Conversion to Roux-en-Y gastric bypass surgery through a robotic-assisted hybrid technique after failed sleeve gastrectomy: Short-term results. / Conversión por técnica híbrida robótica a bypass gástrico en Y de Roux posterior a falla de manga gástrica: resultados a corto plazo.

INTRODUCTION AND AIMS: Laparoscopic sleeve gastrectomy (LSG) is the most widely performed bariatric surgery worldwide but complications and failed procedures are on the rise. AIMS: To determine the reasons for failed LSGs and report the results of conversion to gastric bypass surgery, comparing the outcomes with those of primary gastric bypass surgery. MATERIALS AND METHODS: Patients with failed LSG that underwent conversion to gastric bypass surgery through a robotic-assisted and laparoscopic (hybrid) technique were evaluated. Outcomes and follow-up related to weight loss failure (WLF) were compared with those in patients that underwent primary laparoscopic gastric bypass (pLGB) surgery. RESULTS: Revisional surgery was performed on 13 patients due to WLF, on 3 patients because of refractory gastroesophageal reflux disease (GERD), and on 2 patients due to gastric stricture. There were no differences between the preoperative characteristics of the patients with WLF before undergoing conversion to gastric bypass and the patients that underwent pLGB surgery. At postoperative month 36, the percentage of excess weight loss was greater in the patients that underwent pLGB surgery, than in those with WLF that underwent conversion to gastric bypass (69.17±23.73 vs. 54.17±12.48, respectively; P<0.05). Refractory GERD, symptoms due to gastric stricture, and comorbidities all improved after the revisional surgery. CONCLUSION: Revisional surgery resulted in acceptable weight loss at 36 months of follow-up and favored comorbidity remission. In addition, it resolved symptoms of refractory GERD and gastric stricture.

[Transforming growth factor alpha (TGF-alpha) and epidermoid growth factor (EGF) in polycystic ovary syndrome: potential role in the decrease of apoptosis mechanisms in the follicle]. / El factor de crecimiento transformante-alpha (TGF-alpha) y el factor de crecimiento epidermoide (EGF) en el síndrome de ovarios poliquísticos: posible papel en la disminución de los mecanismos apoptóticos en el folículo.

Knowledgement on ovary function regulation is advancing. Classic concept about endocrine regulation by sexual hormones and gonadotrophin has turning to an hypothesis: autocrine and paracrine factors as intra-ovarian regulators. Follicular growth and steroidogenesis are mainly driven by follicle stimulating hormone (FSH), luteine hormone (LH) and steroids. On the other hand, the presence of intra-ovarian growth factors have an important role in modulation of gonadotrophin effects on ovarian functions. The influence of this factors on follicle growth are described.

Redox state and energy metabolism during liver regeneration: alterations produced by acute ethanol administration.

Ethanol metabolism can induce modifications in liver metabolic pathways that are tightly regulated through the availability of cellular energy and through the redox state. Since partial hepatectomy (PH)-induced liver proliferation requires an oversupply of energy for enhanced syntheses of DNA and proteins, the present study was aimed at evaluating the effect of acute ethanol administration on the PH-induced changes in cellular redox and energy potentials. Ethanol (5 g/kg body weight) was administered to control rats and to two-thirds hepatectomized rats. Quantitation of the liver content of lactate, pyruvate, beta-hydroxybutyrate, acetoacetate, and adenine nucleotides led us to estimate the cytosolic and mitochondrial redox potentials and energy parameters. Specific activities in the liver of alcohol-metabolizing enzymes also were measured in these animals. Liver regeneration had no effect on cellular energy availability, but induced a more reduced cytosolic redox state accompanied by an oxidized mitochondrial redox state during the first 48 hr of treatment; the redox state normalized thereafter. Administration of ethanol did not modify energy parameters in PH rats, but this hepatotoxin readily blocked the PH-induced changes in the cellular redox state. In addition, proliferating liver promoted decreases in the activity of alcohol dehydrogenase (ADH) and of cytochrome P4502E1 (CYP2E1); ethanol treatment prevented the PH-induced diminution of ADH activity. In summary, our data suggest that ethanol could minimize the PH-promoted metabolic adjustments mediated by redox reactions, probably leading to an ineffective preparatory event that culminates in compensatory liver growth after PH in the rat.

Morphological and biochemical effects of a low ethanol dose on rat liver regeneration: role of route and timing of administration.

We have demonstrated that in rats subjected to partial hepatectomy (PH), the regenerating liver had an enhanced metabolism of ethanol, which largely depended on the route and timing of ethanol administration. Therefore, the influence of the administration route and timing for ethanol-induced deleterious effects on the regenerating rat liver was evaluated in animals subjected to 70% PH. Remnant liver showed moderate fatty infiltration, extended distortion of hepatocellular structure, and high mitotic index. Intragastric ethanol administration (1.5 g/kg body weight) considerably reduced the PH-induced changes in liver structures. Ethanol treatment also decreased liver thymidine kinase activity, serum albumin, and glucose levels. Intraperitoneal administration of the same ethanol dose to PH rats promoted lesser alterations on liver regeneration. Independently of its administration route, ethanol abruptly shortened a PH-induced selective increase in serum enzyme activities. These data suggest that the inhibitory effect of a low dose of ethanol on PH-induced liver regeneration is dependent on the timing and route of administration.

Pharmacokinetics of the ethanol bioavailability in the regenerating rat liver induced by partial hepatectomy.

