Antarctic ice-core data reveal that the atmosphere experienced abrupt centennial increases in CO 2 concentration during the last deglaciation (~18-11 thousand years, ka).Establishing the role of ocean circulation in these changes requires high-resolution, accurately-dated marine records. Here we report radiocarbon data from uranium-thorium dated deep-sea corals in the Equatorial Atlantic and Drake Passage over the last 25 ka. Two major deglacial radiocarbon increases occurred in phase with centennial atmospheric CO 2 rises at 14.8 ka and 11.7 ka. We interpret these radiocarbon-enriched signals to represent two short-lived (<500 years) 'overshoot' events with Atlantic meridional overturning stronger than modern. These results provide compelling evidence for a close coupling of ocean circulation and centennial climate events during the last deglaciation.

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Abrupt climate changes in the past have been attributed to variations in Atlantic Meridional Overturning Circulation (AMOC) strength. However, the exact timing and magnitude of past AMOC shifts remain elusive, which continues to limit our understanding of the driving mechanisms of such climate variability. Here we show a consistent signal of the 231Pa/230Th proxy that reveals a spatially coherent picture of western Atlantic circulation changes over the last deglaciation, during abrupt millennial-scale climate transitions. At the onset of deglaciation, we observe an early slowdown of circulation in the western Atlantic from around 19 to 16.5 thousand years ago (ka), consistent with the timing of accelerated Eurasian ice melting. The subsequent weakened AMOC state persists for over a millennium (~16.5–15 ka), during which time there is substantial ice rafting from the Laurentide ice sheet. This timing indicates a role for melting ice in driving a two-step AMOC slowdown, with a positive feedback sustaining continued iceberg calving and climate change during Heinrich Stadial 1.

Oxidative stress is a critical factor in nonalcoholic fatty liver disease pathogenesis. MicroRNA-200a (miR-200a) is reported to target Kelch-like ECH-associated protein 1 (Keap1), which regulates nuclear factor erythroid 2-related factor 2 (Nrf2) anti-oxidant pathway. Polydatin (3,4′,5-trihydroxy-stilbene-3-β-D-glucoside), a polyphenol found in the rhizome of Polygonum cuspidatum, have anti-oxidative, anti-inflammatory and anti-hyperlipidemic effects. However, whether miR-200a controls Keap1/Nrf2 pathway in fructose-induced liver inflammation and lipid deposition and the blockade of polydatin are still not clear. Here, we detected miR-200a down-regulation, Keap1 up-regulation, Nrf2 antioxidant pathway inactivation, ROS-driven thioredoxin-interacting protein (TXNIP) over-expression, NOD-like receptor (NLR) family, pyrin domain containing 3 (NLRP3) inflammasome activation and dysregulation of peroxisome proliferator activated receptor-α (PPAR-α), carnitine palmitoyl transferase-1 (CPT-1), sterol regulatory element binging protein 1 (SREBP-1) and stearoyl-CoA desaturase-1 (SCD-1) in rat livers, BRL-3A and HepG2 cells under high fructose induction. Furthermore, the data from the treatment or transfection of miR-200a minic, Keap1 and TXNIP siRNA, Nrf2 activator and ROS inhibitor demonstrated that fructose-induced miR-200a low-expression increased Keap1 to block Nrf2 antioxidant pathway, and then enhanced ROS-driven TXNIP to activate NLRP3 inflammasome and disturb lipid metabolism-related proteins, causing inflammation and lipid deposition in BRL-3A cells. We also found that polydatin up-regulated miR-200a to inhibit Keap1 and activate Nrf2 antioxidant pathway, resulting in attenuation of these disturbances in these animal and cell models. These findings provide a novel pathological mechanism of fructose-induced redox status imbalance and suggest that the enhancement of miR-200a to control Keap1/Nrf2 pathway by polydatin is a therapeutic strategy for fructose-associated liver inflammation and lipid deposition.