Supplementation of dietary apple cider vinegar as an organic acidifier on the growth performance, digestive enzymes and mucosal immunity of green terror (Andinoacara rivulatus)

The present study was designed to investigate the effects of dietary apple cider vinegar (ACV) on digestive enzyme activity and growth performance as well as immune responses and antibacterial activity of skin mucus in green terror (Andinoacara rivulatus). Fish were fed diets supplemented with 0%, 1%, 2% and 4% of ACV (40.830 ppm acetic acid concentration) for 63 days. The final weight and weight gain values were observed to be significantly higher in fish fed with 2% of ACV compared to the control group (p .05). ACV treatment resulted in a significant increase in the intestinal protease, α‐amylase, lipase and alkaline phosphatase activities compared to control (p < .05). The activities of digestive enzymes in fish fed with 2% and 4% of ACV diets were significantly higher than the other groups (p < .05). The total protein content, alternative haemolytic complement, alkaline phosphatase, total immunoglobulins and lysozyme activities of skin mucus increased significantly in fish fed with ACV diets (p < .05). In conclusion, administration of ACV enhanced digestive enzyme activity, growth performance, immune responses and the immune properties of skin mucus, and it can be used as a natural growth promoter and immunostimulant in green terror culture

Fanconi-Bickel syndrome versus osteogenesis imperfeeta: An Iranian case with a novel mutation in glucose transporter 2 gene, and review of literature

Fanconi-Bickel syndrome is an extremely rare hereditary metabolic disease, characterized by hepatomegaly due to glycogen storage, refractory hypophosphatemic rickets, marked growth retardation and proximal renal tubular acidosis. Recurrent bone fractures are one of the hallmark findings. It is a single gene disorder; the responsible gene belongs to the facilitative glucose transporters 2 (GLUT2) family gene or (SLC2A2) mapped to the q26.1-26.3 locus on chromosome 3, and encodes the GLUT protein 2. This protein is expressed in pancreatic ί-cells, hepatocytes, renal tubules, and intestinal mucosa. Several mutations in the GLUT2 gene have been reported in different ethnicities. Herein we report an Iranian girl with a missed diagnosis of osteogenesis imperfecta. She was referred with the history of frequent fractures, and severe motor delay and was suspected to osteogenesis imperfecta. Following the case we detected refractory rickets instead of OI, sever growth failure, proximal renal tubulopathy and RTA, and enlarged kidneys, progressive hepatomegaly, and GSD on liver biopsy. Glucose and galactose tolerance tests confirmed abnormal carbohydrate metabolism. Molecular analysis on GLUT2 gene revealed a homozygous novel mutation in exon 5; it was 15 nucleotide deletion and 7 nucleotide insertion and caused a frame shift mutation, produced a premature truncated protein (P.A229QFsX19). This mutation has not been reported before in the relevant literature