Zobrazeno 1 - 10
of 29
pro vyhledávání: ''
Publikováno v:
Molecular Endocrinology. 30:402-416
The arcuate nucleus of the hypothalamus represents a key center for the control of appetite and feeding through the regulation of 2 key neuronal populations, notably agouti-related peptide/neuropeptide Y and proopimelanocortin (POMC)/cocaine- and amp
Autor:
Darawan Pinthong, Supachoke Mangmool, Sarawuth Phosri, Motohiro Nishida, Tsukasa Shimauchi, Tananat Denkaew, Warisara Parichatikanond
Publikováno v:
Molecular Endocrinology. 30:118-132
Insulin resistance is a condition in which cells are defective in response to the actions of insulin in tissue glucose uptake. Overstimulation of β-adrenergic receptors (βARs) leads to the development of heart failure and is associated with the pat
Publikováno v:
Molecular Endocrinology. 29:1787-1791
Recently, several LH/human chorionic gonadotropin (hCG) receptor-independent activities for hCG have been described, including activation of the TGF-β receptor (TGFβR) by hyperglycosylated hCG and stimulation of trophoblast invasion. Because the hC
Autor:
Haochen Li, Thurl E. Harris, Chien Li, Hongxia Chao, Zhen Yan, Vitor A. Lira, Rebecca C. Grande
Publikováno v:
Molecular Endocrinology. 29:831-841
Type 2 corticotropin-releasing factor receptor (CRFR2) is expressed in skeletal muscle and stimulation of the receptor has been shown to inhibit the effect of insulin on glucose uptake in muscle cells. Currently, little is known about the mechanisms
Publikováno v:
Molecular Endocrinology. 29:682-692
Type 2 diabetes mellitus (T2DM) is characterized by pancreatic islet failure due to loss of β-cell secretory function and mass. Studies have identified a link between a variance in the gene encoding melatonin (MT) receptor 2, T2DM, and impaired insu
Publikováno v:
Molecular Endocrinology. 29:528-541
Progranulin (PGRN) has recently emerged as an important regulator for glucose metabolism and insulin sensitivity. However, the underlying mechanisms of PGRN in the regulation of insulin sensitivity and autophagy remain elusive. In this study, we aime
Autor:
Adolfo Garcia-Ocaña, Ann Marie Segal, Juan Carlos Alvarez-Perez, Paul L. Harris, Antonella Maffei
Publikováno v:
Molecular endocrinology (Baltim. Md.) 29 (2015): 542–547. doi:10.1210/me.2014-1273
info:cnr-pdr/source/autori:Maffei A, Segal AM, Alvarez-Perez JC, Garcia-Ocaña A, Harris PE./titolo:Anti-incretin, Anti-proliferative Action of Dopamine on ?-Cells./doi:10.1210%2Fme.2014-1273/rivista:Molecular endocrinology (Baltim. Md.)/anno:2015/pagina_da:542/pagina_a:547/intervallo_pagine:542–547/volume:29
info:cnr-pdr/source/autori:Maffei A, Segal AM, Alvarez-Perez JC, Garcia-Ocaña A, Harris PE./titolo:Anti-incretin, Anti-proliferative Action of Dopamine on ?-Cells./doi:10.1210%2Fme.2014-1273/rivista:Molecular endocrinology (Baltim. Md.)/anno:2015/pagina_da:542/pagina_a:547/intervallo_pagine:542–547/volume:29
Human islet ?-cells exploit an autocrine dopamine (DA)-mediated inhibitory circuit to regulate insulin secretion. ?-Cells also express the DA active transporter and the large neutral amino acid transporter heterodimer enabling them to import circulat
Publikováno v:
Molecular Endocrinology. 29:396-410
Pancreatic β-cells with severely knocked down cytosolic malic enzyme (ME1) and mitochondrial NAD(P) malic enzyme (ME2) show normal insulin secretion. The mitochondrial NADP malic enzyme (ME3) is very low in pancreatic β-cells, and ME3 was previousl
Autor:
Georgia A. Martin, Robert B. Gilchrist, Xiao-Yan Liang, David G. Mottershead, Lesley J. Ritter, Jing-Jie Li, Satoshi Sugimura, Thomas D. Mueller, Melissa White
Publikováno v:
Molecular Endocrinology. 29:40-52
Growth differentiation factor 9 (GDF9) is an oocyte-derived growth factor that plays a critical role in ovarian folliculogenesis and oocyte developmental competence and belongs to the TGF-β family of proteins. Recombinant human GDF9 (hGDF9) is secre
Publikováno v:
Molecular Endocrinology. 29:108-120
Type 2 diabetes mellitus (T2DM) is caused by relative insulin deficiency, subsequent to both reduced β-cell mass and insufficient insulin secretion, and both augmenting β-cell mass and β-cell function are therapeutic strategies for treating T2DM.