will take place on Tuesday, 25 September 2018 from 17:15 to 18:15 hours in CBBM, EG, B1/B2.
Host: Prof. Dr. Henrik Oster
Institute of Neurobiology
University of Lübeck
Abstract
GLP-1 acts at multiple levels to control the energy metabolism. It increases insulin and reduces glucagon secretion at the pancreas, promoting energy fluxes in the sense of anabolism. At same time, GLP-1 augments CRF release and promotes the activation of the HPA axis as well as the sympathetic nervous system. Both these actions resulting in increased levels of glucocorticoids and catecholamines in circulation may contribute to avoid an excessive activity of insulin and thereby prevent hypoglycaemia. In addition, ghrelin levels became reduced, which also has a mild anabolic effect. Through all these mechanisms, GLP-1 may contribute to postprandial satiation. In type II diabetes, there is a reduction in GLP-1 levels and secretion, despite of characteristic hyperinsulinism and hyperglucagonism. In addition, increased activity of the sympathetic nervous system and the HPA neuroendocrine axis has been described. Increased expression of 11-βHSD1 in adipose tissue is also commonly present, elevating local levels of glucocorticoids. It is not clear whether the increase in glucocorticoids and catecholamines might contribute to hyperglycaemia and hyperinsulinism, but, on the contrary, the increase in HPA and SNS activity may be a direct consequence of what is interpreted by the whole system as a metabolic very stressing condition for cells: the reduced capacity to use glucose linked to insulin resistance. The administration of exogenous GLP-1R agonists may work at different levels to balance the energy metabolism, increasing insulin secretion and reducing glucagon when needed at post-prandial, later increasing cell sensitivity to insulin and activating counter-regulatory HPA and SNS to prevent insulin excessive action.
Biosketch
Yolanda Diz-Chaves began her scientific career in 1997, at the laboratory of Endocrine Physiology, in the Functional Biology and Health Sciences Department, at the University of Vigo in Spain. In that laboratory she did her Master of Sciences (1997‐1999) and her Doctoral Thesis (1999‐2003). From 2003 to 2005, she completed her postdoctoral training at the Victor Ségalen Bordeaux 2 University (France) for working in the Laboratory of “Homéostasie‐Allostasie‐Pathologie” studying the relation between stress an obesity.
From 2005‐2013, she worked at the Laboratory of Neuroactive Steroids, at the Cajal Institute (CSIC) in Madrid. She was funded by the European Project "EWA: Estrogens and Women Aging" (May 2006‐April 2008), obtaining the contract for the incorporation of researchers (JAE, doctors; CSIC, co‐financed by European Social Fund). During this period she studied the neuroprotective effects of neurosteroids in animal models of neuroinflammation as the prenatal stress model.
From 2014‐present, she has been working as Postdoctoral Senior Researcher in the Laboratory of Endocrinology (Center of Biomedical Research (CINBIO), University of Vigo). Since 2017 she obtained the contract for emergent researcher in CINBIO funded by Xunta de Galicia. She studies the extrapancreatic effects of GLP-1 in the regulation of metabolism and the neuroprotective effects in a prenatal stress model of diabesity.
