Cafeteria Diet Feeding in Young Rats Leads to Hepatic Steatosis and Increased Gluconeogenesis under Fatty Acids and Glucagon Influence

Gluconeogenesis overstimulation due to hepatic insulin resistance is the best-known mechanism behind elevated glycemia in obese subjects with hepatic steatosis. This suggests that glucose production in fatty livers may differ from that of healthy livers, also in response to other gluconeogenic determinant factors, such as the type of substrate and modulators. Thus, the aim of this study was to investigate the effects of these factors on hepatic gluconeogenesis in cafeteria diet-induced obese adult rats submitted to a cafeteria diet at a young age. The livers of the cafeteria group exhibited higher gluconeogenesis rates when glycerol was the substrate, but lower rates were found when lactate and pyruvate were the substrates. Stearate or glucagon caused higher stimulations in gluconeogenesis in cafeteria group livers, irrespective of the gluconeogenic substrates. An increased mitochondrial NADH/NAD+ ratio and a reduced rate of 14CO2 production from [14C] fatty acids suggested restriction of the citric acid cycle. The higher glycogen and lipid levels were possibly the cause for the reduced cellular and vascular spaces found in cafeteria group livers, likely contributing to oxygen consumption restriction. In conclusion, specific substrates and gluconeogenic modulators contribute to a higher stimulation of gluconeogenesis in livers from the cafeteria group.

Interhemispheric gradient of atmospheric radiocarbon reveals natural variability of Southern Ocean winds

Tree ring Δ14C data (Reimer et al., 2004; McCormac et al., 2004) indicate that atmospheric Δ14C varied on multi-decadal to centennial timescales, in both hemispheres, over the pre-industrial period AD 950–1830. Although the Northern and Southern Hemispheric Δ14C records display similar variability, it is difficult from these data alone to distinguish between variations driven by 14CO2 production in the upper atmosphere (Stuiver, 1980) and exchanges between carbon reservoirs (Siegenthaler, 1980). Here we consider rather the Interhemispheric Gradient in atmospheric Δ14C as revealing of the background pre-bomb air-sea Disequilbrium Flux between 14CO2 and CO2. As the global maximum of the Disequilibrium Flux is squarely centered in the open ocean regions of the Southern Ocean, relatively modest perturbations to the winds over this region drive significant perturbations to the Interhemispheric Gradient. The analysis presented here implies that changes to Southern Ocean windspeeds are likely a main driver of the observed variability in the Interhemispheric Gradient over 950–1830, and further, that this variability may be larger than the Southern Ocean wind trends that have been reported for recent decades (notably 1980–2004). This interpretation also implies a significant weakening of the winds over the Southern Ocean within a few decades of AD 1375, associated with the transition between the Medieval Climate Anomaly and the Little Ice Age. The driving forces that could have produced such a shift in the winds remain unkown.

Influence of repeated applications of glyphosate on its persistence and soil bioactivity

Pesticide degradation studies are essential to evaluate its impact in the environment and on non-target organisms. The effect of repeated soil applications of the herbicide glyphosate on its dissipation and on soil microorganisms was studied by radiometric and microbial techniques. Results indicated fast dissipation of the [14C]-glyphosate or [14C]metabolites extractable residues (half-life of 0.92±0.29 month), but increasing half-lives of total mineralization ranging from 2.2 to 3.4 months as the number of applications increased from 1 to 4. No significant correlation was found between 14CO2 production and dehydrogenase activity.

Leptin inhibits insulin-stimulated incorporation of glucose into lipids and stimulates glucose decarboxylation in isolated rat adipocytes

Leptin is an adipocyte hormone involved in the regulation of energy homeostasis. Generally accepted biological effects of leptin are inhibition of food intake and stimulation of metabolic rate in ob/ob mice, that are defective in the leptin gene. In contrast to these centrally mediated effects of leptin, we are reporting here on leptin effects on glucose incorporation into lipids and glucose decarboxylation in adipocytes isolated from male lean albino rats. Adipocytes previously cultivated (15 h) in the presence of leptin presented a 25% (P < 0.05) reduction of the insulin stimulated incorporation of glucose into lipids. Concurrently, the basal conversion of (U-14C)D-glucose into 14CO2 increased (110%) in the leptin cultivated adipocytes and reached values (1.54 nmol/10(5) cells) similar to the insulin stimulated group (not cultivated with leptin) (1.40 nmol/10(5) cells). In addition, in the presence of insulin, the leptin cultivated adipocytes elicited a 162% (P < 0.05) increase in 14CO2 production that was significantly higher than the increase observed for the not-leptin-cultivated insulin group (92%). We conclude that leptin: 1) directly inhibits the insulin stimulated glucose incorporation into lipids; 2) stimulates glucose decarboxylation, and also potentiates the effect of insulin on glucose decarboxylation in isolated adipocytes. Leptin per se does not alter glucose incorporation into lipids.

