Abnormalities of the somatotrophic axis in the obese agouti mouse
暂无分享,去创建一个
N. Martin | S. Bloom | D. Carmignac | M. Ghatei | C. Small | M. Patterson | M. Ghatei | M. Ghatei | S. Bloom | A. Sajedi | S. Bloom | P. Houston | C. Small | NM Martin | D. Carmignac | D F Carmignac
[1] N. Martin,et al. Pre-obese and obese agouti mice are sensitive to the anorectic effects of peptide YY3–36 but resistant to ghrelin , 2004, International Journal of Obesity.
[2] T. Horvath,et al. Disruption of neural signal transducer and activator of transcription 3 causes obesity, diabetes, infertility, and thermal dysregulation. , 2004, Proceedings of the National Academy of Sciences of the United States of America.
[3] H. Watanobe,et al. Evaluation of the Role of Melanocortin 3 and 4 Receptors in Leptin-Stimulated and Spontaneous Growth Hormone Secretion in Rats , 2003, Neuroendocrinology.
[4] A. Grüters,et al. Obesity due to proopiomelanocortin deficiency: three new cases and treatment trials with thyroid hormone and ACTH4-10. , 2003, The Journal of clinical endocrinology and metabolism.
[5] Mohammad A Ghatei,et al. Inhibition of food intake in obese subjects by peptide YY3-36. , 2003, The New England journal of medicine.
[6] I. Robinson,et al. Transgenesis and neuroendocrine physiology: a transgenic rat model expressing growth hormone in vasopressin neurones , 2003, The Journal of physiology.
[7] Tim Cheetham,et al. Clinical spectrum of obesity and mutations in the melanocortin 4 receptor gene. , 2003, The New England journal of medicine.
[8] M. Aubert,et al. The Melanocortin Agonist Melanotan‐II Reduces the Orexigenic and Adipogenic Effects of Neuropeptide Y (NPY) but Does not Affect the NPY‐Driven Suppressive Effects on the Gonadotropic and Somatotropic Axes in the Male Rat , 2003, Journal of neuroendocrinology.
[9] S. Bloom,et al. The Hypothalamic Mechanisms of the Hypophysiotropic Action of Ghrelin , 2002, Neuroendocrinology.
[10] B. Levin,et al. Reduced central leptin sensitivity in rats with diet-induced obesity. , 2002, American journal of physiology. Regulatory, integrative and comparative physiology.
[11] M. Phillip,et al. Leptin Acts as a Growth Factor on the Chondrocytes of Skeletal Growth Centers , 2002, Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research.
[12] H. Yoshimatsu,et al. Hyperleptinemia in A(y)/a mice upregulates arcuate cocaine- and amphetamine-regulated transcript expression. , 2002, American journal of physiology. Endocrinology and metabolism.
[13] A. Mark,et al. The concept of selective leptin resistance: evidence from agouti yellow obese mice. , 2002, Diabetes.
[14] T. Pedrazzini,et al. Chronic administration of neuropeptide Y into the lateral ventricle of C57BL/6J male mice produces an obesity syndrome including hyperphagia, hyperleptinemia, insulin resistance, and hypogonadism , 2001, Molecular and Cellular Endocrinology.
[15] G. Frost,et al. Ghrelin enhances appetite and increases food intake in humans. , 2001, The Journal of clinical endocrinology and metabolism.
[16] T. Wells,et al. Skeletal Growth Acceleration with Growth Hormone Secretagogues in Transgenic Growth Retarded Rats: Pattern‐Dependent Effects and Mechanisms of Desensitization , 2001, Journal of neuroendocrinology.
[17] E. Ravussin,et al. Circulating ghrelin levels are decreased in human obesity. , 2001, Diabetes.
[18] S. Yakar,et al. The somatomedin hypothesis: 2001. , 2001, Endocrine reviews.
[19] M. Aubert,et al. Chronic blockade of the melanocortin 4 receptor subtype leads to obesity independently of neuropeptide Y action, with no adverse effects on the gonadotropic and somatotropic axes. , 2000, Endocrinology.
[20] S. Bloom,et al. The novel hypothalamic peptide ghrelin stimulates food intake and growth hormone secretion. , 2000, Endocrinology.
[21] Yue Feng,et al. Inactivation of the mouse melanocortin-3 receptor results in increased fat mass and reduced lean body mass , 2000, Nature Genetics.
[22] R. Cone,et al. A Unique Metalolic Sysdrone Causes Obesity in the Melanocortin-3 Receptor-Deficient Mouse. , 2000, Endocrinology.
[23] C. Steppan,et al. Leptin is a potent stimulator of bone growth in ob/ob mice , 2000, Regulatory Peptides.
[24] S. Woods,et al. Central nervous system control of food intake , 2000, Nature.
[25] S. O’Rahilly,et al. Dominant and recessive inheritance of morbid obesity associated with melanocortin 4 receptor deficiency. , 2000, The Journal of clinical investigation.
[26] G. Barsh,et al. Anatomy of an Endogenous Antagonist: Relationship between Agouti-Related Protein and Proopiomelanocortin in Brain , 1999, The Journal of Neuroscience.
[27] L. Yaswen,et al. Obesity in the mouse model of pro-opiomelanocortin deficiency responds to peripheral melanocortin , 1999, Nature Medicine.
[28] Navarra,et al. The Effect of Growth Hormone Secretagogues and Neuropeptide Y on Hypothalamic Hormone Release from Acute Rat Hypothalamic Explants , 1999, Journal of neuroendocrinology.
[29] W. J. Visek,et al. Caloric restriction abolishes enhanced metabolic efficiency induced by ectopic agouti protein in yellow mice. , 1999, Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine.
