The black hole behind the cut

We study the analytic structure of the heavy-heavy-light-light holographic correlators in the supergravity approximation of the AdS3 × S 3/CFT2 duality. As an explicit example, we derive the correlator where the heavy operator is a classical microstate of the 5D supersymmetric black hole and its dual geometry interpolates as a function of a continuous parameter between global AdS3 and the extremal BTZ black hole. The simplest perturbation of this interpolating geometry by a light field is described by the Heun equation and we exploit the relation of its connection coefficients to the Liouville CFT to analytically compute the correlator in the two limits, focusing in particular on the black hole regime. In this limit we find that the real poles of the correlator become dense and can be approximated by a cut. We show that, when the charges of the heavy state are in the black hole regime, the discontinuity across the cut has complex poles corresponding to the quasi-normal modes of BTZ. This behaviour is qualitatively similar to what is expected for the large central charge limit of a typical black hole microstate

Prolonged changes in hepatic mitochondrial activity and insulin sensitivity by high fructose intake in adolescent rats

Persistence of damage induced by unhealthy diets during youth has been little addressed. Therefore, we investigated the impact of a short‐term fructose‐rich diet on liver metabolic activity in adolescent rats and the putative persistence of alterations after removing fructose from the diet. Adolescent rats were fed a fructose‐rich diet for three weeks and then switched to a control diet for further three weeks. Body composition and energy balance were not affected by fructose‐rich diet, while increased body lipids and lipid gain were found after the rescue period. Switching to a control diet reversed the upregulation of plasma fructose, uric acid, lipocalin, and haptoglobin, while plasma triglycerides, alanine aminotransferase, lipopolysaccharide, and tumor necrosis factor alpha remained higher. Hepatic steatosis and ceramide were increased by fructose‐rich diet, but reversed by returning to a control diet, while altered hepatic response to insulin persisted. Liver fatty acid synthase and stearoyl‐CoA desaturase (SCD) activities were upregulated by fructose‐rich diet, and SCD activity remained higher after returning to the control diet. Fructose‐induced upregulation of complex II‐driven mitochondrial respiration, peroxisome proliferator‐activated receptor‐gamma coactivator 1 alpha, and peroxisome proliferator activated receptor α also persisted after switching to control diet. In conclusion, our results show prolonged fructose‐induced dysregulation of liver metabolic activity

Prolonged changes in hepatic mitochondrial activity and insulin sensitivity by high fructose intake in adolescent rats

Persistence of damage induced by unhealthy diets during youth has been little addressed. Therefore, we investigated the impact of a short-term fructose-rich diet on liver metabolic activity in adolescent rats and the putative persistence of alterations after removing fructose from the diet. Adolescent rats were fed a fructose-rich diet for three weeks and then switched to a control diet for further three weeks. Body composition and energy balance were not affected by fructose-rich diet, while increased body lipids and lipid gain were found after the rescue period. Switching to a control diet reversed the upregulation of plasma fructose, uric acid, lipocalin, and haptoglobin, while plasma triglycerides, alanine aminotransferase, lipopolysaccharide, and tumor necrosis factor alpha remained higher. Hepatic steatosis and ceramide were increased by fructose-rich diet, but reversed by returning to a control diet, while altered hepatic response to insulin persisted. Liver fatty acid synthase and stearoyl-CoA desaturase (SCD) activities were upregulated by fructose-rich diet, and SCD activity remained higher after returning to the control diet. Fructose-induced upregulation of complex II-driven mitochondrial respiration, peroxisome proliferator-activated receptor-gamma coactivator 1 alpha, and peroxisome proliferator activated receptor alpha also persisted after switching to control diet. In conclusion, our results show prolonged fructose-induced dysregulation of liver metabolic activity