpha and Natural Ways To Activate It.
Protein names
Recommended name:
Peroxisome proliferator-activated receptor alphaAlternative name(s):
PPAR-alphaNuclear receptor subfamily 1 group C member 1
- RS135551 (PPARA) ??
- RS1800206 (PPARA) ??
- RS4253623 (PPARA) ??
- RS4253655 (PPARA) ??
- RS4253728 (PPARA) ??
- RS4253772 (PPARA) ??
- RS4823613 (PPARA) ??
- RS9615264 (PPARA) ??
To see your genotype, you should be logged in and have a file with your genotype uploaded.
Top Gene-Substance Interactions
PPARA Interacts with These Diseases
| Disease | Score |
Fixes
Omega-6/Linoleic acid metabolites/Arachidonic acid, as well as other polyunsaturated fatty acids, are the main ways we naturally activate PPAR alpha (R). This is probably why omega-6's have some benefits in various studies.
It's good to get a good balance of DHA/EPA, MUFAs and Omega 6's, with some saturated fat (not excess like some paleo recommends). PPAR alpha is also stimulated by stress, cortisol, and insulin (R).
PPARa is activated by oleylethanolamide, a naturally occurring lipid that regulates satiety.
My favorite ways to increase PPAR-alpha:
- Cold (R)
- Exercise (R),
- Fasting (R) - fasting increases SIRT1 via activation of PPAR-alpha in mice (R).
- Fish oil/DHA (R),
- Hydroxytyrosol (R),
- Cinnamon (R)
Other ways to increase PPAR-alpha:
Substances That Increase PPARA
| Substances | Interaction | Organism | Category |
Substances That Decrease PPARA
| Substances | Interaction | Organism | Category |
Advanced Summary
May be required for the propagation of clock information to metabolic pathways regulated by PER2.
PPAR-a inhibits COX2 (R). PPAR-a can help increase IGF-1, which will help you build muscle. Mice without PPAR-alpha have 40% less IGF-1 (R). Mice without PPAR alpha have 20X less UCP-3 (R), which is important for fat loss. This and other mechanisms make PPAR alpha important for fat loss. PPAR-a causes insulin resistance in the liver (R).
Conditions with Increased Gene Activity
| Condition | Change (log2fold) | Comparison | Species | Experimental variables | Experiment name |
|---|
Conditions with Decreased Gene Activity
| Condition | Change (log2fold) | Comparison | Species | Experimental variables | Experiment name |
|---|
Technical
The following transcription factors affect gene expression:
- PPAR-alpha
- PPAR-gamma1
- PPAR-gamma2
- ER-alpha
- C/EBPalpha
- HNF-4alpha2
- HNF-4alpha1
- STAT5B
- AP-1
- c-Jun
- PGC-1alpha
- SIRT1
- RXR-alpha
Tissue specificity:
Skeletal muscle, liver, heart and kidney.
Gene Pathways:
Molecular Function:
- Rna Polymerase Ii Core Promoter Proximal Region Sequence-Specific Dna Binding
- Transcriptional Activator Activity, Rna Polymerase Ii Core Promoter Proximal Region Sequence-Specific Binding
- Transcriptional Repressor Activity, Rna Polymerase Ii Core Promoter Proximal Region Sequence-Specific Binding
- Rna Polymerase Ii Repressing Transcription Factor Binding
- Transcriptional Activator Activity, Rna Polymerase Ii Transcription Factor Binding
- Dna Binding
- Transcription Factor Activity, Sequence-Specific Dna Binding
- Steroid Hormone Receptor Activity
- Rna Polymerase Ii Transcription Factor Activity, Ligand-Activated Sequence-Specific Dna Binding
- Transcription Factor Binding
- Drug Binding
- Zinc Ion Binding
- Lipid Binding
- Ubiquitin Conjugating Enzyme Binding
- Sequence-Specific Dna Binding
Biological Processes:
- Negative Regulation Of Transcription From Rna Polymerase Ii Promoter
- Response To Hypoxia
- Transcription Initiation From Rna Polymerase Ii Promoter
- Lipid Metabolic Process
- Fatty Acid Metabolic Process
- Heart Development
- Epidermis Development
- Negative Regulation Of Macrophage Derived Foam Cell Differentiation
- Negative Regulation Of Receptor Biosynthetic Process
- Negative Regulation Of Cholesterol Storage
- Negative Regulation Of Sequestering Of Triglyceride
- Fatty Acid Transport
- Positive Regulation Of Fatty Acid Beta-Oxidation
- Negative Regulation Of Appetite
- Response To Insulin
- Circadian Regulation Of Gene Expression
- Behavioral Response To Nicotine
- Wound Healing
- Lipoprotein Metabolic Process
- Regulation Of Circadian Rhythm
- Cellular Lipid Metabolic Process
- Positive Regulation Of Gluconeogenesis
- Negative Regulation Of Blood Pressure
- Negative Regulation Of Glycolytic Process
- Positive Regulation Of Transcription, Dna-Templated
- Positive Regulation Of Transcription From Rna Polymerase Ii Promoter
- Positive Regulation Of Fatty Acid Oxidation
- Negative Regulation Of Inflammatory Response
- Enamel Mineralization
- Regulation Of Glycolytic Process By Positive Regulation Of Transcription From Rna Polymerase Ii Promoter
- Regulation Of Cellular Ketone Metabolic Process By Positive Regulation Of Transcription From Rna Polymerase Ii Promoter
- Regulation Of Lipid Transport By Positive Regulation Of Transcription From Rna Polymerase Ii Promoter
- Negative Regulation Of Neuron Death
- Negative Regulation Of Pri-Mirna Transcription From Rna Polymerase Ii Promoter
- Negative Regulation Of Leukocyte Cell-Cell Adhesion
- Negative Regulation Of Transcription Regulatory Region Dna Binding