hydrolase/obesity

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[Thrombocyte lysosomal hydrolase activity in patients with ischemic heart disease, hyperlipidemia and obesity against a background of different diets].

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Investigation of lysosomal hydrolase activity in platelets of patients has revealed drastic activation of cathepsins B, C and phospholipase A1, the degree of which rose in the following range: coronary heart disease; coronary heart disease aggravated by obesity: obesity and hyperlipidemia (type II).

Overweight and obesity associated with a missense polymorphism in fatty acid amide hydrolase (FAAH).

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BACKGROUND The brain endogenous cannabinoid system modulates reward and craving pathways and consequently may affect body weight. A naturally occurring missense polymorphism in the gene encoding fatty acid amide hydrolase (FAAH), the primary enzyme for inactivation of endocannabinoids, is associated

The influence of the fatty acid amide hydrolase 385C>A single nucleotide polymorphisms on obesity susceptibility.

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The chronic over-activation of the endogenously produced cannabinoids in obesity has been demonstrated in several studies. A common 385C>A single nucleotide polymorphism of the fatty acid amide hydrolase, one the most important inactivating enzymes of endogenous cannabinoids, has been shown to be

Mutation screen and association studies for the fatty acid amide hydrolase (FAAH) gene and early onset and adult obesity.

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BACKGROUND The orexigenic effects of cannabinoids are limited by activation of the endocannabinoid degrading enzyme fatty acid amide hydrolase (FAAH). The aim of this study was to analyse whether FAAH alleles are associated with early and late onset obesity. METHODS We initially assessed association

C358A missense polymorphism of the endocannabinoid-degrading enzyme fatty acid amide hydrolase (FAAH) and visfatin levels in obese females.

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BACKGROUND Recently, it has been shown that the polymorphism 385 C/A of FAAH (fatty acid amide hydrolase) was associated with overweight and obesity. Visfatin has been identified as a protein expressed in visceral adipose tissue with contradictory functions in glucose metabolism. OBJECTIVE The aim

The fatty acid amide hydrolase (FAAH) Pro129Thr polymorphism is not associated with severe obesity in Greek subjects.

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Fatty amid acid hydrolase (FAAH) has been implicated at both protein and gene level with obesity. An association between Pro129Thr variant of the FAAH gene and obesity has been described, but various studies have yielded conflicting results. Our aim was to determine whether this polymorphism is

Leukotriene A ₄ hydrolase deficiency protects mice from diet-induced obesity by increasing energy expenditure through neuroendocrine axis

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Obesity is a health problem worldwide, and brown adipose tissue (BAT) is important for energy expenditure. Here, we explored the role of leukotriene A₄ hydrolase (LTA₄ H), a key enzyme in the synthesis of the lipid mediator leukotriene B₄ (LTB₄ ), in

Soluble epoxide hydrolase as a therapeutic target for obesity-induced disorders: roles of gut barrier function involved

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Emerging research supports that soluble epoxide hydrolase (sEH), an enzyme involved in eicosanoid metabolism, could be a promising target for obesity-associated disorders. The sEH enzyme is overexpressed in many tissues of obese animals. Genetic ablation or pharmacological inhibition of sEH

Cytochrome P450 monooxygenase/soluble epoxide hydrolase-mediated eicosanoid pathway in colorectal cancer and obesity-associated colorectal cancer.

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Colorectal cancer (CRC) is the third most common cancer and the second leading cause of cancer-related deaths in the United States. Furthermore, it is well established that obese individuals have high risks of developing CRC, and obesity-associated CRC represents an unmet medical problem in the

Potential anti-obesity effects of a long-acting cocaine hydrolase.

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A long-acting cocaine hydrolase, known as CocH3-Fc(M3), engineered from human butyrylcholinesterase (BChE) was tested, in this study, for its potential anti-obesity effects. Mice on a high-fat diet gained significantly less body weight when treated weekly with 1 mg/kg CocH3-Fc(M3) compared to

[Effects of polyphenols on activity of glycosyl hydrolases in the cecum of rats fed obesity inducing diets].

