Prostaglandin Metabolism in Children With Diabetes Mellitus. I. Plasma Prostaglandin E2, F2α, TXB2, and Serum Fatty Acid Levels

Arisaka, Madoka; Arisaka, Osamu; Fukuda, Yutaka; Yamashiro, Yuichiro

doi:10.1097/00005176-198611000-00009

Cited by 29 publications

(13 citation statements)

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“…Fatty acid compositional data obtained in diabetic adults indicated significant reduction of the principal n-3 and n-6 LC-PUFAs, DHA and AA, in plasma and thrombocyte membrane lipids [13,14]. In diabetic children, a significant reduction of plasma DHGLA and AA values was reported together with significant enhancement of plasma prostaglandin E 2 and PGF 2a concentrations [6]. These latter observations suggested that n-6 LC-PUFA might be utilized to a greater extent for prostaglandin synthesis in diabetics than in healthy controls.…”

Section: Discussionmentioning

confidence: 89%

Polyunsaturated fatty acids in plasma lipids of diabetic children during and after diabetic ketoacidosis

Décsi¹,

Szabó²,

Kozári³

et al. 2005

Acta Paediatrica

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Section: Discussionmentioning

confidence: 89%

Polyunsaturated fatty acids in plasma lipids of diabetic children during and after diabetic ketoacidosis

Décsi¹,

Szabó²,

Kozári³

et al. 2005

Acta Paediatrica

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“…Diabetic patients have consistently higher serum levels of pro-inflammatory cytokines such as prostaglandin E2 (PGE2), 74 TNF-α, 75 IL-6, 76 and leukotriene B4. 77 This is in agreement with the postulated roles of PGE2, 78 TNF-α, 79 IL-6, 80 and leukotriene B4 78 as pro-inflammatory cytokines in the pathogenesis of chronic tendinopathy.…”

Section: Persistent Low-grade Chronic Inflammationmentioning

confidence: 99%

Tendinopathy in diabetes mellitus patients—Epidemiology, pathogenesis, and management

Lui

2017

Scandinavian Med Sci Sports

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Chronic tendinopathy is a frequent and disabling musculo-skeletal problem affecting the athletic and general populations. The affected tendon is presented with local tenderness, swelling, and pain which restrict the activity of the individual. Tendon degeneration reduces the mechanical strength and predisposes it to rupture. The pathogenic mechanisms of chronic tendinopathy are not fully understood and several major non-mutually exclusive hypotheses including activation of the hypoxia-apoptosis-pro-inflammatory cytokines cascade, neurovascular ingrowth, increased production of neuromediators, and erroneous stem cell differentiation have been proposed. Many intrinsic and extrinsic risk/causative factors can predispose to the development of tendinopathy. Among them, diabetes mellitus is an important risk/causative factor. This review aims to appraise the current literature on the epidemiology and pathology of tendinopathy in diabetic patients. Systematic reviews were done to summarize the literature on (a) the association between diabetes mellitus and tendinopathy/tendon tears, (b) the pathological changes in tendon under diabetic or hyperglycemic conditions, and (c) the effects of diabetes mellitus or hyperglycemia on the outcomes of tendon healing. The potential mechanisms of diabetes mellitus in causing and exacerbating tendinopathy with reference to the major non-mutually exclusive hypotheses of the pathogenic mechanisms of chronic tendinopathy as reported in the literature are also discussed. Potential strategies for the management of tendinopathy in diabetic patients are presented.

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“…Interestingly, AA-derived PGF2␣ levels are increased in diabetic humans (44,45). The link between free fatty acid levels and the pathogenesis of noninsulin-dependent diabetes has been recognized for many years (46).…”

Section: Downloaded Frommentioning

confidence: 99%

Prostaglandins Promote and Block Adipogenesis through Opposing Effects on Peroxisome Proliferator-activated Receptor γ

Reginato

Krakow

Bailey

et al. 1998

Journal of Biological Chemistry

275

192

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Fat cell differentiation is a critical aspect of obesity and diabetes. Dietary fatty acids are converted to arachidonic acid, which serves as precursor of prostaglandins (PGs). PGJ2 derivatives function as activating ligands for peroxisome proliferator-activated receptor ␥ (PPAR␥), a nuclear hormone receptor that is central to adipogenic determination. We report here that PGF2␣ blocks adipogenesis through activation of mitogen-activated protein kinase, resulting in inhibitory phosphorylation of PPAR␥. Both mitogen-activated protein kinase activation and PPAR␥ phosphorylation are required for the anti-adipogenic effects of PGF2␣. Thus, PG signals generated at a cell surface receptor regulate the program of gene expression required for adipogenesis by modulating the activity of a nuclear hormone receptor that is directly activated by other PG signals. The balance between PGF2␣ and PGJ2 signaling may thus be central to the development of obesity and diabetes.Altered levels of free fatty acids or their metabolites commonly occur in obesity and diabetes (1, 2), and fatty acid uptake is increased in these disorders (3). Levels of arachidonic acid (AA), 1 which is derived from dietary essential fatty acids, are high relative to other fatty acids in obesity and diabetic states (4), and high levels of AA may exacerbate diabetes by negatively regulating glucose uptake (5). AA serves as precursor for eicosanoid signaling molecules including leukotrienes, hydroxyeicosatetraenoic acids, and prostaglandins (PGs) (6). Many eicosanoids signal via cell surface G-protein-coupled receptors (GPCRs) (7). Others including 8 S hydroxyeicosatetraenoic acids, leukotriene B4, and a number of PGs including PGJ2 and derivatives such as 15-deoxy-⌬12,14-PGJ2 (15d-PGJ2) bind and activate members of the nuclear hormone receptor superfamily (8) called peroxisome proliferator-activated receptors (PPARs) ␣ and ␥ (9 -12).Obesity is due to increased size and number of adipocytes. PPAR␥, the nuclear receptor for PGJ2 derivatives, plays a central role in adipogenesis (12)(13)(14). PPAR␥ is the target of thiazolidinediones, an exciting new class of antidiabetic drugs that function as direct ligands for PPAR␥ and have also been shown to be adipogenic (10,(15)(16)(17). An endogenous PPAR␥ ligand is therefore likely to be an important metabolic regulator.The rate-limiting step in PGJ2 biosynthesis is catalyzed by cyclooxygenase (COX) (18). The actions of different enzymes upon the COX product PGH2 lead to numerous PGs that have different effects on growth, differentiation, and function of many tissues, including PGF2␣ (7). PGF2␣ is known to be synthesized by preadipocytes but does not activate PPAR␥ (9) and by contrast has a potent inhibitory effect upon adipocyte differentiation (19,20). Thus, products of AA metabolism downstream of COX have opposing effects upon adipogenesis. Although the adipogenic effects of PGJ2 derivatives involve direct activation of nuclear PPAR␥, PGF2␣ utilizes a specific GPCR on the cell surface to initiate intracellular signal...

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Prostaglandin Metabolism in Children With Diabetes Mellitus. I. Plasma Prostaglandin E2, F2α, TXB2, and Serum Fatty Acid Levels

Cited by 29 publications

References 0 publications

Polyunsaturated fatty acids in plasma lipids of diabetic children during and after diabetic ketoacidosis

Polyunsaturated fatty acids in plasma lipids of diabetic children during and after diabetic ketoacidosis

Tendinopathy in diabetes mellitus patients—Epidemiology, pathogenesis, and management

Prostaglandins Promote and Block Adipogenesis through Opposing Effects on Peroxisome Proliferator-activated Receptor γ

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