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Targeting ocean conservation outcomes through threat reduction
Funder: Discovery and Accelerator grants from Natural Science and Engineering Research Council and the Canada Research Chair programAbstractNations have committed to reductions in the global rate of species extinctions through the Sustainable Development Goals 14 and 15, for ocean and terrestrial species, respectively. Biodiversity loss is worsening despite rapid growth in the number and extent of protected areas, both at sea and on land. Resolving this requires targeting the locations and actions that will deliver positive conservation outcomes for biodiversity. The Species Threat Abatement and Restoration (STAR) metric, developed by a consortium of experts, quantifies the contributions that abating threats and restoring habitats in specific places offer towards reducing extinction risk based on the IUCN Red List of Threatened SpeciesTM. STAR is now recommended as an appropriate metric by recent disclosure frameworks for companies to report their impacts on nature and STAR has seen widespread uptake within the private sector. However, it is currently only available for the terrestrial realm. We extend the coverage of the threat abatement component of the STAR metric (START), used to identify locations where positive interventions could make a large contribution to reducing global species extinction risk and where developments that increase threats to species should be mitigated, to the marine realm for 1646 marine species. Reducing unsustainable fishing provides the greatest opportunity to lower species extinction risk, comprising 43% of the marine START score. Three-quarters (75%) of the global marine START score falls entirely outside the boundaries of protected areas and only 2.7% falls within no-take protected areas. The STAR metric can be used both to guide protected area expansion and to target other actions, such as establishment and enforcement of fishing limits, to recover biodiversity.</jats:p
Metabolic pathways promoting intrahepatic fatty acid accumulation in methionine and choline deficiency:implications for the pathogenesis of steatohepatitis
The pathological mechanisms that distinguish simple steatosis from steatohepatitis (or NASH, with consequent risk of cirrhosis and hepatocellular cancer) remain incompletely defined. Whereas both a methionine- and choline-deficient diet (MCDD) and a choline-deficient diet (CDD) lead to hepatic triglyceride accumulation, MCDD alone is associated with hepatic insulin resistance and inflammation (steatohepatitis). We used metabolic tracer techniques, including stable isotope ([13C4]palmitate) dilution and mass isotopomer distribution analysis (MIDA) of [13C2]acetate, to define differences in intrahepatic fatty acid metabolism that could explain the contrasting effect of MCDD and CDD on NASH in C57Bl6 mice. Compared with control-supplemented (CS) diet, liver triglyceride pool sizes were similarly elevated in CDD and MCDD groups (24.37 ± 2.4, 45.94 ± 3.9, and 43.30 ± 3.5 μmol/liver for CS, CDD, and MCDD, respectively), but intrahepatic neutrophil infiltration and plasma alanine aminotransferase (31 ± 3, 48 ± 4, 231 ± 79 U/l, P < 0.05) were elevated only in MCDD mice. However, despite loss of peripheral fat in MCDD mice, neither the rate of appearance of palmitate (27.2 ± 3.5, 26.3 ± 2.3, and 28.3 ± 3.5 μmol·kg−1·min−1) nor the contribution of circulating fatty acids to the liver triglyceride pool differed between groups. Unlike CDD, MCDD had a defect in hepatic triglyceride export that was confirmed using intravenous tyloxapol (142 ± 21, 122 ± 15, and 80 ± 7 mg·kg−1·h−1, P < 0.05). Moreover, hepatic de novo lipogenesis was significantly elevated in the MCDD group only (1.4 ± 0.3, 2.3 ± 0.4, and 3.4 ± 0.4 μmol/day, P < 0.01). These findings suggest that important alterations in hepatic fatty acid metabolism may promote the development of steatohepatitis. Similar mechanisms may predispose to hepatocyte damage in human NASH