adenosine triphosphate/obezita

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Attenuation of hyperinsulinemia by NN414, a SUR1/Kir6.2 selective K-adenosine triphosphate channel opener, improves glucose tolerance and lipid profile in obese Zucker rats.

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Chronic attenuation of hyperinsulinemia by diazoxide (DZ), a K-adenosine triphosphate (ATP) channel opener and an inhibitor of glucose-mediated insulin secretion, improved glucose tolerance and lipid profile and decreased the rate of weight gain in obese Zucker rats. To determine whether suppression

Hepatic fat and adenosine triphosphate measurement in overweight and obese adults using 1H and 31P magnetic resonance spectroscopy.

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OBJECTIVE Magnetic resonance spectroscopy (MRS) measures hepatic fat and adenosine triphosphate (ATP), but magnetic resonance studies are challenging in obese subjects. We aimed to evaluate the inter- and intrarater reliability and stability of hepatic fat and ATP measurements in a cohort of

Nicotinamide adenine dinucleotide phosphate-converting enzymes and adenosine triphosphate citrate lyase in some tissues and organs of New Zealand obese mice with special reference to the enzyme pattern of the pancreatic islets.

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In order to obtain a quantitative estimate of the capacity of the pancreatic islets for provision of cytoplasmic acetyl-coenzyme A and for the turnover of nicotinamide adenine dinucleotide phosphate and its reduced form (NADP+/NADPH), the following enzymes were assayed in islets taken from New

Adenosine triphosphate-sensitive potassium (K(ATP)) channel activity is coupled with insulin resistance in obesity and type 2 diabetes mellitus.

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ATP sensitive potassium (K(ATP)) channels reside in the plasma membrane of many excitable cells such as pancreatic beta-cells, heart, skeletal muscle and brain, where they link cellular metabolic energy to membrane electrical activity. They are composed of two subunits, K+ ion selective pore (Kir)

Higher dietary fructose is associated with impaired hepatic adenosine triphosphate homeostasis in obese individuals with type 2 diabetes.

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Fructose consumption predicts increased hepatic fibrosis in those with nonalcoholic fatty liver disease (NAFLD). Because of its ability to lower hepatic adenosine triphosphate (ATP) levels, habitual fructose consumption could result in more hepatic ATP depletion and impaired ATP recovery. The degree

Ablation of the cholesterol transporter adenosine triphosphate-binding cassette transporter G1 reduces adipose cell size and protects against diet-induced obesity.

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The ATP-binding cassette transporter G1 (ABCG1) catalyzes export of cellular cholesterol from macrophages and hepatocytes. Here we identify an additional function of ABCG1 in the regulation of adiposity in screens of the Drosophila melanogaster and the New Zealand obese (NZO) mouse genomes.

Puerariae flos alleviates metabolic diseases in Western diet-loaded, spontaneously obese type 2 diabetic model mice.

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Puerariae flos extract (PFE) has been reported to have many effects, including preventing the development of hangovers, liver protective effects, and an estrogenic effect. In addition, some papers reported that PFE is effective against metabolic diseases, with hypolipidemic and hypoglycemic effects.

Downregulation of Kir6.1/SUR2B channels in the obese rat aorta.

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OBJECTIVE This study was designed to evaluate the contribution of adenosine triphosphate-dependent potassium channels to the increase in blood pressure observed in obese rats. METHODS The experiment was performed in male Sprague-Dawley rats. Glibenclamide-sensitive currents were measured in vascular

Recent data on obesity research: β-aminoisobutyric acid.

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The world-wide epidemic of obesity is now affecting up to a third of the adult population. Research attempting to contribute to management of this health scourge has been recently refocused on the essential role of physical activity. Muscle activity induces a dramatic increase in transcription of

Diastolic Dysfunction Induced by a High-Fat Diet Is Associated with Mitochondrial Abnormality and Adenosine Triphosphate Levels in Rats.

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BACKGROUND Obesity is well-known as a risk factor for heart failure, including diastolic dysfunction. However, this mechanism in high-fat diet (HFD)-induced obese rats remain controversial. The purpose of this study was to investigate whether cardiac dysfunction develops when rats are fed with a HFD

Energy expenditure and oxygen consumption as novel biomarkers of obesity-induced cardiac disease in rats.

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The purpose of the present study was to determine calorimetric parameters to predict obesity adverse effects on oxidative stress and cardiac energy metabolism. Male Wistar 24 rats were divided into three groups (n = 8): given standard chow and water (C), receiving standard chow and 30% sucrose in

Effects of weight loss on myocardial energetics and diastolic function in obesity.

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A reduced myocardial phosphocreatine/adenosine triphosphate (PCr/ATP) ratio is linked to both diastolic dysfunction and heart failure. Although obesity is well known to cause diastolic dysfunction a link to impaired cardiac energetics has only recently been established. We assessed whether or not

ABCA1 single nucleotide polymorphisms on high-density lipoprotein-cholesterol and overweight: the D.E.S.I.R. study.

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The adenosine triphosphate-binding cassette A1 (ABCA1) gene plays a key role in reverse cholesterol transport. Some ABCA1 gene polymorphisms have been associated with high-density lipoprotein-cholesterol (HDL-C) concentrations. The aim of this study was to assess the effect of three polymorphisms,

Plasma Amino Acids Stimulate Uncoupled Respiration of Muscle Subsarcolemmal Mitochondria in Lean but not Obese Humans.

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Obesity is associated with mitochondrial dysfunction in skeletal muscle. Increasing the plasma amino acid (AA) concentrations stimulates mitochondrial adenosine triphosphate (ATP) production in lean individuals. To determine whether acute elevation in plasma AAs enhances muscle mitochondrial

Functional adenosine triphosphate-sensitive potassium channel is required in high-carbohydrate diet-induced increase in β-cell mass.

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UNASSIGNED A high-carbohydrate diet is known to increase insulin secretion and induce obesity. However, whether or not a high-carbohydrate diet affects β-cell mass (BCM) has been little investigated. METHODS Both wild-type (WT) mice and adenosine triphosphate-sensitive potassium channel-deficient

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