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BackgroundTherapeutic use of leaves of M. oleifera has been evaluated in diabetes because of its possible capacity to decrease blood glucose and lipids concentration after ingestion, as result of the polyphenols content and others compounds. Nevertheless most results have been obtain from leaf extract, therefore this study would use leaf powder as the regular way of consumption of population to know effects over toxicity glucose, triglycerides, cholesterol, corporal weight, and predominant groups of microbiota.MethodsPowdered leaf was administrated in different doses to know toxicity and genotoxicity using LD50 and micronuclei assay. Hyperglycemia was induced by alloxan on Sprague Dawley rats. Glucose and body weight were measured once a week meanwhile cholesterol and triglycerides were analyzed at the end of the study by commercial kits. Different organs were examined by hematoxylin-eosin technique. Lactic acid bacteria and Enterobacteriaceae were enumerated from stool samples.ResultsThe tested doses revealed no lethal dose and no significant differences in genotoxicity parameter. The consumption of the leaves showed a hypoglycemic effect (< 250 mg/dL in diabetic M. oleifera treated group), however in corporal weight showed an increased (> 30 g over no M. oleifera treated groups). There was no change in enumeration of lactic acid bacteria (8.4 CFU/g) but there were differences in the predominance of type of lactobacillus and enterobacteria enumeration.ConclusionsThese results help to increase information over the most popular use of M. oleifera and its safety. However there are needed more studies over the hypoglycemic mechanisms and effects over intestinal microbiota.

Clostridium perfringens (Cp.) is the cause of human foodborne desease. Meat and poultry products are identified as the main source of infection for humans. Cp. can be found in poultry litter, feces, soil, dust, and healthy birds’ intestinal contents. Cp. strains are known to secrete over 20 identified toxins and enzymes that could potentially be the principal virulence factors, capable of degrading mucin, affecting enterocytes, and the small intestine epithelium, involved in necrotic enteritis (NE) pathophysiology, also leading to immunological responses, microbiota modification and anatomical changes. Different environmental and dietary factors can determine the colonization of this microorganism. It has been observed that the incidence of Cp-associated to NE in broilers has increased in countries that have stopped using antibiotic growth promoters. Since the banning of such antibiotic growth promoters, several strategies for Cp. control have been proposed, including dietary modifications, probiotics, prebiotics, synbiotics, phytogenics, organic acids, and vaccines. However, there are aspects of the pathology that still need to be clarified to establish better actions to control and prevention. This paper reviews the current knowledge about Cp. as foodborne pathogen, the pathophysiology of NE, and recent findings on potential strategies for its control.

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