It is well known that a single ethanol administration is capable of inhibiting the two-thirds partial hepatectomy (PH)-induced liver regeneration (LR); nonetheless, it has not been elucidated how ethanol metabolism by the remnant liver is exerting the deleterious ethanol actions on LR. Indeed, pharmacokinetics analysis of ethanol elimination is lacking in rats subjected to PH, which might extend our understanding in the mechanisms that account for the ethanol-induced inhibition on LR after PH in the rat. Therefore, the present study is a pharmacokinetics analysis comparing intragastric and intraperitoneal administrations of ethanol to rats under PH, at several times after surgery (0 to 96 hr postsurgery). Our results show that PH rats had a much lower blood ethanol peak than sham-operated, when intragastrically administered during the first 4 hr after surgery that was transient and normalized at 6 hr post-PH. The area under the curve for blood ethanol was higher in PH animals, starting after 6 hr postsurgery and extended to the all replicative period, and returned within the control values thereafter. The quantity of ethanol absorbed after its intraperitoneal injection was essentially the same as the administered dose for all of the groups tested. Hence, ethanol bioavailability diminished due to an enhanced rate of the first-pass metabolism for ethanol in PH rats at the very early times post-PH. At later times of PH, ethanol bioavailability was practically normalized, and these effects were accompanied by a drastic increase in the liver capacity to metabolize ethanol, mainly at 48 to 96 hr after surgery, as calculated as ethanol elimination per gram of liver, as well as by total body weight. The very early changes in ethanol bioavailability in PH rats were not accounted for gastric ethanol retention in these animals. In conclusion, first-pass metabolism importantly participates in the modified ethanol bioavailability at very early times after PH, an event presumably attained to gastric catabolism of ethanol. However, the very enhanced metabolism of ethanol showed by the regenerating liver, particularly after the first 24 hr postsurgery, seems to be the main factor affecting ethanol pharmacokinetics in rats subjected to PH. The underlying mechanisms in this liver enhancement of ethanol oxidation by PH rats remains to be elucidated.

Modifications of intracellular calcium release channels and calcium mobilization following 70% hepatectomy.

The aim of this study was to investigate the properties of ryanodine and IP3 receptors in regenerating liver following 70% hepatectomy, and to evaluate the hepatic Ca2+ distribution and mobilization during this process. Specific [3H]ryanodine and [3H]IP3 binding to hepatic smooth endoplasmic reticulum membranes, as well as subcellular Ca2+ determination by atomic absorption flame photometry and Ca2+ mobilization by INDO-1 AM spectrofluorescence in hepatocytes, was performed in regenerating livers after surgical 70% hepatectomy. Incorporation of 14C amino acids into proteins and of 32P into phospholipids was done in subcellular fractions. Ryanodine receptor Kd presented a dramatic increase after 12 h of surgery and remained high up to 2 days of treatment. IP3 receptor Bmax showed a significant augmentation starting at 6 h after hepatectomy and returning to normal values after 1 week. Cytosolic total calcium content decreased from 12 h until 4 days after hepatectomy whereas the microsomal and mitochondrial total calcium increased at 1 and 2-4 days of liver regeneration, which coincided with the differential turnover of proteins and phospholipids in these fractions. ATP-induced Ca2+ transients in hepatocytes of 24-h-hepatectomized rats confirmed the altered sensitivity of the ryanodine receptor toward its ligand, since 10 times more ryanodine was necessary to alter the ATP-induced Ca2+ transient. The data support the notion that the calcium release channels are targets of mechanisms of metabolic control during the proliferative response following 70% hepatectomy and might be part of the modified intracellular Ca2+ dynamics during liver regeneration.

Sucrose administration to partially hepatectomized rats: a possible model to study ethanol-induced inhibition of liver regeneration.

Although acute ethanol treatment drastically inhibits liver regeneration after partial hepatectomy, the exact mechanisms involved remain obscure. On the other hand, it is known that early carbohydrate administration promotes a more successful restoration of the liver mass. Therefore, carbohydrate administration could be an experimental approach for studying ethanol action on the regenerating liver. In rats subjected to two-thirds partial hepatectomy, ethanol was administered alone or in combination with a variety of carbohydrates (glucose, fructose, glucose plus fructose, sucrose and maltose). In liver samples, regeneration parameters and histological assessment were performed. Blood ethanol and metabolites reflecting liver function were assayed. Ethanol intake strongly decreased the incorporation of [3H]thymidine into liver DNA, the concentration of DNA/g of tissue, and thymidine kinase activity. In this group, severe alterations in cell structure (i.e. abundant fat droplets and abnormal mitochondria) were found. Carbohydrates readily improved the survival rate of ethanol-intoxicated hepatectomized rats. Sucrose was effective in reverting the ethanol-induced alterations in liver structure and the parameters of liver regeneration, and partially blocked the ethanol-induced alterations in serum levels of albumin, triacylglycerols and ammonia without modifying the blood levels and clearance of ethanol. Data suggest that the beneficial action of sucrose might be related to an adequate supply of energetic sources at early times of liver regeneration, rather than altering ethanol bioavailability. Thus, the present model could be an experimental approach for studying the metabolic alterations involved in the ethanol-induced inhibition of the liver regeneration.

Acute ethanol intake produces lipid peroxidation in rat red blood cells membranes.

The effect of acute ethanol intake on lipid peroxidation (LP) and proteins in red blood cells (RBC) was explored. The amount of malondialdehyde (MDA; an indicator of LP) was elevated transiently when the maximal ethanol level in whole blood was observed. In contrast, erythrocyte membrane proteins were not affected. In in vitro experiments both ethanol and acetaldehyde did not alter the MDA levels. These results indicate that the metabolism of ethanol or acetaldehyde beyond the RBCs is required in order to detect LP on these cells.