Attenuation of Diabetic Hyperphagia in Neuropeptide Y-Deficient Mice
نویسندگان
چکیده
منابع مشابه
Attenuation of diabetic hyperphagia in neuropeptide Y--deficient mice.
The combined effects of increased hypothalamic signaling by neuropeptide Y (NPY) and decreased signaling by melanocortins are hypothesized to stimulate food intake when body fat stores are depleted. To investigate NPY's role in the hyperphagic response to uncontrolled diabetes, streptozotocin (STZ) (200 mg/kg intraperitoneally) or saline vehicle was given to NPY-deficient (Npy(--/--)) and wild-...
متن کاملInsulin secretion is increased in pancreatic islets of neuropeptide Y-deficient mice.
Neuropeptide Y (NPY), whose role in appetite regulation is well known, is also expressed in pancreatic islets. Although previous studies indicated that application of NPY to pancreatic islets inhibits insulin secretion, its physiological role in the regulation of insulin secretion is not fully understood. We hypothesized that NPY in islets tonically suppresses insulin secretion and the reductio...
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OBJECTIVE Tankyrase (TNKS) is a Golgi-associated poly-ADP-ribose polymerase that is implicated in the regulation of GLUT4 trafficking in 3T3-L1 adipocytes. Its chromosomal locus 8p23.1 is linked to monogenic forms of diabetes in certain kindred. We hypothesize that TNKS is involved in energy homeostasis in mammals. RESEARCH DESIGN AND METHODS Gene-trap techniques were used to ablate TNKS expr...
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To elucidate the role of neuropeptide Y (NPY)-Y1 receptor (Y1-R) in food intake, energy expenditure, and other possible functions, we have generated Y1-R-deficient mice (Y1-R-/-) by gene targeting. Contrary to our hypothesis that the lack of NPY signaling via Y1-R would result in impaired feeding and weight loss, Y1-R-/- mice showed a moderate obesity and mild hyperinsulinemia without hyperphag...
متن کاملDistinct forebrain and caudal brainstem contributions to the neuropeptide Y mediation of ghrelin hyperphagia.
Neuropeptide Y (NPY) has been implicated in the downstream mediation of ghrelin hyperphagia, with the site of action for both peptides considered to be intrinsic to the hypothalamus. Here, however, we observed robust hyperphagia with caudal brainstem (CBS) (fourth intracerebroventricular) ghrelin delivery and, moreover, that this response was reversed with coadministration of either of two NPY ...
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ژورنال
عنوان ژورنال: Diabetes
سال: 2002
ISSN: 0012-1797,1939-327X
DOI: 10.2337/diabetes.51.3.778