Activation of peroxisome proliferator-activated receptor (PPAR) <mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mi>&#x03B1;</mml:mi></mml:math>, <mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mi>&#x03B4;</mml:mi></mml:math>, and <mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mi>&#x03B3;</mml:mi></mml:math> subtypes increases expression of genes involved in fatty acid transport and oxidation and alters adiposity in animal models of obesity and type-2 diabetes. PPARpan agonists which activate all three receptor subtypes have antidiabetic activity in animal models without the weight gain associated with selective PPAR<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mi>&#x03B3;</mml:mi></mml:math> agonists. Herein we report the effects of selective PPAR agonists (GW9578, a PPAR<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mi>&#x03B1;</mml:mi></mml:math> agonist, GW0742,  a PPAR<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mi>&#x03B4;</mml:mi></mml:math> agonist, GW7845, a PPAR<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mi>&#x03B3;</mml:mi></mml:math> agonist), combination of PPAR<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mi>&#x03B1;</mml:mi></mml:math> and <mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mi>&#x03B4;</mml:mi></mml:math> agonists, and PPARpan (PPAR<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mrow><mml:mi>&#x03B1;</mml:mi><mml:mo>/</mml:mo><mml:mi>&#x03B3;</mml:mi><mml:mo>/</mml:mo><mml:mi>&#x03B4;</mml:mi></mml:mrow></mml:math>) activators (GW4148 or GW9135) on body weight (BW), body composition, food consumption, fatty acid oxidation, and serum chemistry of diet-induced obese AKR/J mice.  PPAR<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mi>&#x03B1;</mml:mi></mml:math> or PPAR<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mi>&#x03B4;</mml:mi></mml:math> agonist treatment induced a slight decrease in fat mass (FM) while a PPAR<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mi>&#x03B3;</mml:mi></mml:math> agonist increased BW and FM commensurate with increased food consumption. The reduction in BW and food intake after cotreatment with PPAR<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mi>&#x03B1;</mml:mi></mml:math> and <mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mi>&#x03B4;</mml:mi></mml:math> agonists appeared to be synergistic. GW4148, a PPARpan agonist, induced a significant and sustained reduction in BW and FM similar to an efficacious dose of rimonabant, an antiobesity compound.  GW9135, a PPARpan agonist with weak activity at PPAR<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mi>&#x03B4;</mml:mi></mml:math>, induced weight loss initially followed by rebound weight gain reaching vehicle control levels by the end of the experiment. We conclude that PPAR<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mi>&#x03B1;</mml:mi></mml:math> and PPAR<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mi>&#x03B4;</mml:mi></mml:math> activations are critical to effective weight loss induction. These results suggest that the PPARpan compounds may be expected to maintain the beneficial insulin sensitization effects of a PPAR<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mi>&#x03B3;</mml:mi></mml:math> agonist while either maintaining weight or producing weight loss.

W. Wallace Harrington

Christy S. Britt

Joan G. Wilson

Naphtali O. Milliken

Jane G. Binz

David C. Lobe

William R. Oliver

Michael C. Lewis

Diane M. Ignar

The Effect of PPAR<svg style="vertical-align:-0.1638pt" height="7.9499998" version="1.1" viewBox="0 0 9.7749996 7.9499998" width="9.7749996" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg"><g transform="matrix(.017,-0,0,-.017,.062,7.675)"><path id="x1D6FC" d="M545 106q-67 -118 -134 -118q-24 0 -40 37.5t-30 129.5h-2q-47 -72 -103 -119.5t-108 -47.5q-47 0 -76 45.5t-29 119.5q0 113 85 204t174 91q47 0 70 -33.5t43 -119.5h3q32 47 80 140l55 13l10 -9q-47 -80 -138 -201q17 -99 27.5 -136t22.5 -37q23 0 69 61zM333 204&#xA;q-14 98 -31 149.5t-50 51.5q-49 0 -94 -70t-45 -164q0 -55 15.5 -86t40.5 -31q70 0 164 150z" /></g></svg>, PPAR<svg style="vertical-align:-0.1638pt" height="12.4375" version="1.1" viewBox="0 0 8.9125004 12.4375" width="8.9125004" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg"><g transform="matrix(.017,-0,0,-.017,.062,12.162)"><path id="x1D6FF" d="M494 514l-10 -15q-56 76 -106.5 117t-110.5 41q-45 0 -45 -30q0 -28 109 -152q59 -68 86 -118.5t27 -107.5q0 -62 -29.5 -119.5t-86.5 -96.5q-64 -45 -138 -45q-76 0 -121.5 53t-45.5 136q0 74 40.5 135t98.5 95q43 26 87 42q-40 59 -57.5 92t-17.5 62q0 46 39 77.5&#xA;t90 31.5q54 0 97.5 -35.5t65 -78.5t28.5 -84zM359 234q0 84 -90 191q-47 -17 -74 -47q-81 -89 -81 -200q0 -71 32.5 -109.5t72.5 -38.5q47 0 80 33t46.5 77.5t13.5 93.5z" /></g></svg>, PPAR<svg style="vertical-align:-3.56265pt" height="12.175" version="1.1" viewBox="0 0 8.6374998 12.175" width="8.6374998" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg"><g transform="matrix(.017,-0,0,-.017,.062,7.675)"><path id="x1D6FE" d="M478 372q0 -39 -31 -97t-61 -98t-78 -98q-45 -55 -73 -102q-13 -79 -13 -197q-11 -11 -43.5 -25.5t-53.5 -15.5l-15 17q5 35 26 101.5t47 123.5q8 72 -1.5 174.5t-37.5 178.5q-14 37 -29 37q-20 0 -67 -65l-25 21q37 60 73 90.5t63 30.5q47 0 72 -112q13 -56 17.5 -141.5&#xA;t0.5 -143.5h2q155 193 155 297q0 26 -12 47q-5 8 -5 15q0 16 12.5 27t29.5 11q21 0 34 -21t13 -55z" /></g></svg>, and PPARpan Agonists on Body Weight, 
Body Mass, and Serum Lipid Profiles in Diet-Induced Obese AKR/J Mice

