"No pienses en un oso blanco". Sobre un caso de trastorno de la conducta alimentaria de larga evolución.

Sin resumen

How does financial literacy influence undergraduates’ risk-taking propensity?

Previous evidence is contradictory about the financial literacy-individual’s risk-taking propensity relationship. Therefore, this article attempts to examine the relationship between financial literacy and risk-taking propensity in a university environment, considering for the first time the financial literacy’s multidimensional nature (i.e., financial knowledge, financial attitude, and financial behaviour). Applying Covariance-Based Structural Equation Models to 568 Spanish undergraduates, our results show that: (1) financial knowledge and financial behaviour directly and positively affect risk-taking propensity; (2) financial attitude indirectly and positively affects risk-taking propensity through financial behaviour. These findings are relevant since they provide new insights into the association mechanism that explains the financial literacy-undergraduates’ risk-taking propensity relationship.Antonio Molina-García’s work was funded by the Spanish Ministry of Education and Vocational Training (FPU) (FPU20/02328). Funding for open access charge: Universidad de Málaga / CBUA

Ghrelin and lipid metabolism: key partners in energy balance

Disclaimer: this is not the definitive version of record of this article. This manuscript has been accepted for publication in "Journal of Molecular Endocrinology", but the version presented here has not yet been copy-edited, formatted or proofed. Consequently, Bioscientifica acepts no responsability for any errors on omissions it may contain. The definitive version is now freely avaliable at doi 10.1677/JME-10-0068[Abstract] Ghrelin, the endogenous ligand of the GH secretagogue receptor, has a pleiotropic role in the modulation of energy balance. Recent evidence has demonstrated that besides its orexigenic role, ghrelin regulates central and peripheral lipid metabolism through specific control of hypothalamic AMP-activated protein kinase (AMPK), a critical metabolic gauge regulating both cellular and whole-body energy homeostasis. In this review, we summarize the new milestones of ghrelin's actions on energy balance, with particular focus on its molecular interaction with hypothalamic AMPK and fatty acid metabolism. Understanding this new metabolic pathway can provide new therapeutic targets for the treatment of obesity and the metabolic syndrome.European Commission; FP7/2007–2013 no. 245009European Commission; FP7/2007–2013; nº 018734Xunta de Gailcia; PS07/12Xunta de Gailcia; PGIDIT06PXIB208063PRXunta de Gailcia; 10PXIB208164PRInstituto de Salud Carlos III; PI051024Instituto de Salud Carlos III;PI070413Instituto de Salud Carlos III; PS09/01880Ministerio de Educacion y Ciencia; RyC-2008-02219Ministerio de Educacion y Ciencia; BFU2008Ministerio de Educacion y Ciencia; RyC-2007-0021

A gliclazide complex based on palladium towards Alzheimer's disease: promising protective activity against Aβ-induced toxicity in C. elegans

A new palladium coordination compound based on gliclazide with the chemical formula [Pd(glz)2] (where glz = gliclazide) has been synthesized and characterised. The structural characterization reveals that this material consists of mononuclear units formed by a Pd2+ ion coordinated to two molecules of the glz ligand, in which palladium ions exhibit a distorted plane-square coordination sphere. This novel material behaves like a good and selective inhibitor of butyrylcholinesterase, one of the most relevant therapeutic targets against Alzheimer’s disease. Analysis of the enzyme kinetics showed a mixed mode of inhibition, the title compound being capable of interacting with both the free enzyme and the enzyme–substrate complex. Finally, the palladium compound shows promising protective activity against Ab-induced toxicity in the Caenorhabditis elegans model, which has never been reported

Hypothalamic mTOR signaling mediates the orexigenic action of ghrelin

Current evidence suggests that ghrelin, a stomach derived peptide, exerts its orexigenic action through specific modulation of Sirtuin1 (SIRT1)/p53 and AMP-activated protein kinase (AMPK) pathways, which ultimately increase the expression of agouti-related protein (AgRP) and neuropeptide Y (NPY) in the arcuate nucleus of the hypothalamus (ARC). However, there is a paucity of data about the possible action of ghrelin on alternative metabolic pathways at this level. Here, we demonstrate that ghrelin elicits a marked upregulation of the hypothalamic mammalian target of rapamycin (mTOR) signaling pathway. Of note, central inhibition of mTOR signaling with rapamycin decreased ghrelin's orexigenic action and normalized the mRNA expression of AgRP and NPY, as well as their key downstream transcription factors, namely cAMP response-element binding protein (pCREB) and forkhead box O1 (FoxO1, total and phosphorylated). Taken together, these data indicate that, in addition to previous reported mechanisms, ghrelin also promotes feeding through modulation of hypothalamic mTOR pathway

