alpha carboxylase/التهاب

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Overexpression of acetyl-coenzyme A carboxylase beta increases proinflammatory cytokines in cultured human renal proximal tubular epithelial cells.

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BACKGROUND We have identified the acetyl-coenzyme A carboxylase beta gene (ACACB) as a strong susceptibility gene to diabetic nephropathy in individuals with type 2 diabetes. To elucidate the mechanism by which ACACB contributes to conferring susceptibility to diabetic nephropathy, we examined the

A gene polymorphism in acetyl-coenzyme A carboxylase beta may be associated with the C-reactive protein level in a prediabetic and diabetic population.

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A recent study reported a significant association between the T-allele in intron 18 of the acetyl-coenzyme A carboxylase beta (ACACB) gene (C>T polymorphism) and nephropathy caused by diabetes mellitus (DM). Considering the involvement of chronic inflammation in the pathophysiology of DM, the

Activation of AMP-Activated Protein Kinase by Adenine Alleviates TNF-Alpha-Induced Inflammation in Human Umbilical Vein Endothelial Cells.

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The AMP-activated protein kinase (AMPK) signaling system plays a key role in cellular stress by repressing the inflammatory responses induced by the nuclear factor-kappa B (NF-κB) system. Previous studies suggest that the anti-inflammatory role of AMPK involves activation by adenine, but the

Exercise training in ovariectomized rats stimulates estrogenic-like effects on expression of genes involved in lipid accumulation and subclinical inflammation in liver.

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We hypothesized that the reduction in liver fat accumulation known to occur with exercise training in ovariectomized (Ovx) rats is associated with reduced expression of genes involved in lipogenesis while favoring the expression of transcription factors regulating lipid oxidation. We also tested the

Amelioration of diet-induced metabolic syndrome and fatty liver with Sitagliptin via regulation of adipose tissue inflammation and hepatic Adiponectin/AMPK levels in mice.

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Chronic consumption of unhealthy diet and sedentary lifestyle induces fatty liver and metabolic complications. Adipocytes get overloaded with lipid succeeding low-grade inflammation and disrupting adipokine release. This research aims to investigate the effect of sitagliptin on white adipose tissue

Inflammation-associated interleukin-6/signal transducer and activator of transcription 3 activation ameliorates alcoholic and nonalcoholic fatty liver diseases in interleukin-10-deficient mice.

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Alcoholic and nonalcoholic steatohepatitis are characterized by fatty liver plus inflammation. It is generally believed that steatosis promotes inflammation, whereas inflammation in turn aggregates steatosis. Thus, we hypothesized the deletion of interleukin (IL)-10, a key anti-inflammatory

Antiobesity and anti-inflammation effects of Hakka stir-fried tea of different storage years on high-fat diet-induced obese mice model via activating the AMPK/ACC/CPT1 pathway

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Background: As a typical representative of metabolic syndrome, obesity is also one of the extremely dangerous factors of cardiovascular diseases. Thus, the prevention and treatment of obesity has gradually become a global campaign. There

Puerarin inhibits apoptosis and inflammation in myocardial cells via PPARα expression in rats with chronic heart failure.

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Chronic heart failure affects myocardial energy metabolism and cardiac function. Puerarin has been reported to improve cardiac function through regulation of energy metabolism in mice with myocardial infarction. The aim of the current study was to determine whether puerarin can improve body weight

Adenosine monophosphate-activated protein kinase activation and suppression of inflammatory response by cell stretching in rabbit synovial fibroblasts.

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Joint mobilization is known to be beneficial in osteoarthritis (OA) patients. This study aimed to investigate the effect of stretching on adenosine monophosphate-activated protein kinase (AMPK) activity and its role in modulating inflammation in rabbit synovial fibroblasts. Uniaxial stretching of

Farnesoid X Receptor Agonism, Acetyl-Coenzyme A Carboxylase Inhibition, and Back Translation of Clinically Observed Endpoints of De Novo Lipogenesis in a Murine NASH Model.

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A promising approach for the treatment of nonalcoholic steatohepatitis (NASH) is the inhibition of enhanced hepatic de novo lipogenesis (DNL), which is the synthesis of fatty acids from nonlipid sources. This study assesses three approaches to DNL suppression in a newly developed dietary NASH

Diet-induced obesity associated with steatosis, oxidative stress, and inflammation in liver.

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BACKGROUND Obesity induces steatosis and increases oxidative stress, as well as chronic inflammation in the liver. The balance between lipogenesis and lipolysis is disrupted in obese animals. At a cellular level, the changes in metabolic sensors and energy regulators are poorly understood. We

ACC1 (Acetyl Coenzyme A Carboxylase 1) Is a Potential Immune Modulatory Target of Cerebral Ischemic Stroke.

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Background and Purpose- Cerebral ischemic stroke elicits profound responses of CD4⁺ T cells, which in turn significantly affect the ischemic brain injury. ACC1 (acetyl coenzyme A carboxylase 1) is a key enzyme that has been recently found to propagate CD4⁺ T cell-associated

Acetyl-coenzyme A carboxylase inhibition reduces de novo lipogenesis in overweight male subjects: A randomized, double-blind, crossover study.

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NDI-010976, an allosteric inhibitor of acetyl-coenzyme A carboxylases (ACC) ACC1 and ACC2, reduces hepatic de novo lipogenesis (DNL) and favorably affects steatosis, inflammation, and fibrosis in animal models of fatty liver disease. This study was a randomized, double-blind, placebo-controlled,

Dietary calcium regulates the risk renal injury in high fat diet induced obese rats by regulating renal lipid metabolism, oxidative stress and inflammation.

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Context: The antiobesity effect of dietary calcium by preventing fat accumulation and weight gain was well established from several epidemiological and animal studies.Objective: To evaluate the effect of dietary calcium against obesity-associated with renal injury in high fat diet

Olumacostat Glasaretil, a Promising Topical Sebum-Suppressing Agent that Affects All Major Pathogenic Factors of Acne Vulgaris.

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Hunt et al. show that olumacostat glasaretil, an inhibitor of acetyl coenzyme A carboxylase, reduces saturated and monounsaturated fatty acyl chains in sebaceous lipids. Topical olumacostat glasaretil application decreases hamster ear sebaceous gland size and shows efficacy in treating patients with

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Herbal & Natural Medicine

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