Francine M. Gregoire

Sander Kersten

Wallace Harrington

PPARS and Obesity

The increasing prevalence of obesity is a fundamental contributor to the growing prevalence of the metabolic syndrome. Rexinoids, a class of compounds that selectively bind and activate RXR, are being studied as a potential option for the treatment of metabolic syndrome. These compounds have glucose-lowering, insulin-sensitizing, and antiobesity effects in animal models of insulin resistance and type 2 diabetes. However, undesirable side effects such as hypertriglyceridemia and suppression of the thyroid hormone axis also occur. This review examines and compares the effects of four RXR-selective ligands: LGD1069, LG100268, AGN194204, and LG101506, a selective RXR modulator. Similar to selective modulators of other nuclear receptors such as the estrogen receptor (SERMs), LG101506 binding to RXR selectively maintains the desirable characteristic effects of rexinoids while minimizing the undesirable effects. These recent findings suggest that, with continued research efforts, RXR-specific ligands with improved pharmacological profiles may eventually be available as additional treatment options for the current epidemic of obesity, insulin resistance, type 2 diabetes, and all of the associated metabolic sequelae.

Jane A. Pinaire

Anne  Reifel-Miller

Therapeutic Potential of Retinoid X Receptor Modulators for the Treatment of the Metabolic Syndrome

At a time when the twin epidemics of obesity and type 2 diabetes threaten to engulf even the most well-resourced Western healthcare systems, the nuclear receptor peroxisome proliferator-activated receptor <mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mi>&#x03B3;</mml:mi></mml:math> (PPAR<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mi>&#x03B3;</mml:mi></mml:math>) has emerged as a <em>bona fide</em> therapeutic target for treating human metabolic disease. The novel insulin-sensitizing antidiabetic thiazolidinediones (TZDs, e.g., rosiglitazone, pioglitazone), which are licensed for use in the treatment of type 2 diabetes, are high-affinity PPAR<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mi>&#x03B3;</mml:mi></mml:math> ligands, whose beneficial effects extend beyond improvement in glycaemic control to include amelioration of dyslipidaemia, lowering of blood pressure, and favourable modulation of macrophage lipid handling and inflammatory responses. However, a major drawback to the clinical use of exisiting TZDs is weight gain, reflecting both enhanced adipogenesis and fluid retention, neither of which is desirable in a population that is already overweight and prone to cardiovascular disease. Accordingly, the &#8216;&#8216;search is on&#8217;&#8217; to identify the next generation of PPAR<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mi>&#x03B3;</mml:mi></mml:math> modulators that will promote maximal clinical benefit by targeting specific facets of the metabolic syndrome (glucose intolerance/diabetes, dyslipidaemia, and hypertension), while simultaneously avoiding undesirable side effects of PPAR<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mi>&#x03B3;</mml:mi></mml:math> activation (e.g., weight gain). This paper outlines the important clinical and laboratory observations made in human subjects harboring genetic variations in PPAR<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mi>&#x03B3;</mml:mi></mml:math> that support such a therapeutic strategy.

