Prostaglandins and Obesity

Curtis-Prior, P.B.

doi:10.1016/s0140-6736(75)91690-6

Cited by 25 publications

(10 citation statements)

References 20 publications

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“…Increased prostaglandin levels have been described in the plasma of normotensive obese patients [12], suggesting that abnormal regulation of the cyclo-oxygenase pathway may also occur in human obesity. The results of our experiments suggest further that endothelin receptor antagonists may contribute to vasoprotection by inhibiting endothelium-dependent vasoconstrictor activity by pressure-independent mechanisms.…”

Section: Discussionmentioning

confidence: 99%

Effects of obesity on endothelium-dependent reactivity during acute nitric oxide synthase inhibition: modulatory role of endothelin

Traupe

d’Uscio

Muenter³

et al. 2002

Clinical Science

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This study investigated vascular reactivity in response to acetylcholine, in the presence of acute inhibition of nitric oxide synthase, in the carotid artery and aorta of obese C57Bl6/J mice fed on a high-fat diet for 30 weeks, and of control mice. A subgroup of obese animals was also treated with the ET(A) receptor antagonist darusentan (50 mg x kg(-1) x day(-1)). In vascular rings from control animals, acetylcholine caused endothelium-dependent contractions in the carotid artery, but not in the aorta. In vascular rings from obese mice, contractility to acetylcholine was also evident in the aorta, and that in the carotid artery was increased compared with control mice. ET(A) receptor blockade by darusentan treatment of the obese mice prevented enhanced vasoconstriction to acetylcholine, resulting in mild vasodilatation. Thus obesity increases endothelium-dependent vasoconstriction in the absence of endothelial nitric oxide. This effect can be completely prevented by chronic ET(A) receptor blockade, suggesting that endothelin modulates increased endothelium-dependent vasoconstriction in obesity.

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Section: Discussionmentioning

confidence: 99%

Effects of obesity on endothelium-dependent reactivity during acute nitric oxide synthase inhibition: modulatory role of endothelin

Traupe

d’Uscio

Muenter³

et al. 2002

Clinical Science

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“…The diverse actions of PGE 2 can be explained by the existence of these multiple EP subtypes with different signal transduction pathways ( 6,9 ). It has been shown that COX products, such as PGE 2 and PGF 2 ␣ , inhibit adipocyte development (10)(11)(12). A recent study suggested that COX-2 may be involved in body fat regulation ( 13 ).…”

Section: Rna Isolation and Real Time Rt-pcrmentioning

confidence: 99%

Prostaglandin E2-EP4 signaling suppresses adipocyte differentiation in mouse embryonic fibroblasts via an autocrine mechanism

Inazumi

Shirata

Morimoto

et al. 2011

Journal of Lipid Research

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Adipogenesis is a crucial aspect in controlling body fat mass ( 1, 2 ). Acquisition of the mature adipocyte phenotype is a highly regulated process in which mesenchymal stem cells (MSC) undergo differentiation, resulting in both an increase in size and number of mature adipocytes in adipose tissue. Adipose tissue is important not only for energy storage but also as an endocrine organ that regulates energy homeostasis by secreting various adipokines, such as cytokines, chemokines, growth factors, and lipid mediators ( 3 ). The presence of receptors for adipokines in preadipocytes and adipocytes has been shown, suggesting that secreted adipokines have autocrine effects and regulate their own differentiation and functions ( 4 ). Although it has been shown that a number of factors, including adipokines, regulate adipogenesis in various settings, most of the evidence comes from supraphysiological or pharmacological doses of these molecules to elicit a response. Hence, their physiological signifi cance in local milieu has not been established.Prostaglandins (PG) are arachidonate metabolites synthesized by the action of cyclooxygenase (COX) as the rate-limiting enzyme. COX has been shown to exist as two isomers, COX-1 and COX-2. PGs exert a wide range of actions through their binding to plasma membrane receptors ( 5, 6 ). For instance, PGF 2 ␣ exerts its actions via specifi c interactions with the prostanoid FP receptor, which activates phopholipase C, resulting in phophatidylinositol breakdown ( 7 ). In contrast, PGE 2 exerts action through its Abstract The prostaglandin (PG) receptors EP4 and FP have the potential to exert negative effects on adipogenesis, but the exact contribution of endogenous PG-driven receptor signaling to this process is not fully understood. In this study, we employed an adipocyte differentiation system from mouse embryonic fi broblasts (MEF) and compared the effects of each PG receptor-defi ciency on adipocyte differentiation.

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“…Moreover, fat accumulation in the liver is associated with increased hepatic synthesis of prothrombotic and proinflammatory mediators as PAI‐1, fibrinogen, C‐reactive protein (CRP), and inflammatory cytokines . In metabolic obesity, a biochemical error occurs that leads to overproduction of PGs together with a significant association between increasing BMI and systemic oxidant stress . In addition, an association between overweight/obesity has been shown to be associated with enhanced oxidant stress and formation of isoPs .…”

Section: Introductionmentioning

confidence: 99%

Eicosanoids and Their Drugs in Cardiovascular Diseases: Focus on Atherosclerosis and Stroke

Capra

Bäck

Barbieri

et al. 2012

Medicinal Research Reviews

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Eicosanoids are biologically active lipids in both physiologic and pathophysiologic situations. These mediators rapidly generate at sites of inflammation and act through specific receptors that following the generation of a signal transduction cascade, lead to coordinated cellular responses to specific stimuli. Prostanoids, that is, prostaglandins and thromboxane A(2), are active products of the cyclooxygenase pathway, while leukotrienes and lipoxins derive from the lipoxygenase pathway. In addition, a complex family of prostaglandin isomers called isoprostanes is derived as free-radical products of oxidative metabolism. While there is a wide consensus on the importance of the balance between proaggregating (thromboxane A(2)) and antiaggregating (prostacyclin) cyclooxygenase products in cardiovascular homeostasis, an increasing body of evidence suggests a key role also for other eicosanoids generated by lipoxygenases, epoxygenases, and nonenzymatic pathways in cardiovascular diseases. This intricate network of lipid mediators is unique considering that from a single precursor, arachidonic acid, may derive an array of bioproducts that interact within each other synergizing or, more often, behaving as functional antagonists.

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Prostaglandins and Obesity

Cited by 25 publications

References 20 publications

Effects of obesity on endothelium-dependent reactivity during acute nitric oxide synthase inhibition: modulatory role of endothelin

Effects of obesity on endothelium-dependent reactivity during acute nitric oxide synthase inhibition: modulatory role of endothelin

Prostaglandin E2-EP4 signaling suppresses adipocyte differentiation in mouse embryonic fibroblasts via an autocrine mechanism

Eicosanoids and Their Drugs in Cardiovascular Diseases: Focus on Atherosclerosis and Stroke

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