Climate Change and Trophic Response of the Antarctic Bottom Fauna

BACKGROUND: As Earth warms, temperate and subpolar marine species will increasingly shift their geographic ranges poleward. The endemic shelf fauna of Antarctica is especially vulnerable to climate-mediated biological invasions because cold temperatures currently exclude the durophagous (shell-breaking) predators that structure shallow-benthic communities elsewhere. METHODOLOGY/PRINCIPAL FINDINGS: We used the Eocene fossil record from Seymour Island, Antarctic Peninsula, to project specifically how global warming will reorganize the nearshore benthos of Antarctica. A long-term cooling trend, which began with a sharp temperature drop approximately 41 Ma (million years ago), eliminated durophagous predators-teleosts (modern bony fish), decapod crustaceans (crabs and lobsters) and almost all neoselachian elasmobranchs (modern sharks and rays)-from Antarctic nearshore waters after the Eocene. Even prior to those extinctions, durophagous predators became less active as coastal sea temperatures declined from 41 Ma to the end of the Eocene, approximately 33.5 Ma. In response, dense populations of suspension-feeding ophiuroids and crinoids abruptly appeared. Dense aggregations of brachiopods transcended the cooling event with no apparent change in predation pressure, nor were there changes in the frequency of shell-drilling predation on venerid bivalves. CONCLUSIONS/SIGNIFICANCE: Rapid warming in the Southern Ocean is now removing the physiological barriers to shell-breaking predators, and crabs are returning to the Antarctic Peninsula. Over the coming decades to centuries, we predict a rapid reversal of the Eocene trends. Increasing predation will reduce or eliminate extant dense populations of suspension-feeding echinoderms from nearshore habitats along the Peninsula while brachiopods will continue to form large populations, and the intensity of shell-drilling predation on infaunal bivalves will not change appreciably. In time the ecological effects of global warming could spread to other portions of the Antarctic coast. The differential responses of faunal components will reduce the endemic character of Antarctic subtidal communities, homogenizing them with nearshore communities at lower latitudes

Bace1-dependent amyloid processing regulates hypothalamic leptin sensitivity in obese mice

Obesity places an enormous medical and economic burden on society. The principal driver appears to be central leptin resistance with hyperleptinemia. Accordingly, a compound that reverses or prevents leptin resistance should promote weight normalisation and improve glucose homeostasis. The protease Bace1 drives beta amyloid (Aβ) production with obesity elevating hypothalamic Bace1 activity and Aβ₁–₄₂ production. Pharmacological inhibition of Bace1 reduces body weight, improves glucose homeostasis and lowers plasma leptin in diet-induced obese (DIO) mice. These actions are not apparent in ob/ob or db/db mice, indicating the requirement for functional leptin signalling. Decreasing Bace1 activity normalises hypothalamic inflammation, lowers PTP1B and SOCS3 and restores hypothalamic leptin sensitivity and pSTAT3 response in obese mice, but does not affect leptin sensitivity in lean mice. Raising central Aβ₁–₄₂ levels in the early stage of DIO increases hypothalamic basal pSTAT3 and reduces the amplitude of the leptin pSTAT3 signal without increased inflammation. Thus, elevated Aβ₁–₄₂ promotes hypothalamic leptin resistance, which is associated with diminished whole-body sensitivity to exogenous leptin and exacerbated body weight gain in high fat fed mice. These results indicate that Bace1 inhibitors, currently in clinical trials for Alzheimer’s disease, may be useful agents for the treatment of obesity and associated diabetes

Leptina e sua influência na patofisiologia de distúrbios alimentares Leptin and its influence in the pathophysiology of eating disorders

A leptina é uma proteína secretada pelos adipócitos com papel regulador em vários sistemas do organismo, como sistema imune, respiratório e reprodutivo, bem como no balanço energético via ação hipotalâmica. Sua ação primária ocorre no núcleo hipotalâmico arqueado, no qual inicia uma cascata de eventos para inibição da ingestão energética e aumento do gasto energético. As concentrações de leptina são influenciadas pela adiposidade, fatores hormonais e nutricionais. A restrição e os episódios de compulsão alimentar, presentes na anorexia nervosa e bulimia, respectivamente, são considerados, na literatura científica, fatores determinantes na leptinemia. Seus níveis também alterados no tratamento desses distúrbios alimentares sugerem uma relação entre as alterações neuroendócrinas e conseqüentes modificações nos sinais de fome e saciedade, com a patogenia ou manutenção dos quadros clínicos. Trabalhos têm encontrado impacto dessas alterações na saúde dos pacientes, em curto e longo prazos. Esta revisão tem como objetivo esclarecer quais são as funções da leptina nos tecidos nervoso e periférico, quais os mecanismos que interferem na sua concentração nos distúrbios alimentares e como isso reflete na saúde do paciente anoréxico ou bulímico.<br>Leptin, a protein secreted by adipocytes, has a regulatory function in several organism systems such as the immune, respiratory, and reproductive systems and in the energy balance via hypothalamic action. Its primary action occurs in the arcuate hypothalamic nucleus, where it begins a cascade of events that inhibits energy intake and enhances energy consumption. The concentration of leptin is influenced by adiposity and hormonal and nutritional factors. The scientific literature considers food restriction and binge episodes of anorexia nervosa and bulimia, respectively, as determining factors of leptin circulation. Leptin levels are also altered during the treatment of these food disturbances, which indicates a relation between neuroendocrine alterations and eventual modifications in hunger and satiety signals and pathogenesis or clinical state of patients. Studies have reported on the short and long-term impact of these alterations on health. Therefore, this review aims to explain the function of leptin in the central and peripheral nervous systems, the mechanisms that interfere with its concentrations in food disturbances, and how this reflects on the health of anorectic and bulimic patients

Correlation of renin angiotensin and aldosterone system activity with subcutaneous and visceral adiposity: the framingham heart study

<p>Abstract</p> <p>Background</p> <p>Animal studies suggest that local adipocyte-mediated activity of the renin-angiotensin-aldosterone system (RAAS) contributes to circulating levels, and may promote the development of obesity-related hypertension in rodents.</p> <p>Methods</p> <p>We examined relations of systemic RAAS activity, as assessed by circulating plasma renin activity (PRA), serum aldosterone level, and aldosterone:renin ratio (ARR), with specific regional adiposity measures in a large, community-based sample. Third Generation Framingham Heart Study participants underwent multidetector computed tomography assessment of SAT and VAT volumes during Exam 1 (2002 and 2005). PRA and serum aldosterone were measured after approximately 10 minutes of supine rest; results were log-transformed for analysis. Correlation coefficients between log-transformed RAAS measures and adiposity measurements were calculated, adjusted for age and sex. Partial correlations between log-transformed RAAS measures and adiposity measurements were also calculated, adjusted for standard CVD risk factors.</p> <p>Results</p> <p>Overall, 992 women and 897 men were analyzed (mean age 40 years; 7% hypertension; 3% diabetes). No associations were observed with SAT (renin r = 0.04, p = 0.1; aldosterone r = -0.01, p = 0.6) or VAT (renin r = 0.03, p = 0.2; aldosterone r = -0.03, p = 0.2). Similar results were observed for ARR, in sex-stratified analyses, and for BMI and waist circumference. Non-significant partial correlations were also observed in models adjusted for standard cardiovascular risk factors.</p> <p>Conclusions</p> <p>Regional adiposity measures were not associated with circulating measures of RAAS activity in this large population-based study. Further studies are required to determine whether adipocyte-derived RAAS components contribute to systemic RAAS activity in humans.</p