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The record of past climate highlights recurrent and intense millennial anomalies, characterised by a distinct pattern of inter-polar temperature change, termed the ‘thermal bipolar seesaw’, which is widely believed to arise from rapid changes in the Atlantic overturning circulation. By forcing a suppression of North Atlantic convection, models have been able to reproduce many of the general features of the thermal bipolar seesaw; however, they typically fail to capture the full magnitude of temperature change reconstructed using polar ice cores from both hemispheres. Here we use deep-water temperature reconstructions, combined with parallel oxygenation and radiocarbon ventilation records, to demonstrate the occurrence of enhanced deep convection in the Southern Ocean across the particularly intense millennial climate anomaly, Heinrich Stadial 4. Our results underline the important role of Southern Ocean convection as a potential amplifier of Antarctic warming, and atmospheric CO2 rise, that is responsive to triggers originating in the North Atlantic.

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The record of past climate highlights recurrent and intense millennial anomalies, characterised by a distinct pattern of inter-polar temperature change, termed the ‘thermal bipolar seesaw’, which is widely believed to arise from rapid changes in the Atlantic overturning circulation. By forcing a suppression of North Atlantic convection, models have been able to reproduce many of the general features of the thermal bipolar seesaw; however, they typically fail to capture the full magnitude of temperature change reconstructed using polar ice cores from both hemispheres. Here we use deep-water temperature reconstructions, combined with parallel oxygenation and radiocarbon ventilation records, to demonstrate the occurrence of enhanced deep convection in the Southern Ocean across the particularly intense millennial climate anomaly, Heinrich Stadial 4. Our results underline the important role of Southern Ocean convection as a potential amplifier of Antarctic warming, and atmospheric CO2 rise, that is responsive to triggers originating in the North Atlantic.

Hepatic fat accumulation is associated with diabetes and hepatocellular carcinoma (HCC). Here, we characterize the metabolic response that high-fat availability elicits in livers before disease development. After a short term on a high-fat diet (HFD), otherwise healthy mice showed elevated hepatic glucose uptake and increased glucose contribution to serine and pyruvate carboxylase activity compared with control diet (CD) mice. This glucose phenotype occurred independently from transcriptional or proteomic programming, which identifies increased peroxisomal and lipid metabolism pathways. HFD-fed mice exhibited increased lactate production when challenged with glucose. Consistently, administration of an oral glucose bolus to healthy individuals revealed a correlation between waist circumference and lactate secretion in a human cohort. In vitro, palmitate exposure stimulated production of reactive oxygen species and subsequent glucose uptake and lactate secretion in hepatocytes and liver cancer cells. Furthermore, HFD enhanced the formation of HCC compared with CD in mice exposed to a hepatic carcinogen. Regardless of the dietary background, all murine tumors showed similar alterations in glucose metabolism to those identified in fat exposed nontransformed mouse livers, however, particular lipid species were elevated in HFD tumor and nontumor-bearing HFD liver tissue. These findings suggest that fat can induce glucose-mediated metabolic changes in nontransformed liver cells similar to those found in HCC. Significance: With obesity-induced hepatocellular carcinoma on a rising trend, this study shows in normal, nontransformed livers that fat induces glucose metabolism similar to an oncogenic transformation.