Mark  Gurnell

&#x2018;Striking the Right Balance&#x2019; in Targeting PPAR<svg style="vertical-align:-3.56265pt" height="12.175" version="1.1" viewBox="0 0 8.6374998 12.175" width="8.6374998" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg"><g transform="matrix(.017,-0,0,-.017,.062,7.675)"><path id="x1D6FE" d="M478 372q0 -39 -31 -97t-61 -98t-78 -98q-45 -55 -73 -102q-13 -79 -13 -197q-11 -11 -43.5 -25.5t-53.5 -15.5l-15 17q5 35 26 101.5t47 123.5q8 72 -1.5 174.5t-37.5 178.5q-14 37 -29 37q-20 0 -67 -65l-25 21q37 60 73 90.5t63 30.5q47 0 72 -112q13 -56 17.5 -141.5&#xA;t0.5 -143.5h2q155 193 155 297q0 26 -12 47q-5 8 -5 15q0 16 12.5 27t29.5 11q21 0 34 -21t13 -55z" /></g></svg> in the Metabolic Syndrome: Novel Insights from Human Genetic Studies

The interest in genetic manipulations of PPARs is as old as their discovery as receptors of ligands with beneficial clinical activities. Considering the effects of PPAR ligands on critical aspects of systemic physiology, including obesity, lipid metabolism, insulin resistance, and diabetes, gene knockout (KO) in mice is the ideal platform for both hypothesis testing and discovery of new PPAR functions in vivo. With the fervent pursuit of the magic bullet to eradicate the obesity epidemic, special emphasis has been placed on the impacts of PPARs on obesity and its associated diseases. As detailed in this review, understanding how PPARs regulate gene expression and basic metabolic pathways is a necessary intermediate en route to deciphering their effects on obesity. Over a decade and dozens of genetic modifications of PPARs into this effort, valuable lessons have been learned, but we are left with more questions to be answered. These lessons and future prospects are the subject of this review.

Yaacov Barak

Suyeon Kim

Genetic Manipulations of PPARs: Effects on Obesity and Metabolic Disease

Peroxisome proliferator-activated receptor <mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mi>&#x03B3;</mml:mi></mml:math> (PPAR-<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mi>&#x03B3;</mml:mi></mml:math>) is a key regulator of lipid metabolism and energy balance implicated in the development of insulin resistance and obesity.  The identification of putative natural and synthetic ligands and activators of PPAR-<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mi>&#x03B3;</mml:mi></mml:math> has helped to unravel the molecular basis of its function, including molecular details regarding ligand binding, conformational changes of the receptor, and cofactor binding, leading to  the emergence of the concept of selective PPAR-<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mi>&#x03B3;</mml:mi></mml:math> modulators (SPPAR<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mi>&#x03B3;</mml:mi></mml:math>Ms). SPPAR<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mi>&#x03B3;</mml:mi></mml:math>Ms bind in distinct manners to the ligand-binding pocket of PPAR-<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mi>&#x03B3;</mml:mi></mml:math>, leading to alternative receptor conformations, differential cofactor recruitment/displacement, differential gene expression, and ultimately differential biological responses.  Based on this concept, new and improved antidiabetic agents for the treatment of diabetes are in development.  This review summarizes the current knowledge on the mechanism of action and biological effects of recently characterized SPPAR<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mi>&#x03B3;</mml:mi></mml:math>Ms, including metaglidasen/halofenate, PA-082, and the angiotensin receptor antagonists, recently characterized as a new class of SPPAR<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mi>&#x03B3;</mml:mi></mml:math>Ms.

Fang  Zhang

Brian E. Lavan

Selective Modulators of PPAR-<svg style="vertical-align:-3.56265pt" height="12.175" version="1.1" viewBox="0 0 8.6374998 12.175" width="8.6374998" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg"><g transform="matrix(.017,-0,0,-.017,.062,7.675)"><path id="x1D6FE" d="M478 372q0 -39 -31 -97t-61 -98t-78 -98q-45 -55 -73 -102q-13 -79 -13 -197q-11 -11 -43.5 -25.5t-53.5 -15.5l-15 17q5 35 26 101.5t47 123.5q8 72 -1.5 174.5t-37.5 178.5q-14 37 -29 37q-20 0 -67 -65l-25 21q37 60 73 90.5t63 30.5q47 0 72 -112q13 -56 17.5 -141.5&#xA;t0.5 -143.5h2q155 193 155 297q0 26 -12 47q-5 8 -5 15q0 16 12.5 27t29.5 11q21 0 34 -21t13 -55z" /></g></svg> Activity: Molecular Aspects Related to Obesity and Side-Effects