Influence of ghrelin and growth hormone deficiency on AMP-activated protein kinase and hypothalamic lipid metabolism

This is the peer reviewed version of the article which has been published in final form at Wiley Online Library. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for self-archiving[Abstract] Current evidence demonstrates that the stomach-derived hormone ghrelin, a potent growth hormone (GH) secretagogue, promotes feeding through a mechanism involving the short-term activation of hypothalamic AMP-activated protein kinase (AMPK), which in turn results in decreased hypothalamic levels of malonyl-CoA and increased carnitine palmitoyltransferase 1 (CPT1) activity. Despite this evidence, no data have been reported about the effect of chronic, central ghrelin administration on hypothalamic fatty acid metabolism. In the present study, we examined the differences in hypothalamic fatty acid metabolism in the presence and absence of GH, by using a model for the study of GH-deficiency, namely the spontaneous dwarf rat and the effect of long-term central ghrelin treatment and starvation on hypothalamic fatty acid metabolism in this animal model. Our data showed that GH-deficiency induces reductions in both de novo lipogenesis and β-oxidation pathways in the hypothalamus. Thus, dwarf rats display reductions in fatty acid synthase (FAS) mRNA expression both in the ventromedial nucleus of the hypothalamus (VMH) and whole hypothalamus, as well as in FAS protein and activity. CPT1 activity was also reduced. In addition, in the present study, we show that chronic ghrelin treatment does not promote AMPK-induced changes in the overall fluxes of hypothalamic fatty acid metabolism in normal rats and that this effect is independent of GH status. By contrast, we demonstrated that both chronic ghrelin and fasting decreased FAS mRNA expression in the VMH of normal rats but not dwarf rats, suggesting GH status dependency. Overall, these results suggest that ghrelin plays a dual time-dependent role in modulating hypothalamic lipid metabolism. Understanding the molecular mechanism underlying the interplay between GH and ghrelin on hypothalamic lipid metabolism will allow new strategies for the design and development of suitable drugs for the treatment of GH-deficiency, obesity and its comorbidities.Galicia. Consellería de Innovación, Industria e Comercio; PGIDIT06PXIB208063PRGalicia. Consellería de Cultura, Educación e Ordenación Universitaria; GRC2006/66Xunta de Galicia; PS07/12Instituto de Salud Carlos III; PI061700Instituto de Salud Carlos III; PS09/01880Instituto de Salud Carlos III; PI051024Instituto de Salud Carlos III; PI070413Ministerio de Educacion y Ciencia; BFU2008Ministerio de Educacion y Ciencia; RyC-2007-00211Unión Europea; Health-F2-2008-22371

Sequential Exposure to Obesogenic Factors in Females Rats: From Physiological Changes to Lipid Metabolism in Liver and Mesenteric Adipose Tissue

During their lifetime, females are subjected to different nutritional and hormonal factors that could increase the risk of obesity and associated comorbidities. From early postnatal periods until the postmenopausal phase, exposure to over nutrition, high-energy diet and oestrogen deficiency, are considered as significant obesity risk factors in women. In this study, we assessed how key transitional life events and exposure to different nutrition influence energy homeostasis in a rat model. Specifically, we assessed the sequential exposure to postnatal over nutrition, high-fat diet (HFD) after weaning, followed later by ovariectomy (OVX; as a model of menopause). Each obesity risk factor increased significantly body weight (BW) and adiposity, with additive effects after sequential exposure. Increased energy intake in both HFD and/or OVX groups, and decreased locomotor activity and energy expenditure after OVX can explain these metabolic changes. Our study also documents decreased lipogenic pathway in mesenteric adipose tissue after HFD and/or OVX, independent of previous postnatal programming, yet only HFD evoked this effect in liver. In addition, we report an increase in the expression of the hepatic PEPCK depending on previous metabolic status. Overall, our results identify the impact of different risk factors, which will help in understanding the development of obesity in females