The influence of near surface sediment hydrothermalism on the TEX₈₆ tetraether lipid-based proxy and a new correction for ocean bottom lipid overprinting

The diversity and relative abundances of tetraether lipids produced by Thaumarchaeota in soils and sediments increasingly is used to assess environmental change. For instance, the TetraEther indeX of 86 carbon atoms (TEX86), based on archaeal isoprenoidal glycerol dialkyl glycerol tetraether (iGDGT) lipids, is frequently applied to reconstruct past sea-surface temperatures (SST). Yet, it is unknown how the ratio fully responds to environmental and or geochemical variations and if the produced signals are the adaptive response by Thaumarchaeota to climate driven temperature changes in the upper water column. We present the results of a four push-core transect study of surface sediments collected along an environmental gradient at the Cathedral Hill hydrothermal vent system in Guaymas Basin, Gulf of California. The transect crosses a region where advecting hydrothermal fluids reach 155 °C within the upper 21 cm below the seafloor (cmbsf) close to the vent center to near ambient conditions at the vent periphery. The recovered iGDGTs closest to the vent center experienced high rates of turnover with up to 94 % of lipid pool being lost within the upper 21 cmbsf. Here, we show that turnover is non-selective across TEX86 GDGT lipid classes and does not independently affect the ratio. However, as evident by TEX86 ratios being highly correlated to the Cathedral Hill vent sediment porewater temperatures (R2 = 0.84), the ratio can be strongly impacted by the combination of severe lipid loss when it is coupled to the addition of in situ iGDGT production from archaeal communities living in the vent sediments. The resulting signal overprint produces absolute temperature offsets of up to 4 °C based on the TEX86H-calibration relative to modern climate records of the region. The overprint is also striking given the flux of GDGTs from the upper water column that is estimated to represent ~93 % of the combined intact polar lipid (IPL) and core GDGT lipid pool initially deposited on the seafloor. A model to correct the overprint signal using IPLs is therefore presented that can similarly be applied to all near-surface marine sediment systems where calibration models or climate reconstructions are made based on the TEX86 measure.

Systematic assessment of lipid profiles for the discovery of tissue contributors to the circulating lipid pool in cold exposure

Plasma lipid levels are altered in chronic conditions such as type 2 diabetes and cardiovascular disease as well as acute stresses such as fasting and cold exposure. Advances in mass spectrometry based lipidomics have uncovered the complexity of the plasma lipidome which includes over 500 lipids that serve functional roles including energy substrate and signaling molecule. The plasma lipid pool is maintained through regulation of tissue production, secretion, and uptake. A major challenge is establishing the tissues of origin and uptake for various plasma lipids, which is necessary to determine the lipid function. Using cold exposure as an acute stress, we performed global lipidomics on the plasma and nine tissues that may contribute to the circulating pool. We found that numerous species of plasma acylcarnitines (ACars) and ceramides were significantly changed with cold exposure. Through computational assessment, we identified the liver and brown adipose tissue (BAT) as major contributors and consumers of circulating ACars, in agreement with our previous work. We further identified the kidney and intestine as novel contributors to the circulating ACar pool and validated these findings with gene expression analysis. Regression analysis also identified that the BAT and kidney as regulators of the plasma ceramide pool. These studies provide an adaptable computational tool to assess tissue contribution to the plasma lipid pool. Our findings have implications in understanding the function of plasma ACars and ceramides, which are elevated in metabolic diseases.

Accumulation of Plasma-Derived Lipids in the Lipid Core and Necrotic Core of Human Atheroma: Imaging Mass Spectrometry and Histopathological Analyses

Objective: To clarify the pathogenesis of human atheroma, the origin of deposited lipids, the developmental mechanism of liponecrotic tissue, and the significance of the oxidation of phospholipids were investigated using mass spectrometry-aided imaging and immunohistochemistry. Approach and Results: Atherosclerotic lesions in human coronary arteries were divided into 3 groups: pathological intimal thickening with lipid pool, atheroma with lipid core, and atheroma with necrotic core. The lipid pool and lipid core were characterized by the deposition of extracellular lipids. The necrotic core comprised extracellular lipids and liponecrotic tissue. The proportion of cholesteryl linoleate in cholesteryl linoleate+cholesteryl oleate fraction in the extracellular lipid and liponecrotic regions differed significantly from that of the macrophage foam cell–dominant region, and the plasma-derived components (apoB and fibrinogen) were localized in the regions. The liponecrotic region was devoid of elastic and collagen fibers and accompanied by macrophage infiltration in the surrounding tissue. Non–oxidized phospholipid (Non-OxPL), OxPL, and Mox macrophages were detected in the three lesions. In the atheroma with lipid core and atheroma with necrotic core, non-OxPL tended to localize in the superficial layer, whereas OxPL was distributed evenly. Mox macrophages were colocalized with OxPL epitopes. Conclusions: In human atherosclerosis, plasma-derived lipids accumulate to form the lipid pool of pathological intimal thickening, lipid core of atheroma with lipid core, and necrotic core of atheroma with necrotic core. The liponecrotic tissue in the necrotic core appears to be developed by the loss of elastic and collagen fibers. Non-OxPL in the accumulated lipids is oxidized to form OxPL, which may contribute to the lesion development through Mox macrophages.

The Emerging Physiological Role of AGMO 10 Years after Its Gene Identification

The gene encoding alkylglycerol monooxygenase (AGMO) was assigned 10 years ago. So far, AGMO is the only known enzyme capable of catalysing the breakdown of alkylglycerols and lyso-alkylglycerophospholipids. With the knowledge of the genetic information, it was possible to relate a potential contribution for mutations in the AGMO locus to human diseases by genome-wide association studies. A possible role for AGMO was implicated by genetic analyses in a variety of human pathologies such as type 2 diabetes, neurodevelopmental disorders, cancer, and immune defence. Deficient catabolism of stored lipids carrying an alkyl bond by an absence of AGMO was shown to impact on the overall lipid composition also outside the ether lipid pool. This review focuses on the current evidence of AGMO in human diseases and summarises experimental evidence for its role in immunity, energy homeostasis, and development in humans and several model organisms. With the progress in lipidomics platform and genetic identification of enzymes involved in ether lipid metabolism such as AGMO, it is now possible to study the consequence of gene ablation on the global lipid pool and further on certain signalling cascades in a variety of model organisms in more detail.