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adenyl cyclase/obesity

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14 結果

[Membrane adenyl cyclase activity in adipose tissue of obese hyperglycemic Bar-Harbor mice].

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Adenyl cyclase and cyclic AMP-phosphodiesterase activity in the isolated islets of Langerhans of normal and obese mice.

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Application of agents active at the alpha 2-adrenoceptor of fat cells to the treatment of obesity--a critical appraisal.

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The extent of cyclic AMP (cAMP) mediated lipolysis in adipose tissue cells of man and several other animal species is regulated by the interplay of alpha- and beta-adrenoceptors modulating adenyl cyclase activity. Although the naturally-occurring catecholamines, and isoprenaline, are thought to act

Glycogen metabolism and cyclic AMP levels in isolated islets of lean and genetically obese mice.

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The levels of glycogen and cyclic AMP, incorporation of glucose into glycogen and activities of glycogen synthetase and phosphorylase were determined in pancreatic islets isolated from genetically obese mice and their lean litter-mates. Islets from obese mice had elevated glycogen levels, increased

FABP4 is secreted from adipocytes by adenyl cyclase-PKA- and guanylyl cyclase-PKG-dependent lipolytic mechanisms.

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OBJECTIVE Fatty acid-binding protein 4 (FABP4) is expressed in adipocytes, and elevated plasma FABP4 level is associated with obesity-mediated metabolic phenotype. Postprandial regulation and secretory signaling of FABP4 has been investigated. METHODS Time courses of FABP4 levels were examined

[The discovery of neuromedin U and its pivotal role in the central regulation of energy homeostasis].

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Neuromedin U (NMU) is a structurally highly conserved neuropeptide and has been paired with the G-protein-coupled receptors (GPCRs) NMUR1 and NMUR2, which were formerly classified in the orphan receptor family. Activation of the G protein Gq/11 subunit causes a pertussis toxin (PTX)-insensitive
OBJECTIVE Resistin, a novel hormone, is expressed in mouse, rat and human adipose tissue. Its resistance to insulin is controversial. We hypothesized that resistin has the similar roles like those of tumour necrosis factor-alpha (TNF-alpha), a putative mediator of insulin resistance, and they are in

First diagnosis of Martin-Albright syndrome in a 58-year-old patient.

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Albright hereditary osteodystrophy (AHO), also known as Martin-Albright syndrome (MAS), is a rare autosomal dominantly transmitted disease characterized by short stature, obesity, mental retardation, a round facies, and brachymetacarpia and -tarsia, as well as cutaneous calcification. The disease is

Repetitive hypoglycaemia increases serum adrenaline and induces monocyte adhesion to the endothelium in rat thoracic aorta.

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OBJECTIVE Severe hypoglycaemia associated with diabetes management is a potential risk for cardiovascular diseases. However, the effect and mechanism of hypoglycaemia on the progression of atherosclerosis remains largely unknown. As a first step towards elucidating the above, we investigated the

Insulin resistance and type 2 diabetes mellitus: its relationship with the beta 3-adrenergic receptor.

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The beta 3 subtype of adrenaline and noradrenaline receptors has been extensively characterized at structural and functional levels. Ligand binding and adenyl cyclase activation studies have helped to define their unique beta-adrenergic profile. Humans, other larger mammals, and rodents share most

Pseudohypoparathyroidism with normal serum calcium level.

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A mildly obese 15-year-old boy had short stature with rounded facies and short, stubby hands and toes. He had the fully expressed syndrome of pseudohypoparathyroidism but was the only member of his family who had all the somatic characteristics of this disease. The serum parathyroid hormone level

Protein kinase A signaling as an anti-aging target.

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Protein kinase A (PKA) is a multi-unit protein kinase that mediates signal transduction of G-protein-coupled receptors through its activation by adenyl cyclase (AC)-mediated cAMP. The vital importance of PKA signaling to cellular function is reflected in the widespread expression of PKA subunit

CRTC3 links catecholamine signalling to energy balance.

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The adipose-derived hormone leptin maintains energy balance in part through central nervous system-mediated increases in sympathetic outflow that enhance fat burning. Triggering of β-adrenergic receptors in adipocytes stimulates energy expenditure by cyclic AMP (cAMP)-dependent increases in
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