Mass transfer limitation in PAH-contaminated soil remediation

Batch experiments were conducted to determine the effects of Triton X-100, a nonionic phenolic ethoxylate surfactant, on the biodegradation of soil-bound naphthalene and phenanthrene. Two different types of soils, one contaminated with polynuclear aromatic hydrocarbons (PAHs) for different lengths of time, 2 days to 10 months, in the laboratory and the other, a field-contaminated soil from a manufactured gas plant (MGP) site, were used. Biodegradation of PAHs was measured by monitoring the 14CO2 production for the artificially contaminated soils and the residual PAHs in soil phase for the MGP soil. Without adding surfactant, the mineralization rate of phenanthrene was significantly smaller in the 1 0-month contaminated soil compared to that in the 2-day contaminated soil. Presumably, mineralization was mass-transfer limited in the soil with longer contamination period. Triton X-100 significantly enhanced mineralization in the 10 month-old soil but none in the 2-day old soil. The MGP soil, weathered over 2-3 decades, exhibited even greater enhancement of mineralization. Mineralization of PAHs in aged soils appears to be controlled by mass transfer rather than the rate of biodegradation. Surfactants increase the rate of release of soil-bound contaminant and thus help promote biodegradation.

Hepatic zonation of the catabolism of arginine and ornithine in the perfused rat liver

The metabolism of 14C-labelled arginine and ornithine was studied in the isolated, nonrecirculating, perfused rat liver. The catabolism of these amino acids required ornithine aminotransferase since treatment of rats with gabaculine, an inhibitor of this enzyme, decreased substantially the production of 14CO2 from the 14C-labelled amino acids. In the liver, ornithine aminotransferase is restricted to a small population of hepatocytes proximal to the terminal hepatic vein [Kuo, F. C., Hwu, W. L., Valle, D. and Darnell Jr., J. E. (1991) Proc. Natl. Acad. Sci. U.S.A. 88, 9468-9472], i.e. the perivenous subpopulation of hepatocytes. Catabolism of arginine requires arginase to convert arginine to ornithine which can then be catabolized through ornithine aminotransferase. The presence of arginase activity in the perivenous hepatocytes was demonstrated by experiments in which livers were perfused with [14C]arginine in both antegrade and retrograde directions. Identical rates of 14CO2 production were obtained in these experiments, a result which could only occur if the process of arginine catabolism through ornithine aminotransferase can be carried out in its entirety in the perivenous cells.

Enhanced hepatic gluconeogenic capacity for selected precursors after endurance training

The effects of endurance training (running 90 min/day, 30 m/min, approximately 10% grade) on hepatic gluconeogenesis were studied in 24-h-fasted rats by using the isolated liver perfusion technique. After isolation, livers were perfused (single pass) for 30 min with Krebs-Henseleit bicarbonate buffer and fresh bovine red blood cells (hematocrit 20–24%) with no added substrate. Alanine (10 mM), dihydroxyacetone (20 mM), or glutamine (10 mM) was then added to the reservoir, and perfusions continued for 60 min. No significant differences were observed in perfusate pH, hematocrit, bile production, or serum alanine aminotransferase effluxing from livers from trained or control animals for any perfusion. Livers from trained animals that were perfused with 10 mM alanine demonstrated significantly higher rates of glucose production compared with livers from control animals (0.51 +/- 0.04 vs. 0.40 +/- 0.02 micromol.min-1.g liver-1, respectively). Elevations of a similar magnitude were observed for rates of [14C]alanine incorporation into [14C]glucose in livers from trained vs. control animals (8,797 +/- 728 vs. 6,962 +/- 649 dpm.min-1.g liver-1, respectively). Significant increases were also observed in hepatic alanine uptake (30%), oxygen consumption (23%), urea release (22%), and 14CO2 production (29%) of livers of endurance-trained animals. In contrast, no significant differences between groups were observed for hepatic glucose output after perfusions with either dihydroxyacetone (1.75 +/- 0.06 micromol.min-1.g liver-1) or glutamine (0.62 +/- 0.04 micromol.min-1.g liver-1). Further, during perfusions with dihydroxyacetone and glutamine, training had no significant impact on precursor uptake, oxygen consumption, or urea output. The current findings indicate a training-induced adaptation for hepatic gluconeogenesis located below the level of the triose phosphates.