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The results of experimental studies indicate that the preventive and therapeutic effects of polyphenols in obesity are accompanied by a significant decrease in the severity of dysbiosis caused by the predominance of fats and simple carbohydrates in the diet, especially fructose, and the restoration

[C358A polymorphism of the endocannabinoid degrading enzyme fatty acid amide hydrolase (FAAH) and adipocytokine levels in the morbidly obese].

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BACKGROUND The 385 C/A polymorphism of fatty acid amide hydrolase (FAAH) has recently been demonstrated to be associated with overweight and obesity. The aim of our study was to investigate the association between missense polymorphism (cDNA 385 C->A) of the FAAH gene and anthropometric parameters,

Soluble Epoxide Hydrolase Inhibition by t-TUCB Promotes Brown Adipogenesis and Reduces Serum Triglycerides in Diet-Induced Obesity

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Brown adipose tissue (BAT) is an important target for obesity treatment and prevention. Soluble epoxide hydrolase (sEH) converts bioactive epoxy fatty acids (EpFAs) into less active diols. sEH inhibitors (sEHI) are beneficial in many chronic diseases by stabilizing EpFAs. However, roles of sEH and

Relation of C358A polymorphism of the endocannabinoid degrading enzyme fatty acid amide hydrolase (FAAH) with obesity and insulin resistance.

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OBJECTIVE Recently, it has been demonstrated that the polymorphism 385 C->A of FAAH (fatty acid amide hydrolase) was associated with overweight and obesity. The aim of our study was to investigate the relationship of missense polymorphism (cDNA 385 C-A) of FAAH gene on obesity anthropometric

Human adipose triglyceride lipase (PNPLA2) is not regulated by obesity and exhibits low in vitro triglyceride hydrolase activity.

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OBJECTIVE The recent identification of murine adipose triglyceride lipase (ATGL, now known as patatin-like phospholipase domain containing 2 [PNPLA2]), gene product of Pnpla2, has questioned the unique role of hormone sensitive lipase (HSL, now known as LIPE), gene product of Lipe, in fat cell

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hydrolase/obesity

[Thrombocyte lysosomal hydrolase activity in patients with ischemic heart disease, hyperlipidemia and obesity against a background of different diets].

Overweight and obesity associated with a missense polymorphism in fatty acid amide hydrolase (FAAH).

The influence of the fatty acid amide hydrolase 385C>A single nucleotide polymorphisms on obesity susceptibility.

Mutation screen and association studies for the fatty acid amide hydrolase (FAAH) gene and early onset and adult obesity.

C358A missense polymorphism of the endocannabinoid-degrading enzyme fatty acid amide hydrolase (FAAH) and visfatin levels in obese females.

The fatty acid amide hydrolase (FAAH) Pro129Thr polymorphism is not associated with severe obesity in Greek subjects.

Leukotriene A 4 hydrolase deficiency protects mice from diet-induced obesity by increasing energy expenditure through neuroendocrine axis

Soluble epoxide hydrolase as a therapeutic target for obesity-induced disorders: roles of gut barrier function involved

Cytochrome P450 monooxygenase/soluble epoxide hydrolase-mediated eicosanoid pathway in colorectal cancer and obesity-associated colorectal cancer.

Potential anti-obesity effects of a long-acting cocaine hydrolase.

[Effects of polyphenols on activity of glycosyl hydrolases in the cecum of rats fed obesity inducing diets].

[C358A polymorphism of the endocannabinoid degrading enzyme fatty acid amide hydrolase (FAAH) and adipocytokine levels in the morbidly obese].

Soluble Epoxide Hydrolase Inhibition by t-TUCB Promotes Brown Adipogenesis and Reduces Serum Triglycerides in Diet-Induced Obesity

Relation of C358A polymorphism of the endocannabinoid degrading enzyme fatty acid amide hydrolase (FAAH) with obesity and insulin resistance.

Human adipose triglyceride lipase (PNPLA2) is not regulated by obesity and exhibits low in vitro triglyceride hydrolase activity.

Baz done ki pi konplè remèd fèy medsin te apiye nan syans

Leukotriene A ₄ hydrolase deficiency protects mice from diet-induced obesity by increasing energy expenditure through neuroendocrine axis