arachidonic acid/obesity

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Eicosapentaenoic acid/arachidonic acid ratio and weight loss during hospitalization for glycemic control among overweight Japanese patients with type 2 diabetes: a retrospective observational study.

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The study aimed to examine the relationship between levels of serum eicosapentaenoic acid (EPA), arachidonic acid (AA), as well as EPA/AA ratio and weight loss during hospitalization in participants considered to be overweight, with type 2 diabetes.The

Arachidonic acid status negatively associates with forearm bone outcomes and glucose homeostasis in children with overweight condition or obesity.

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Long-chain polyunsaturated fatty acids are implicated in musculoskeletal health in adults. This study examined whether fatty acid status relates to bone health outcomes in children with overweight condition or obesity (BMI Z-score 3.1 ± 0.1, 9.0 ± 0.2 y, n=108). Non-dominant forearm bone density

Associations among FADS1 rs174547, eicosapentaenoic acid/arachidonic acid ratio, and arterial stiffness in overweight subjects.

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We aimed to evaluate the longitudinal interaction effects between the minor allele of FADS1 rs174547 and overweight on n-3 and n-6 long-chain polyunsaturated fatty acid (PUFA) levels and pulse wave velocity (PWV). Plasma PUFA levels were measured via GC-MS, and arterial stiffness was determined as

Characteristics of obese children with low content of arachidonic acid in plasma lipids.

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BACKGROUND Although there have been many studies on the relationship between obesity and long-chain polyunsaturated fatty acid (LCPUFA), the results and their interpretation are controversial, especially in children. Arachidonic acid (AA), the product of n-6 LCPUFA, is reported to be related to

Association of adipose tissue arachidonic acid content with BMI and overweight status in children from Cyprus and Crete.

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The relationships between n-3 and n-6 fatty acids in subcutaneous fat, BMI and overweight status were investigated in eighty-eight children from Crete and Cyprus. Overweight status, BMI and serum lipid levels were similar in children at both locations, but Cretan children had higher levels of total

Effect of male sex and obesity on platelet arachidonic acid in spontaneous hypertensive heart failure rats.

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Sexual dimorphism is observed in the progression to congestive heart failure and, ultimately, in longevity in spontaneously hypertensive heart failure (SHHF) rats. As platelet activation may impact development of cardiovascular diseases, we studied the effects of obesity and sex on platelet

Arachidonic acid maldistribution in obesity.

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Arachidonic acid is an important regulator of cellular function via its effects on the physical properties of membranes, in its free form, or as a substrate for eicosanoids. Dietary studies indicate that its production is regulated, but the mechanisms of this regulation and factors influencing

Stimulation of leptin release by arachidonic acid and prostaglandin E(2) in adipose tissue from obese humans.

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The purpose of this study was to examine the effect of arachidonic acid and its metabolites on leptin formation by explants of human adipose tissue over a 48-hour incubation in primary culture. We found that arachidonic acid or prostaglandin E(2) (PGE(2)) stimulated leptin release by explants of

Augmented insulinotropic action of arachidonic acid through the lipoxygenase pathway in the obese Zucker rat.

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OBJECTIVE The metabolism of arachidonic acid (AA) has been shown to be altered in severe insulin resistance that is present in obese (fa/fa) Zucker rats. We examined the effects and mechanism of action of AA on basal and glucose-stimulated insulin secretion in pancreatic islets isolated from obese

Pro-inflammatory phospholipid arachidonic acid/eicosapentaenoic acid ratio of dysmetabolic severely obese women.

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BACKGROUND Fatty acids (FAs) and adipokines such as adiponectin or interleukin-6 (IL-6) are known to modulate inflammation and the development of metabolic syndrome. Whether FA composition assessed in plasma triacylglycerols (TAGs), phospholipids (PLs) and non-esterified fatty acids (NEFAs) and

Thr-encoding allele homozygosity at codon 54 of FABP 2 gene may be associated with impaired delta 6 desatruase activity and reduced plasma arachidonic acid in obese children.

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BACKGROUND Alanine-for-threonine substitution at codon 54 (A54T polymorphism) in the fatty acid-binding protein 2 gene (FABP2) has been associated with hypertriglyceridemia and insulin resistance. Impairment in the activity of delta 6 and 5 desaturases is also supposed to be a factor predisposing

Obesity is positively associated with arachidonic acid-derived 5- and 11-hydroxyeicosatetraenoic acid (HETE).

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Oxylipids are oxygenated polyunsaturated fatty acid (PUFA) metabolites that are responsible for the onset and resolution of the inflammatory response. Enzymatic oxygenation through the lipoxygenase (LOX) or cytochrome P450 (CYP) pathways can form oxylipids that have either proinflammatory or

Arachidonic acid sex-dependently affects obesity through linking gut microbiota-driven inflammation to hypothalamus-adipose-liver axis.

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Unraveling the role of dietary lipids is beneficial to treat obesity and metabolic dysfunction. Nonetheless, how dietary lipids affect existing obesity remains unknown. Arachidonic acid (AA), a derivative of linoleic acid, is one of the crucial n-6 fatty acids. The aim of this study was to

Arachidonic acid exacerbates diet-induced obesity and reduces bone mineral content without impacting bone strength in growing male rats.

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Long-chain polyunsaturated fatty acids modulate bone mass and adipocyte metabolism. Arachidonic acid (AA, C20:4 n-6) is elevated in obesity and postulated to stimulate bone resorption. This study aimed to determine the effect of AA on bone mass, quality, and adiposity in diet-induced obesity during

Altered arachidonic acid metabolism via COX-1 and COX-2 contributes to the endothelial dysfunction of penile arteries from obese Zucker rats.

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OBJECTIVE The aim of the current study was to investigate the role of arachidonic acid (AA) metabolism via cyclooxygenase (COX) in the endothelial dysfunction of penile arteries from pre-diabetic, obese Zucker rats (OZR). METHODS Penile arteries from OZR and from lean Zucker rats (LZR) were mounted

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