Acetic acid, CH3COOH, is thought to be the primary compound responsible for weight loss in an apple cider vinegar diet. Two studies done in Japan by the Central Research Institute of the Mizkan Group state that acetic acid in vinegar may have the ability to reduce fatty acid deposits in rats and humans at a genetic level. Mizkan researchers noted an activity increase in the PPAR-alpha after vinegar was ingested. The
PPAR-alpha is an organelle, functioning like a small organ inside the body's cells, eliminating toxins and releasing enzymes that oxidize fatty acids and stimulate the burning of calories.
Study on Lecithin for Heart-Health
Researchers from the Washington University School of Medicine in St. Louis, MO, reported in the August, 2009 issue of Cell that they may have found a connection between lecithin and the protein PPAR-alpha. PPAR-alpha is a protein in the liver that works to metabolize lipids and glucose. When PPAR-alpha is not functioning properly and bad cholesterol and triglyceride levels rise, doctors prescribe drugs called fibrates to provoke PPAR-alpha to work properly. However, the study found that lecithin may actually be able to replace fibrates to provoke PPAR-alpha into working without the side-effects of prescription drugs.
The study used specially created mice that were unable to create fatty acid synthase in the liver. Fatty acid synthase converts the sugars we eat into fatty acids which play a part in energy metabolism. The researchers were surprised to find that the mice without fatty acid synthase were exactly like those that couldn’t produce PPAR-alpha. When given fibrates, the mice returned to normal, leaving researchers to believe that fatty acid synthase was connected to activating PPAR-alpha. From this research they found that phosphatidylcholine, a compound of lecithin, works to bind with PPAR-alpha to activate it so the body can effectively metabolize lipids and glucose. The effective metabolizing of lipids and glucose helps reduce the amount of fats in the blood which can lead to heart disease and diabetes.
PPARalpha as a mediator of androgen effects on T cell autoimmunity. We are interested in how male sex hormones act to limit the activity of auto-aggressive T cells in EAE. We have found that androgens suppress the production of pro-inflammatory cytokines by these cells. We have also made the discovery that the nuclear receptor peroxisome proliferator-activated receptor alpha (PPARalpha) is expressed at higher levels in male as compared to female T helper cells and that the expression of this molecule is sensitive to the levels of androgens. Our studies also indicate that the activity of PPARalpha controls the development of T helper 1 inflammation selectively in male mice during EAE. Our current research effort is directed towards understanding the mechanism of how this molecule and other PPAR molecules may limit the development of autoimmunity.
Br J Dermatol. 2003 Aug;149(2):229-36. Related Articles, Links
Peroxisome proliferator-activated receptors in cutaneous biology.
Kuenzli S, Saurat JH.
Department of Dermatology, University Hospital, Geneva, Switzerland.
Peroxisome proliferator-activated receptors (PPARs) are ligand-activated transcription factors that regulate the expression of target genes involved in many cellular functions including cell proliferation, differentiation and immune/inflammation response. The PPAR subfamily consists of three isotypes: PPAR alpha, PPAR beta/delta and PPAR gamma, which have all been identified in keratinocytes. PPAR beta/delta is the predominant subtype in human keratinocytes, whereas PPAR alpha and PPAR gamma are expressed at much lower levels and increase significantly upon keratinocyte differentiation. PPAR beta/delta is not linked to differentiation, but is significantly upregulated upon various conditions that result in keratinocyte proliferation, and during skin wound healing. In vitro and in vivo evidence suggests that PPARs appear to play an important role in skin barrier permeability, inhibiting epidermal cell growth, promoting epidermal terminal differentiation and regulating skin inflammatory response by diverse mechanisms. These proprieties are pointing in the direction of PPARs being key regulators of skin conditions characterized by hyperproliferation, inflammatory infiltrates and aberrant differentiation such as psoriasis, but may also have clinical implications in inflammatory skin disease (e.g. atopic dermatitis), proliferative skin disease, wound healing, acne and protease inhibitor associated lipodystrophia.
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Peroxisome proliferator-activated receptors in inflammation control
P Delerive, JC Fruchart, and B Staels
Peroxisome proliferator-activated receptors (PPARs) are ligand-activated transcription factors belonging to the nuclear receptor superfamily. PPARalpha is highly expressed in liver, skeletal muscle, kidney, heart and the vascular wall. PPARgamma is predominantly detected in adipose tissue, intestine and macrophages. PPARs are activated by fatty-acid derivatives and pharmacological agents such as fibrates and glitazones which are specific for PPARalpha and PPARgamma respectively. PPARs regulate lipid and lipoprotein metabolism, glucose homeostasis, cell proliferation and differentiation, and apoptosis. PPARalpha controls intra- and extracellular lipid metabolisms whereas PPARgamma triggers adipocyte differentiation and promotes lipid storage. In addition, PPARs also modulate the inflammatory response. PPAR activators have been shown to exert anti-inflammatory activities in various cell types by inhibiting the expression of proinflammatory genes such as cytokines, metalloproteases and acute-phase proteins. PPARs negatively regulate the transcription of inflammatory response genes by antagonizing the AP-1, nuclear factor-kappaB (NF-kappaB), signal transducer and activator of transcription and nuclear factor of activated T-cells signalling pathways and by stimulating the catabolism of proinflammatory eicosanoids. These recent findings indicate a modulatory role for PPARs in inflammation with potential therapeutical applications in chronic inflammatory diseases.
