guanine/obesity

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Changes in the phosphorylation state of the inhibitory guanine-nucleotide-binding protein Gi-2 in hepatocytes from lean (Fa/Fa) and obese (fa/fa) Zucker rats.

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Treatment of intact, 32Pi-labelled hepatocytes from lean Zucker rats with a range of agents including 12-O-tetradecanoyl-phorbol 13-acetate (TPA), vasopressin, and angiotensin II elicited substantial increases in the phosphorylation of the alpha-subunit of the inhibitory G protein of adenylate

The interaction of guanine nucleotides with the adenylate cyclase complex in white adipocyte membranes of lean and obese (ob/ob) mice.

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The ability of the guanine nucleotides (Gpp(NH)p and GTP-gamma-S) and of fluoride to stimulate adenylate cyclase is equal in the white adipocyte of lean and ob/ob mice. This suggests that the interaction between the guanine nucleotide regulatory component (N) and the catalytic unit of adenylate

Evaluation of inhibitory guanine nucleotide regulatory protein Gi function in hepatocyte and liver membranes from obese Zucker (fa/fa) rats and their lean (Fa/?) littermates.

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Previous studies have shown that hepatocyte and liver membranes from insulin resistant animals exhibit an impairment of inhibitory guanine nucleotide binding regulatory protein, Gi function, such that a Gi defect may contribute towards the diabetic syndrome. In the current studies, it is shown that

mRNA and protein levels of the stimulatory guanine nucleotide regulatory protein Gs are lower in the testis of obese (ob/ob) mice.

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Probing of total testis RNA with a cDNA corresponding to the alpha s subunit of the guanine nucleotide regulatory protein (G-protein) showed that levels of mRNA were markedly reduced in the ob/ob mouse compared to its +/+ control. The lowered level of mRNA resulted in lowered protein synthesis as

The Rho-guanine nucleotide exchange factor PDZ-RhoGEF governs susceptibility to diet-induced obesity and type 2 diabetes.

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Adipose tissue is crucial for the maintenance of energy and metabolic homeostasis and its deregulation can lead to obesity and type II diabetes (T2D). Using gene disruption in the mouse, we discovered a function for a RhoA-specific guanine nucleotide exchange factor PDZ-RhoGEF (Arhgef11) in white

Multiple defects occur in the guanine nucleotide regulatory protein system in liver plasma membranes of obese (fa/fa) but not lean (Fa/Fa) Zucker rats: loss of functional Gi and abnormal Gs function.

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Hepatocyte membranes from both lean and obese Zucker rats exhibited adenylate cyclase activity that could be stimulated by glucagon, forskolin, NaF and elevated concentrations of p[NH]ppG. In membranes from lean animals, functional Gi was detected by the ability of low concentrations of p[NH]ppG to

Expression of guanine-nucleotide-binding proteins in lean and obese insulin-resistant mice.

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To examine whether G protein were affected in the obese insulin-resistant state, the level of various G proteins (alpha i1, alpha i2, alpha i3, alpha o and alpha s) was assessed by immunodetection in lean and experimentally induced obese mice. Crude membranes were prepared from adipose tissues,

Guanine-nucleotide-binding proteins Gi and Gs in fat-cells from normal, hypothyroid and obese human subjects.

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In human adipocyte plasma membranes, pertussis toxin catalysed the ADP-ribosylation of an apparently single 40 kDa protein. The same protein was also observed in Western blots by using an antibody which identifies the C-terminal decapeptide of Gi alpha (alpha subunit of Gi). In analogous

Indirect evidence against a contribution of the guanine nucleotide-binding inhibitory component of adenylate cyclase to impaired lipolysis in the epididymal adipose tissue of congenitally obese (ob/ob) mice.

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The mixed adrenergic agonist epinephrine, at a 10 microM concentration, stimulated cyclic AMP production and glycerol release in the epididymal adipose tissue of ob/ob male mice. These effects when tested, respectively, after 7 min in the presence and after 60 min in the absence of theophylline

Guanine nucleotide binding regulatory proteins in liver from obese humans with and without type II diabetes: evidence for altered "cross-talk" between the insulin receptor and Gi-proteins.

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A novel pathway for physiological "cross-talk" between the insulin receptor and the regulatory Gi-protein has been demonstrated. We tested the hypothesis that a coupling defect between Gi and the insulin receptor is present in the liver of obese patients with and without type II diabetes. Insulin 1

Decreased guanine nucleotide binding and reduced equivalent production by brown adipose tissue in hypothalamic obesity. Recovery after cold acclimation.

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Ginseng (Panax quinquefolius) attenuates leptin-induced cardiac hypertrophy through inhibition of p115Rho guanine nucleotide exchange factor-RhoA/Rho-associated, coiled-coil containing protein kinase-dependent mitogen-activated protein kinase pathway activation.

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Leptin is a 16-kDa peptide primarily derived from white adipocytes and is typically elevated in plasma of obese individuals. Although leptin plays a critical role in appetite regulation, leptin receptors have been identified in numerous tissues including the heart and have been shown to directly

Association between anthropometric measures of obesity, metabolic disturbances and polymorphism G-308A of the tumor necrosis factor-alpha gene in children.

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BACKGROUND TNF--α is one of the most important factors in the development and course of inflammation. It is suggested that polymorphism located in the 5'regulatory region of the TNF-α gene at position 308 (guanine [G]→adenine[A]) may increase the expression of this cytokine in fat tissue and

Hyperandrogenism, mediated by obesity and receptor polymorphisms, promotes aggressive epithelial ovarian cancer biology.

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OBJECTIVE Epidemiologic data suggest that aberrant androgen homeostasis may promote aggressive epithelial ovarian cancer biology. Hyperandrogenism results from both obesity and expression of polymorphic androgen receptor (AR) allelotypes harboring short cytosine-adenine-guanine (CAG) repeat

The regulation of adenylate cyclase in liver membranes of lean and obese mice.

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The modulation of adenylate cyclase by guanosine triphosphate (GTP) and hormones was examined in liver membranes of lean and ob/ob mice, to determine whether a defective regulation of cyclase similar to that found in adipocyte membranes was present. In conjunction with GTP, glucagon was a powerful

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