Chromosomal mapping of ribosomal clusters and telomeric sequences (TTAGG)n in nine species of lobsters (Crustacea, Decapoda)

Lobsters are ubiquitous, economically important decapod crustaceans with apparently conflicting evolutionary relationships. Here, we describe the chromosomal location of the major (45S rDNA) and minor (5S rDNA) ribosomal gene families in four species of Astacidea and five of Achelata, using two-color FISH. The major ribosomal family is located in 4–16 sites per diploid chromosome set, with Nephrops norvegicus (Nephropidae) showing the highest number described so far in Decapoda. The 5S rDNA is located in two sites in eight species; only in the crayfish Procambarus clarkii the 5S FISH signals were detected in four sites together with additional weaker signals. Furthermore, in N. norvegicus the minor ribosomal genes are syntenic with one major ribosomal cluster. Moreover, we located by two-color FISH the pentanucleotide (TTAGG)n telomeric repeat in the Nephropidae studied, showing the occurrence of a colocalization with 45S ribosomal sequences in Homarus gammarus. The comparison of chromosomal locations of repetitive sequences in Mediterranean, Atlantic, and South African lobster species as well as in marine and freshwater ones provides information on chromosomal evolution and cytotaxonomy of Decapoda

Improvement in glycemia after glucose or insulin overload in leptin-infused rats is associated with insulin-related activation of hepatic glucose metabolism

Background: Insulin regulates glucose homeostasis through direct effects on the liver, among other organs, with leptin modulating insulin's hepatic actions. Since central leptin may modify insulin signaling in the liver, we hypothesized that leptin infusion activates hepatic glycogen synthesis following peripheral administration of a bolus of glucose or insulin, thus regulating glycemia. Findings: Oral glucose and intraperitoneal insulin tolerance tests were performed in control, intracerebroventricular leptin-treated and pair-fed rats during 14 days. An improvement in glycemia and an increase in hepatic free glucose and glycogen concentrations after glucose or insulin overload were observed in leptin-treated rats. In order to analyze whether the liver was involved in these changes, we studied activation of insulin signaling by Western blotting and multiplex bead immunoassay after leptin infusion. Our studies revealed an increase in phosphorylation of insulin receptor substrate-1 and Akt in leptin-treated rats. Examination of parameters related to glucose uptake and metabolism in the liver revealed an augment in glucose transporter 2 and a decrease in phosphoenolpyruvate carboxylase protein levels in this group. Conclusions: These results indicate that central leptin increases hepatic insulin signaling, associated with increased glycogen concentrations after glucose or insulin overload, leading to an improvement in glycemia.This work was supported by the Spanish Ministry of Science and Innovation with the help of European FEDER funding (FIS PI13/02195), Ministerio de Ciencia e Innovación (BFU2011-27492 and BFU2014-51836-C2-2-R), the Network Center for Biomedical Research on Obesity and Nutrition (CIBEROBN) Instituto Carlos III and Fundación Endocrinología y Nutrición. S.C. is supported by CIBEROB

Leptin modulates the response of brown adipose tissue to negative energy balance: implication of the gh/igf-i axis

The growth hormone (GH)/insulin-like growth factor I (IGF-I) axis is involved in metabolic control. Malnutrition reduces IGF-I and modifies the thermogenic capacity of brown adipose tissue (BAT). Leptin has effects on the GH/IGF-I axis and the function of BAT, but its interaction with IGF-I and the mechanisms involved in the regulation of thermogenesis remains unknown. We studied the GH/IGF-I axis and activation of IGF-I-related signaling and metabolism related to BAT thermogenesis in chronic central leptin infused (L), pair-fed (PF), and control rats. Hypothalamic somatostatin mRNA levels were increased in PF and decreased in L, while pituitary GH mRNA was reduced in PF. Serum GH and IGF-I concentrations were decreased only in PF. In BAT, the association between suppressor of cytokine signaling 3 and the IGF-I receptor was reduced, and phosphorylation of the IGF-I receptor increased in the L group. Phosphorylation of Akt and cyclic AMP response element binding protein and glucose transporter 4 mRNA levels were increased in L and mRNA levels of uncoupling protein-1 (UCP-1) and enzymes involved in lipid anabolism reduced in PF. These results suggest that modifications in UCP-1 in BAT and changes in the GH/IGF-I axis induced by negative energy balance are dependent upon leptin levels.This research was funded by the Spanish Ministry of Science and Innovation with the help of European FEDER funding (FIS PI19/00166), Ministerio de Economía y Competitividad (BFU 2017-82565-C2-1-R) and the Network Center for Biomedical Research on Obesity and Nutrition (CIBEROBN) Instituto Carlos III. S.C. was supported by CIBEROB

Increased oxidative stress and apoptosis in the hypothalamus of diabetic male mice in the insulin receptor substrate-2 knockout model

Insulin receptor substrate-2-deficient (IRS2-/-) mice are considered a good model to study the development of diabetes because IRS proteins mediate the pleiotropic effects of insulin-like growth factor-I (IGF-I) and insulin on metabolism, mitogenesis and cell survival. The hypothalamus might play a key role in the early onset of diabetes, owing to its involvement in the control of glucose homeostasis and energy balance. Because some inflammatory markers are elevated in the hypothalamus of diabetic IRS2-/- mice, our aim was to analyze whether the diabetes associated with the absence of IRS2 results in hypothalamic injury and to analyze the intracellular mechanisms involved. Only diabetic IRS2-/- mice showed increased cell death and activation of caspase-8 and -3 in the hypothalamus. Regulators of apoptosis such as FADD, Bcl-2, Bcl-xL and p53 were also increased, whereas p-IκB and c-FLIPL were decreased. This was accompanied by increased levels of Nox-4 and catalase, enzymes involved in oxidative stress. In summary, the hypothalamus of diabetic IRS2-/- mice showed an increase in oxidative stress and inflammatory markers that finally resulted in cell death via substantial activation of the extrinsic apoptotic pathway. Conversely, nondiabetic IRS2-/- mice did not show cell death in the hypothalamus, possibly owing to an increase in the levels of circulating IGF-I and in the enhanced hypothalamic IGF-IR phosphorylation that would lead to the stimulation of survival pathways. In conclusion, diabetes in IRS2-deficient male mice is associated with increased oxidative stress and apoptosis in the hypothalamusThis work was supported by the Ministerio de Ciencia e Innovación [BFU2011- 27492 and BFU2014-51836-C2-2-R to J.A.C.; and SAF2012-33283 to A.M.V.]; Fondo de Investigación Sanitaria [PI1302195 to J.A.]; Centro de Investigación Biomédica en Red de Fisiopatologı́a de Obesidad y Nutrición (CIBEROBN); and Centro de Investigación Biomédica en Red Diabetes y Enfermedades asociadas (CIBERDEM), Instituto de Salud Carlos III, and Fundación de Endocrinologı́a y Nutrición

Estradiol uses different mechanisms in astrocytes from the hippocampus of male and female rats to protect against damage Induced by palmitic acid

An excess of saturated fatty acids can be toxic for tissues, including the brain, and this has been associated with the progression of neurodegenerative diseases. Since palmitic acid (PA) is a free fatty acid that is abundant in the diet and circulation and can be harmful, we have investigated the effects of this fatty acid on lipotoxicity in hippocampal astrocytes and the mechanism involved. Moreover, as males and females have different susceptibilities to some neurodegenerative diseases, we accessed the responses of astrocytes from both sexes, as well as the possible involvement of estrogens in the protection against fatty acid toxicity. PA increased endoplasmic reticulum stress leading to cell death in astrocytes from both males and females. Estradiol (E2) increased the levels of protective factors, such as Hsp70 and the anti-inflammatory cytokine interleukin-10, in astrocytes from both sexes. In male astrocytes, E2 decreased pJNK, TNFα, and caspase-3 activation. In contrast, in female astrocytes E2 did not affect the activation of JNK or TNFα levels, but decreased apoptotic cell death. Hence, although E2 exerted protective effects against the detrimental effects of PA, the mechanisms involved appear to be different between male and female astrocytes. This sexually dimorphic difference in the protective mechanisms induced by E2 could be involved in the different susceptibilities of males and females to some neurodegenerative processesThis work was funded by grants from Ministerio de Ciencia e Innovación (BFU2014-51836-C2-2-R to JC and BFU2014-51836-C2-1-R to LG-S) and Fondos de Investigación Sanitaria (Grant PI16/00485 to JA), co-funded by European FEDER Program, and Centro de Investigación Biomédica en Red Fisiopatología de Obesidad y Nutrición (CIBEROBN) of the Instituto de Salud Carlos III, and Fundación de Endocrinología y Nutrició

Cerebral insulin bolus revokes the changes in hepatic lipid metabolism induced by chronic central leptin infusion

Central actions of leptin and insulin on hepatic lipid metabolism can be opposing and the mechanism underlying this phenomenon remains unclear. Both hormones can modulate the central somatostatinergic system that has an inhibitory effect on growth hormone (GH) expression, which plays an important role in hepatic metabolism. Using a model of chronic central leptin infusion, we evaluated whether an increase in central leptin bioavailability modifies the serum lipid pattern through changes in hepatic lipid metabolism in male rats in response to an increase in central insulin and the possible involvement of the GH axis in these effects. We found a rise in serum GH in leptin plus insulin-treated rats, due to an increase in pituitary GH mRNA levels associated with lower hypothalamic somatostatin and pituitary somatostatin receptor-2 mRNA levels. An augment in hepatic lipolysis and a reduction in serum levels of non-esterified fatty acids (NEFA) and triglycerides were found in leptin-treated rats. These rats experienced a rise in lipogenic-related factors and normalization of serum levels of NEFA and triglycerides after insulin treatment. These results suggest that an increase in insulin in leptin-treated rats can act on the hepatic lipid metabolism through activation of the GH axisThis research was funded by the Spanish Ministry of Science and Innovation with the help of European FEDER funding (FIS PI19/00166), Ministerio de Economía y Competitividad (BFU 2017-82565-C2-1-R) and the Network Center for Biomedical Research on Obesity and Nutrition (CIBEROBN) Instituto Carlos III. S.C. was supported by CIBEROB

Increased hypothalamic anti‐inflammatory mediators in non‐diabetic insulin receptor substrate 2‐deficient mice

© 2021 by the authors.Insulin receptor substrate (IRS) 2 is a key mediator of insulin signaling and IRS-2 knockout (IRS2−/−) mice are a preclinical model to study the development of diabetes, as they develop peripheral insulin resistance and beta-cell failure. The differential inflammatory profile and insulin signaling in the hypothalamus of non-diabetic (ND) and diabetic (D) IRS2−/− mice might be implicated in the onset of diabetes. Because the lipid profile is related to changes in inflammation and insulin sensitivity, we analyzed whether ND IRS2−/− mice presented a different hypothalamic fatty acid metabolism and lipid pattern than D IRS2−/− mice and the relationship with inflammation and markers of insulin sensitivity. ND IRS2−/− mice showed elevated hypothalamic anti-inflammatory cytokines, while D IRS2−/− mice displayed a proinflammatory profile. The increased activity of enzymes related to the pentose-phosphate route and lipid anabolism and elevated polyunsaturated fatty acid levels were found in the hypothalamus of ND IRS2−/− mice. Conversely, D IRS2−/− mice have no changes in fatty acid composition, but hypothalamic energy balance and markers related to anti-inflammatory and insulin-sensitizing properties were reduced. The data suggest that the concurrence of an anti-inflammatory profile, increased insulin sensitivity and polyunsaturated fatty acids content in the hypothalamus may slow down or delay the onset of diabetes.This work was supported by the Spanish Ministry of Science and Innovation with the help of European FEDER funding (grant numbers FIS PI19/00166, BFU 2017-82565-C2-1-R, and RTI2018-094052-B-100), Comunidad de Madrid, Spain (S2017/BMD-3684) and the Network Center for Biomedical Research on Obesity and Nutrition (CIBEROBN) and Diabetes (CIBERDEM) Instituto Carlos III. S.C. was supported by CIBEROBN and A.G.M. by Fundación para la Investigación Biomédica Hospital Infantil Universitario Niño Jesús

Chronic central leptin infusion modulates the glycemia response to insulin administration in male rats through regulation of hepatic glucose metabolism

Leptin and insulin use overlapping signaling mechanisms to modify hepatic glucose metabolism, which is critical in maintaining normal glycemia. We examined the effect of an increase in central leptin and insulin on hepatic glucose metabolism and its influence on serum glucose levels. Chronic leptin infusion increased serum leptin and reduced hepatic SH-phosphotyrosine phosphatase 1, the association of suppressor of cytokine signaling 3 to the insulin receptor in liver and the rise in glycemia induced by central insulin. Leptin also decreased hepatic phosphoenolpyruvate carboxykinase levels and increased insulins ability to phosphorylate insulin receptor substrate-1, Akt and glycogen synthase kinase on Ser9 and to stimulate glucose transporter 2 and glycogen levels. Peripheral leptin treatment reproduced some of these changes, but to a lesser extent. Our data indicate that leptin increases the hepatic response to a rise in insulin, suggesting that pharmacological manipulation of leptin targets may be of interest for controlling glycemia

Impacto de la intervención con una adaptación grupal del método de musicoterapia BMGIM en pacientes con Enfermedad Inflamatoria Intestinal (Enfermedad de Crohn y COLITIS Ulcerosa)

Las terapias complementarias no farmacológicas han demostrado las mejoras que producen en pacientes crónicos, en especial las terapias psicológicas (Gracie et al., 2017), dentro de las cuales se encuentra la Musicoterapia (MT). Uno de los métodos de Musicoterapia reconocidos a nivel mundial es el método Bonny de Imaginación Guiada con Música (BMGIM), cuya aplicación ha mostrado la mejora al tratar pacientes con ciertas enfermedades crónicas, como artritis reumatoide (Jacobi & Eisenberg, 2001) y fibromialgia (Torres, 2015a, 2015b). Aun así, no hay estudios específicos que evalúen el impacto de un tratamiento basado en una adaptación grupal del BMGIM en pacientes con enfermedad inflamatoria intestinal (EII), concretamente Colitis Ulcerosa (CU y Enfermedad de Crohn (EC), y ese ha sido el objeto de este estudio de tesis doctoral. El objetivo consiste en determinar la eficacia de la intervención con una adaptación grupal del método de MT BMGIM, en la mejora del estado de salud de pacientes con EII (CU y EC).Medicin

Fire and biodiversity in the Anthropocene

The workshop leading to this paper was funded by the Centre Tecnològic Forestal de Catalunya and the ARC Centre of Excellence for Environmental Decisions. L.T.K. was supported by a Victorian Postdoctoral Research Fellowship (Victorian Government), a Centenary Fellowship (University of Melbourne), and an Australian Research Council Linkage Project Grant (LP150100765). A.R. was supported by the Xunta de Galicia (Postdoctoral Fellowship ED481B2016/084-0) and the Foundation for Science and Technology under the FirESmart project (PCIF/MOG/0083/2017). A.L.S. was supported by a Marie Skłodowska-Curie Individual Fellowship (746191) under the European Union Horizon 2020 Programme for Research and Innovation. L.R. was supported by the Australian Government’s National Environmental Science Program through the Threatened Species Recovery Hub. L.B. was partially supported by the Spanish Government through the INMODES (CGL2014-59742-C2-2-R) and the ERANET-SUMFORESTS project FutureBioEcon (PCIN-2017-052). This research was supported in part by the U.S. Department of Agriculture, Forest Service, Pacific Southwest Research Station.BACKGROUND Fire has shaped the diversity of life on Earth for millions of years. Variation in fire regimes continues to be a source of biodiversity across the globe, and many plants, animals, and ecosystems depend on particular temporal and spatial patterns of fire. Although people have been using fire to modify environments for millennia, the combined effects of human activities are now changing patterns of fire at a global scale—to the detriment of human society, biodiversity, and ecosystems. These changes pose a global challenge for understanding how to sustain biodiversity in a new era of fire. We synthesize how changes in fire activity are threatening species with extinction across the globe, highlight forward-looking methods for predicting the combined effects of human drivers and fire on biodiversity, and foreshadow emerging actions and strategies that could revolutionize how society manages fire for biodiversity in the Anthropocene. ADVANCES Our synthesis shows that interactions with anthropogenic drivers such as global climate change, land use, and biotic invasions are transforming fire activity and its impacts on biodiversity. More than 4400 terrestrial and freshwater species from a wide range of taxa and habitats face threats associated with modified fire regimes. Many species are threatened by an increase in fire frequency or intensity, but exclusion of fire in ecosystems that need it can also be harmful. The prominent role of human activity in shaping global ecosystems is the hallmark of the Anthropocene and sets the context in which models and actions must be developed. Advances in predictive modeling deliver new opportunities to couple fire and biodiversity data and to link them with forecasts of multiple drivers including drought, invasive plants, and urban growth. Making these connections also provides an opportunity for new actions that could revolutionize how society manages fire. Emerging actions include reintroduction of mammals that reduce fuels, green fire breaks comprising low-flammability plants, strategically letting wildfires burn under the right conditions, managed evolution of populations aided by new genomics tools, and deployment of rapid response teams to protect biodiversity assets. Indigenous fire stewardship and reinstatement of cultural burning in a modern context will enhance biodiversity and human well-being in many regions of the world. At the same time, international efforts to reduce greenhouse gas emissions are crucial to reduce the risk of extreme fire events that contribute to declines in biodiversity. OUTLOOK Conservation of Earth’s biological diversity will be achieved only by recognition of and response to the critical role of fire in shaping ecosystems. Global changes in fire regimes will continue to amplify interactions between anthropogenic drivers and create difficult trade-offs between environmental and social objectives. Scientific input will be crucial for navigating major decisions about novel and changing ecosystems. Strategic collection of data on fire, biodiversity, and socioeconomic variables will be essential for developing models to capture the feedbacks, tipping points, and regime shifts characteristic of the Anthropocene. New partnerships are also needed to meet the challenges ahead. At the local and regional scale, getting more of the “right” type of fire in landscapes that need it requires new alliances and networks to build and apply knowledge. At the national and global scale, biodiversity conservation will benefit from greater integration of fire into national biodiversity strategies and action plans and in the implementation of international agreements and initiatives such as the UN Convention on Biological Diversity. Placing the increasingly important role of people at the forefront of efforts to understand and adapt to changes in fire regimes is central to these endeavors.PostprintPeer reviewe