RESUMEN
This study describes the levels of gut lysozyme and IgM, the number, size and density of gut-associated lymphoid tissue (GALT) regions, and the lymphocyte population in Asian seabass following field oral administration of a feed-based vaccine. Fish in a grow-out farm were selected and divided into two groups; Group 1 was vaccinated at week 0, 2, and 6, while Group 2 was not vaccinated. Samplings were done at 2-week intervals when the fish were observed for clinical signs, and gross lesions were recorded. The intestinal tissue and gut lavage fluid were collected. GALT regions (numbers, size, density and population of lymphocytes) were analyzed. Clinical signs such as abnormal swimming pattern and death, and gross lesions including scale loss, ocular opacity, and skin ulceration were observed in both groups. At the end of the study, the incidence rate between both groups were significantly different (p < 0.05). The gut IgM level and lysozyme activity, lymphocyte population, number, size and density of GALT regions of Group 1 were significantly (p < 0.05) higher than Group 2. Therefore, this study concludes that the feed-based vaccine reduces the incidence of vibriosis by stimulating the gut immunity of the vaccinated fish with an enhanced GALT region, specific IgM production against Vibrio harveyi, and lysozyme responses.
RESUMEN
Metabolic Syndrome, a pathological condition affecting approximately 35% of the USA population, is characterized by obesity, insulin resistance, and hypertension. Metabolic syndrome is considered the single most common condition predisposing to the development of various chronic diseases including diabetes and hypertension. Hypomagnesaemia has been consistently observed in association with metabolic syndrome, but it is unclear whether reduced Mg2+ levels are the consequence or a possible cause for the development of the metabolic syndrome and/or its associated pathologies. Research performed in our laboratory showed that rats exposed for 2 weeks to a Mg2+ deficient diet presented decreased glucose accumulation into the hepatocytes together with low Mg2+ level in the circulation and within the liver cells. To better investigate the changes in glucose metabolism, HepG2 were used to mimic in vitro Mg2+ deficiency conditions. HepG2 cells cultured in low extracellular Mg2+ presented a 20% decrease in total cellular Mg2+ content, reduced glucose accumulation, and enhanced glucose 6-phosphate (G6P) transport into the endoplasmic reticulum (ER). The increased G6P transport was associated with its enhanced hydrolysis by the glucose 6-phosphatase, but also conversion to 6-phosphogluconolactone by the glucose 6-phosphate dehydrogenase. The latter process resulted in the increased generation of NADPH within the ER and the increased conversion of cortisone to cortisol by the 11-ß-hydroxysteroid dehydrogenase type-1 (11-ß-OHSD1). Taken together, our results provide compelling evidence that Mg2+ deficiency precedes and actually promotes some of the hepatic dysmetabolisms typical of the metabolic syndrome. The decrease in intrahepatic Mg2+ content up-regulates G6P entry into the hepatic endoplasmic reticulum and its routing into the pentose shunt pathway for energetic purposes. The associated increased in NADPH production within the ER then stimulates cortisol production, setting the conditions for hepatic insulin resistance and further altering liver metabolism.