[30] F. Casanueva,et al. Role of Growth Hormone (GH)-Releasing Hormone and Somatostatin on Leptin-Induced GH Secretion , 1999, Neuroendocrinology.
[31] T. Hökfelt,et al. Hypocretin/Orexin‐ and melanin‐concentrating hormone‐expressing cells form distinct populations in the rodent lateral hypothalamus: Relationship to the neuropeptide Y and agouti gene‐related protein systems , 1998, The Journal of comparative neurology.
[32] L. Vanhaelst,et al. Cafeteria diet-induced obesity is associated with a low spontaneous growth hormone secretion and normal plasma insulin-like growth factor-I concentrations. , 1998, Growth hormone & IGF research : official journal of the Growth Hormone Research Society and the International IGF Research Society.
[33] S. Bloom,et al. A C-terminal fragment of Agouti-related protein increases feeding and antagonizes the effect of alpha-melanocyte stimulating hormone in vivo. , 1998, Endocrinology.
[34] Michael W. Schwartz,et al. Coexpression of Agrp and NPY in fasting-activated hypothalamic neurons , 1998, Nature Neuroscience.
[35] J. Shutter,et al. Overexpression of Agrt leads to obesity in transgenic mice , 1997, Nature Genetics.
[36] G. Barsh,et al. Antagonism of central melanocortin receptors in vitro and in vivo by agouti-related protein. , 1997, Science.
[37] R. Cone,et al. Induction of neuropeptide Y gene expression in the dorsal medial hypothalamic nucleus in two models of the agouti obesity syndrome. , 1997, Molecular endocrinology.
[38] E. Hooghe-Peters,et al. Cafeteria diet-induced obese rats have an increased somatostatin protein content and gene expression in the periventricular nucleus , 1997, Journal of endocrinological investigation.
[39] R. Cone,et al. Targeted Disruption of the Melanocortin-4 Receptor Results in Obesity in Mice , 1997, Cell.
[40] R. Palmiter,et al. Attenuation of the Obesity Syndrome of ob/ob Mice by the Loss of Neuropeptide Y , 1996, Science.
[41] D. Smith,et al. Glucagon-like peptide-1 (GLP-1) releases thyrotropin (TSH): characterization of binding sites for GLP-1 on alpha-TSH cells. , 1996, Endocrinology.
[42] S. Woods,et al. Specificity of Leptin Action on Elevated Blood Glucose Levels and Hypothalamic Neuropeptide Y Gene Expression in ob/ob Mice , 1996, Diabetes.
[43] E. Ravussin,et al. Leptin levels in human and rodent: Measurement of plasma leptin and ob RNA in obese and weight-reduced subjects , 1995, Nature Medicine.
[44] I. Robinson,et al. Hypothalamic GH receptor gene expression in the rat: effects of altered GH status. , 1995, The Journal of endocrinology.
[45] Richard P. Woychik,et al. Agouti protein is an antagonist of the melanocyte-stimulating-hormone receptor , 1994, Nature.
[46] M. Mortrud,et al. Localization of the melanocortin-4 receptor (MC4-R) in neuroendocrine and autonomic control circuits in the brain. , 1994, Molecular endocrinology.
[47] C. Deal,et al. Hormonal control of growth in the genetically obese Zucker rat. I. Linear growth, plasma insulin-like growth factor-I (IGF-I) and IGF-binding proteins. , 1994, Endocrinology.
[48] I. Robinson,et al. Growth hormone binding protein in the rat: effects of gonadal steroids. , 1993, Endocrinology.
[49] S. Mccann,et al. Physiologically significant effect of neuropeptide Y to suppress growth hormone release by stimulating somatostatin discharge. , 1990, Endocrinology.
[50] J. Ilan,et al. Expression of insulin-like growth factor I in cultured rat hepatocytes: effects of insulin and growth hormone. , 1989, Molecular endocrinology.
[51] V. Mendel. Influence of the insulin-to-growth hormone ratio on body composition of mice. , 1980, The American journal of physiology.
[52] Yen Tt,et al. An analysis of the relationships among obesity, plasma insulin, and hepatic lipogenic enzymes in 'viable yellow obese' mice (avy/a). , 1976 .
[53] W. E. Heston,et al. Influence of the Ay gene on mammary-gland tumors, hepatomas, and normal growth in mice. , 1961, Journal of the National Cancer Institute.
[54] E. Müller,et al. Neuroendocrine control of growth hormone secretion , 2004, Naunyn-Schmiedeberg's Archives of Pharmacology.
[55] S. O’Rahilly,et al. Serum ghrelin levels are inversely correlated with body mass index, age, and insulin concentrations in normal children and are markedly increased in Prader-Willi syndrome. , 2003, The Journal of clinical endocrinology and metabolism.
[56] R. Cone,et al. A unique metabolic syndrome causes obesity in the melanocortin-3 receptor-deficient mouse. , 2000, Endocrinology.
[57] B. Levin. Arcuate NPY neurons and energy homeostasis in diet-induced obese and resistant rats. , 1999, The American journal of physiology.
[58] 安永徹. Nutrition related hormonal changes in obese children(肥満児の栄養過多によるホルモン変化について) , 1998 .
[59] M. Aubert,et al. Neuropeptide Y administered chronically into the lateral ventricle profoundly inhibits both the gonadotropic and the somatotropic axis in intact adult female rats. , 1993, Endocrinology.
[60] G. Wolff,et al. Differential responses of yellow Avy/A and agouti A/a (BALB/c X VY) F1 hybrid mice to the same diets: glucose tolerance, weight gain, and adipocyte cellularity. , 1988, International journal of obesity.
[61] M. Greenberg,et al. An Analysis of the Relationships Among Obesity, Plasma Insulin, and Hepatic Lipogenic Enzymes in "Viable Yellow Obese" Mice (Avy/a)* , 1976, Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme.