RV POSEIDON Cruise Report POS420 COWACSS Biological observation and sampling of cold-water corals to investigate impacts on climate change

Trondheim – (Kristiansund) – Kiel 08. – (25.) – 30.09.201

An Obesity Risk SNP (rs17782313) near the MC4R Gene Is Associated with Cerebrocortical Insulin Resistance in Humans

Activation of melanocortin-4 receptor (MC4R) by insulin sensitive neurons is a central mechanism in body weight regulation, and genetic variants in the MC4R gene (e.g., rs17782313) are associated with obesity. By using magnetoencephalography, we addressed whether rs17782313 affects the cerebrocortical insulin response. We measured the cerebrocortical insulin response by using magnetoencephalography in a hyperinsulinemic euglycemic clamp (versus placebo) in 51 nondiabetic humans (26 f/25 m, age 35 ± 3 years, BMI 28 ± 1 kg/m2). The C-allele of rs17782313 was minor allele (frequency 23%), and the genotype distribution (TT 30, TC 19, CC 2) was in Hardy-Weinberg-Equilibrium. Insulin-stimulated cerebrocortical theta activity was decreased in the presence of the C-allele (TT 33 ± 16 fT; TC/CC −27 ± 20 fT; P = .023), and this effect remained significant after adjusting for BMI and peripheral insulin sensitivity (P = .047). Cerebrocortical theta activity was impaired in carriers of the obesity risk allele. Therefore, cerebral insulin resistance may contribute to the obesity effect of rs17782313

Effect of pulse-current-based protocols on the lithium dendrite formation and evolution in all-solid-state batteries

Understanding the cause of lithium dendrites formation and propagation is essential for developing practical all-solid-state batteries. Li dendrites are associated with mechanical stress accumulation and can cause cell failure at current densities below the threshold suggested by industry research (i.e., >5 mA/cm2). Here, we apply a MHz-pulse-current protocol to circumvent low-current cell failure for developing all-solid-state Li metal cells operating up to a current density of 6.5 mA/cm2. Additionally, we propose a mechanistic analysis of the experimental results to prove that lithium activity near solid-state electrolyte defect tips is critical for reliable cell cycling. It is demonstrated that when lithium is geometrically constrained and local current plating rates exceed the exchange current density, the electrolyte region close to the defect releases the accumulated elastic energy favouring fracturing. As the build-up of this critical activity requires a certain period, applying current pulses of shorter duration can thus improve the cycling performance of all-solid-solid-state lithium batteries.publishedVersio

Crumbling Reefs and Cold-Water Coral Habitat Loss in a Future Ocean: Evidence of “Coralporosis” as an Indicator of Habitat Integrity

Ocean acidification is a threat to the net growth of tropical and deep-sea coral reefs, due to gradual changes in the balance between reef growth and loss processes. Here we go beyond identification of coral dissolution induced by ocean acidification and identify a mechanism that will lead to a loss of habitat in cold-water coral reef habitats on an ecosystem-scale. To quantify this, we present in situ and year-long laboratory evidence detailing the type of habitat shift that can be expected (in situ evidence), the mechanisms underlying this (in situ and laboratory evidence), and the timescale within which the process begins (laboratory evidence). Through application of engineering principals, we detail how increased porosity in structurally critical sections of coral framework will lead to crumbling of load-bearing material, and a potential collapse and loss of complexity of the larger habitat. Importantly, in situ evidence highlights that cold-water corals can survive beneath the aragonite saturation horizon, but in a fundamentally different way to what is currently considered a biogenic cold-water coral reef, with a loss of the majority of reef habitat. The shift from a habitat with high 3-dimensional complexity provided by both live and dead coral framework, to a habitat restricted primarily to live coral colonies with lower 3-dimensional complexity represents the main threat to cold-water coral reefs of the future and the biodiversity they support. Ocean acidification can cause ecosystem-scale habitat loss for the majority of cold-water coral reefs.BN/Marie-Eve Aubin-Tam La

Hidden impacts of ocean acidification to live and dead coral framework

Cold-water corals, such as Lophelia pertusa, are key habitat-forming organisms found throughout the world's oceans to 3000 m deep. The complex three-dimensional framework made by these vulnerable marine ecosystems support high biodiversity and commercially important species. Given their importance, a key question is how both the living and the dead framework will fare under projected climate change. Here, we demonstrate that over 12 months L. pertusa can physiologically acclimate to increased CO2, showing sustained net calcification. However, their new skeletal structure changes and exhibits decreased crystallographic and molecular-scale bonding organization. Although physiological acclimatization was evident, we also demonstrate that there is a negative correlation between increasing CO2 levels and breaking strength of exposed framework (approx. 20–30% weaker after 12 months), meaning the exposed bases of reefs will be less effective ‘load-bearers’, and will become more susceptible to bioerosion and mechanical damage by 2100

Inhibition of PTP1B Restores IRS1-Mediated Hepatic Insulin Signaling in IRS2-Deficient Mice

[Objective]: Mice with complete deletion of insulin receptor substrate 2 (IRS2) develop hyperglycaemia, impaired hepatic insulin signaling and elevated gluconeogenesis, whereas mice deficient for protein tyrosine phosphatase (PTP) 1B display an opposing hepatic phenotype characterized by increased sensitivity to insulin. To define the relationship between these two signaling pathways in the regulation of liver metabolism, we used genetic and pharmacological approaches to study the effects of inhibiting PTP1B on hepatic insulin signaling and expression of gluconeogenic enzymes in IRS2−/− deficient mice. [Research design and methods]: We analyzed glucose homeostasis and insulin signaling in liver and isolated hepatocytes from IRS2−/− and IRS2−/−/PTP1B−/−. Additionally, hepatic insulin signaling was assessed in control and IRS2−/− mice treated with resveratrol, an anti-oxidant present in red wine. [Results]: In livers of hyperglycaemic IRS2−/− mice, the expression levels of PTP1B and its association with the insulin receptor (IR) were increased. The absence of PTP1B in the double mutant mice restored hepatic IRS1-mediated phosphatidylinositol (PI) 3-kinase/Akt/Foxo1 signaling. Moreover, resveratrol treatment of hyperglycaemic IRS2−/− mice decreased hepatic PTP1B mRNA and inhibited PTP1B activity, thereby restoring IRS1-mediated PI 3-kinase/Akt/Foxo1 signaling and peripheral insulin sensitivity. [Conclusions]: By regulating the phosphorylation state of IR, PTB1B determines sensitivity to insulin in liver and exerts a unique role in the interplay between IRS1 and IRS2 in the modulation of hepatic insulin action.This work was supported by Ministerio de Ciencia e Innovación Grants (Spain) BFU2008-02420, SAF2009- 08114 (to A.M.V.), BFU2008-04901-C03-03 (to M.R.), BFU2005-00084, and SAF2008-00011 (to D.J.B.) and the Centro de Investigación Biomédica en Red Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM) (Instituto Salud Carlos III). A.G.-R. holds a postdoctoral contract from CIBERDEM.Peer reviewe

Insulin Promotes Glycogen Storage and Cell Proliferation in Primary Human Astrocytes

In the human brain, there are at least as many astrocytes as neurons. Astrocytes are known to modulate neuronal function in several ways. Thus, they may also contribute to cerebral insulin actions. Therefore, we examined whether primary human astrocytes are insulin-responsive and whether their metabolic functions are affected by the hormone.Commercially available Normal Human Astrocytes were grown in the recommended medium. Major players in the insulin signaling pathway were detected by real-time RT-PCR and Western blotting. Phosphorylation events were detected by phospho-specific antibodies. Glucose uptake and glycogen synthesis were assessed using radio-labeled glucose. Glycogen content was assessed by histochemistry. Lactate levels were measured enzymatically. Cell proliferation was assessed by WST-1 assay.We detected expression of key proteins for insulin signaling, such as insulin receptor β-subunit, insulin receptor substrat-1, Akt/protein kinase B and glycogen synthase kinase 3, in human astrocytes. Akt was phosphorylated and PI-3 kinase activity increased following insulin stimulation in a dose-dependent manner. Neither increased glucose uptake nor lactate secretion after insulin stimulation could be evidenced in this cell type. However, we found increased insulin-dependent glucose incorporation into glycogen. Furthermore, cell numbers increased dose-dependently upon insulin treatment.This study demonstrated that human astrocytes are insulin-responsive at the molecular level. We identified glycogen synthesis and cell proliferation as biological responses of insulin signaling in these brain cells. Hence, this cell type may contribute to the effects of insulin in the human brain