Natural Moroccan clays: Comparative study of their application as recyclable catalysts in Knoevenagel condensation

Natural Moroccan clay samples from different regions were purified via simple washing, activated and extensively analyzed by various characterization techniques. A comparative study of these clays as recyclable heterogeneous catalysts for the Knoevenagel condensation was undertaken in EtOH/water as solvent under mild conditions; high yield of the desired α,β-unsaturated products was obtained in a short reaction period (~ 30 min). The recyclable solid catalyst was effective for several runs indicating that these purified clays are potentially eco-friendly heterogeneous catalysts; assorted α,β-unsaturated carbonyl compounds were synthetized in high yields (~ 98%) at 40 °C.     

Bisphenol a induces steatosis in HepaRG cells using a model of perinatal exposure

Human exposure to bisphenol A (BPA) could favor obesity and related metabolic disorders such as hepatic steatosis. Investigations in rodents have shown that these deleterious effects are observed not only when BPA is administered during the adult life but also with different protocols of perinatal exposure. Whether perinatal BPA exposure could pose a risk in human is currently unknown, and thus appropriate in vitro models could be important to tackle this major issue. Accordingly, we determined whether long‐term BPA treatment could induce steatosis in human HepaRG cells by using a protocol mimicking perinatal exposure. To this end, the kinetics of expression of seven proteins differentially expressed during liver development was determined during a 4‐week period of cell culture required for proliferation and differentiation. By analogy with data reported in rodents and humans, our results indicated that the period of cell culture around day 15 and day 18 after seeding could be considered as the “natal” period. Consequently, HepaRG cells were treated for 3 weeks with BPA (from 0.2 to 2000 nM), with a treatment starting during the proliferating period. BPA was able to induce steatosis with a nonmonotonic dose response profile, with significant effects on neutral lipids and triglycerides observed for the 2 nM concentration. However, the expression of many enzymes involved in lipid and carbohydrate homeostasis was unchanged in exposed HepaRG cells. The expression of other potential BPA targets and enzymes involved in BPA biotransformation was also determined, giving answers as well as new questions regarding the mechanisms of action of BPA. Hence, HepaRG cells provide a valuable model that can prove useful for the toxicological assessment of endocrine disruptors on hepatic metabolisms, in particular in the developing liver. © 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 1024–1036, 2017.     

Effect of Halothane Anesthesia on Glucose Utilization and Production in Adolescents

Background: It should be possible to avoid variations in plasma glucose concentration during anesthesia by adjusting glucose infusion rate to whole-body glucose uptake. To study this hypothesis, we measured glucose utilization and production, before and during halothane anesthesia.

Methods: After an overnight fast, six adolescents between 12 and 17 yr of age were infused with tracer doses of [6,6-sup 2 H2]glucose for 2 h before undergoing anesthesia, and the infusion was continued after induction, until the beginning of surgery. Plasma glucose concentration was monitored throughout, and free fatty acids, lactate, insulin, and glucagon concentrations were measured before and during anesthesia.

Results: Despite the use of a glucose-free maintenance solution, plasma glucose concentration increased slightly but significantly 5 min after induction (5.3 plus/minus 0.4 vs. 4.5 plus/minus 0.4 mmol *symbol* 1 sup -1 , P < 0.05). This early increase corresponded to a significant increase in endogenous glucose production over basal conditions (4.1 plus/minus 0.4 vs. 3.6 plus/minus 0.2 mg *symbol* kg sup -1 *symbol* min sup -1, P < 0.05), with no concomitant change in peripheral glucose utilization. Fifteen minutes after induction, both glucose utilization and production rates decreased steadily and were 20% less than basal values by 35 min after induction (2.9 plus/minus 0.3 vs. 3.6 plus/minus 0.2 mg *symbol* kg sup -1 *symbol* min sup -1, P < 0.05). Similarly, glucose metabolic clearance rate decreased by 25% after 35 min. Despite the increase in blood glucose concentration, anesthesia resulted in a significant decrease in plasma insulin concentration.     

Chronic permanent hypoxemia predisposes to mild elevation of liver stiffness

AIM:To evaluate the impact of long term permanent hypoxemia noticed in patients with non operated congenital cyanogenic cyanotic cardiopathy on liver stiffness.METHODS:We included ten adult patients with non operated inoperate cyanotic cardiopathy and ten matched patients for age and gender admitted to the gastroenterology department for proctologic diseases;Clinical and laboratory data were collected[age,gender,body mass index,oxygen saturation,glutamate oxaloacetate transaminase(GOT),glutamate pyruvate transaminase(GPT),glycemia and cholesterol].Measurement of hepatic stiffness by transient elastography was carried out in all patients using the Fibroscan device.All patients underwent an echocardiography to eliminate congestive heart failure.RESULTS:Among the patients with cyanotic cardiopathy,median liver stiffness 5.9±1.3 kPa was greater than control group(4.7±0.4 kPa)(P=0.008).Median levels of GOT,GPT,gamma-glutamyltransferase,glycemia and cholesterol were comparable in cardiopathy and control group.In regression analysis including age,gender,body mass index,oxygen saturation,GOT,GPT,glycemia,cholesterol showed that only oxygen saturation was related to liver stiffness(r=-0.63 P=0.002).CONCLUSION:Chronic permanent hypoxemia can induce mild increase of liver stiffness,but further studies are needed to explore the histological aspects of liver injury induced by chronic permanent hypoxemia.     

Rapid adaptation of rat brain and liver metabolism to a ketogenic diet: an integrated study using 1H- and 13C-NMR spectroscopy

The ketogenic diet (KD) is an effective alternative treatment for refractory epilepsy in children, but the mechanisms by which it reduces seizures are poorly understood. To investigate how the KD modifies brain metabolism, we infused control (CT) and 7-day KD rats with either [1-¹³C]glucose (Glc) or [2,4-¹³C₂]β-hydroxybutyrate (β-HB). Specific enrichments of amino acids (AAs) measured by ¹H- and ¹³C-NMR in total brain perchloric acid extracts were similar between CT and KD rats after [1-¹³C]Glc infusion whereas they were higher in KD rats after [2,4-¹³C₂]β-HB infusion. This suggests better metabolic efficiency of ketone body utilization on the KD. The relative rapid metabolic adaptation to the KD included (1) 11%-higher brain γ-amino butyric acid (GABA)/glutamate (Glu) ratio versus CT, (2) liver accumulation of the ketogenic branched-chain AAs (BCAAs) leucine (Leu) and isoleucine (ILeu), which were never detected in CT, and (3) higher brain Leu and ILeu contents. Since Glu and GABA are excitatory and inhibitory neurotransmitters, respectively, higher brain GABA/Glu ratio could contribute to the mechanism by which the KD reduces seizures in epilepsy. Increased BCAA on the KD may also contribute to better seizure control.