Peroxisome proliferator-activated receptors (PPARs) are transcription factors that act as lipid sensors and adapt the metabolic rates of various tissues to the concentration of dietary lipids. PPARs are pharmacological targets for the treatment of metabolic disorders. PPAR<mml:math id="E2" xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mi>α</mml:mi></mml:math> and PPAR<mml:math id="E3" xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mi>γ</mml:mi></mml:math> are activated by hypolipidemic and insulin-sensitizer compounds, such as fibrates and thiazolidinediones. The roles of PPAR<mml:math id="E4" xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mrow><mml:mi>β</mml:mi><mml:mo>/</mml:mo><mml:mi>δ</mml:mi></mml:mrow></mml:math> in metabolic regulations remained unclear until recently. Treatment of obese monkeys and rodents by specific PPAR<mml:math id="E5" xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mrow><mml:mi>β</mml:mi><mml:mo>/</mml:mo><mml:mi>δ</mml:mi></mml:mrow></mml:math> agonists promoted normalization of metabolic parameters and reduction of adiposity. Recent evidences strongly suggested that some of these beneficial actions are related to activation of fatty acid catabolism in skeletal muscle and also that PPAR<mml:math id="E6" xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mrow><mml:mi>β</mml:mi><mml:mo>/</mml:mo><mml:mi>δ</mml:mi></mml:mrow></mml:math> is involved in the adaptive responses of skeletal muscle to environmental changes, such as long-term fasting or physical exercise, by controlling the number of oxidative myofibers. These observations indicated that PPAR<mml:math id="E7" xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mrow><mml:mi>β</mml:mi><mml:mo>/</mml:mo><mml:mi>δ</mml:mi></mml:mrow></mml:math> agonists might have therapeutic usefulness in metabolic syndrome by increasing fatty acid consumption in skeletal muscle and reducing obesity.

Céline Gaudel

Paul A. Grimaldi

Metabolic Functions of Peroxisome Proliferator-Activated Receptor <svg style="vertical-align:-3.56265pt" height="16.6625" version="1.1" viewBox="0 0 25.7875 16.6625" width="25.7875" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg"><g transform="matrix(.017,-0,0,-.017,.062,12.162)"><path id="x1D6FD" d="M558 587q0 -32 -14 -61t-40 -53.5t-48.5 -41t-54.5 -36.5q144 -51 144 -174q0 -55 -43.5 -108t-104.5 -87q-77 -42 -131 -42q-31 0 -54 20t-31 47l11 18q48 -29 108 -29q79 0 119.5 43t40.5 109t-44.5 107.5t-119.5 50.5l22 47q34 1 65 21q96 61 96 157q0 42 -24 67.5
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t90 31.5q54 0 97.5 -35.5t65 -78.5t28.5 -84zM359 234q0 84 -90 191q-47 -17 -74 -47q-81 -89 -81 -200q0 -71 32.5 -109.5t72.5 -38.5q47 0 80 33t46.5 77.5t13.5 93.5z"/></g></svg> in Skeletal Muscle

Transcriptional cofactors are integral to the proper function and regulation of nuclear receptors. Members of the peroxisome proliferator-activated receptor (PPAR) family of nuclear receptors are involved in the regulation of lipid and carbohydrate metabolism. They modulate gene transcription in response to a wide variety of ligands, a process that is mediated by transcriptional coactivators and corepressors. The mechanisms by which these cofactors mediate transcriptional regulation of nuclear receptor function are still being elucidated. The rapidly increasing array of cofactors has brought into focus the need for a clear understanding of how these cofactors interact in ligand- and cell-specific manners. This review highlights the differential effects of the assorted cofactors regulating the transcriptional action of PPAR<mml:math id="E2" xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mi>γ</mml:mi></mml:math> and summarizes the recent advances in understanding the physiological functions of corepressors and coactivators.

Emily Powell

Peter Kuhn

Wei Xu

Nuclear Receptor Cofactors in PPAR<svg style="vertical-align:-3.56265pt" height="12.175" version="1.1" viewBox="0 0 8.6374998 12.175" width="8.6374998" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg"><g transform="matrix(.017,-0,0,-.017,.062,7.675)"><path id="x1D6FE" d="M478 372q0 -39 -31 -97t-61 -98t-78 -98q-45 -55 -73 -102q-13 -79 -13 -197q-11 -11 -43.5 -25.5t-53.5 -15.5l-15 17q5 35 26 101.5t47 123.5q8 72 -1.5 174.5t-37.5 178.5q-14 37 -29 37q-20 0 -67 -65l-25 21q37 60 73 90.5t63 30.5q47 0 72 -112q13 -56 17.5 -141.5
t0.5 -143.5h2q155 193 155 297q0 26 -12 47q-5 8 -5 15q0 16 12.5 27t29.5 11q21 0 34 -21t13 -55z"/></g></svg>-Mediated Adipogenesis and Adipocyte Energy Metabolism

Uncoupling proteins (UCPs) are mitochondrial membrane transporters involved in the control of energy conversion in mitochondria. Experimental and genetic evidence relate dysfunctions of UCPs with metabolic syndrome and obesity. The PPAR subtypes mediate to a large extent the transcriptional regulation of the UCP genes, with a distinct relevance depending on the UCP gene and the tissue in which it is expressed. UCP1 gene is under the dual control of PPAR<mml:math id="E1" xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mi>γ</mml:mi></mml:math> and PPAR<mml:math id="E2" xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mi>α</mml:mi></mml:math> in relation to brown adipocyte differentiation and lipid oxidation, respectively. UCP3 gene is regulated by PPAR<mml:math id="E3" xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mi>α</mml:mi></mml:math> and PPAR<mml:math id="E4" xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mi>δ</mml:mi></mml:math> in the muscle, heart, and adipose tissues. UCP2 gene is also under the control of PPARs even in tissues in which it is the predominantly expressed UCP (eg, the pancreas and liver). This review summarizes the current understanding of the role of PPARs in UCPs gene expression in normal conditions and also in the context of type-2 diabetes or obesity.

Francesc Villarroya

Roser Iglesias

Marta Giralt

PPARs in the Control of Uncoupling Proteins Gene Expression

The worldwide prevalence of obesity and related metabolic disorders is rising rapidly, increasing the burden on our healthcare system. Obesity is often accompanied by excess fat storage in tissues other than adipose tissue, including liver and skeletal muscle, which may lead to local insulin resistance and may stimulate inflammation, as in steatohepatitis.  In addition, obesity changes the morphology and composition of adipose tissue, leading to changes in protein production and secretion. Some of these secreted proteins, including several proinflammatory mediators, may be produced by macrophages resident in the adipose tissue. The changes in inflammatory status of adipose tissue and liver with obesity feed a growing recognition that obesity represents a state of chronic low-level inflammation. Various molecular mechanisms have been implicated in obesity-induced inflammation, some of which are modulated by the peroxisome proliferator-activated receptors (PPARs). PPARs are ligand-activated transcription factors involved in the regulation of numerous biological processes, including lipid and glucose metabolism, and overall energy homeostasis. Importantly, PPARs also modulate the inflammatory response, which makes them an interesting therapeutic target to mitigate obesity-induced inflammation and its consequences. This review will address the role of PPARs in obesity-induced inflammation specifically in adipose tissue, liver, and the vascular wall.

Rinke Stienstra

Caroline Duval

Michael Müller

PPARs, Obesity, and Inflammation

About this journal

<p><em>PPAR Research</em> publishes articles related to mechanisms involved in the activation of peroxisome proliferator-activated receptors, as well as their role in regulation of cellular differentiation, development, energy homeostasis and metabolic function.</p>


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<p>Chief Editor, Dr Xiao-Jie Lu, is dedicated to basic and translational research on liver diseases. His research at Nanjing Medical University, China, focuses&nbsp;on exploring these diseases' underlying mechanisms that may be translatable to novel diagnostic biomarkers or therapeutic targets.</p>


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PPAR Research publishes articles related to mechanisms involved in the activation of peroxisome proliferator-activated receptors, as well as their role in regulation of cellular differentiation, development, energy homeostasis and metabolic function.

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PPAR Research

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PPAR Research

PPARS and Obesity

PPARS and Obesity

Articles

The Effect of PPAR, PPAR, PPAR, and PPARpan Agonists on Body Weight, Body Mass, and Serum Lipid Profiles in Diet-Induced Obese AKR/J Mice

PPARS and Obesity

Therapeutic Potential of Retinoid X Receptor Modulators for the Treatment of the Metabolic Syndrome

‘Striking the Right Balance’ in Targeting PPAR in the Metabolic Syndrome: Novel Insights from Human Genetic Studies

Genetic Manipulations of PPARs: Effects on Obesity and Metabolic Disease

Selective Modulators of PPAR- Activity: Molecular Aspects Related to Obesity and Side-Effects

Metabolic Functions of Peroxisome Proliferator-Activated Receptor in Skeletal Muscle

Nuclear Receptor Cofactors in PPAR-Mediated Adipogenesis and Adipocyte Energy Metabolism

PPARs in the Control of Uncoupling Proteins Gene Expression

PPARs, Obesity, and Inflammation