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1.
Recent Pat Food Nutr Agric ; 12(1): 29-35, 2021.
Article in English | MEDLINE | ID: mdl-33397263

ABSTRACT

BACKGROUND: Malnutrition induced by dietary restriction produces several metabolic changes that affect body weight, the digestive system, and annex organs, including the liver. Malnutrition generates an inflammatory state and increases oxidative stress. The liver is one of the body vital organs, becoming necessary to analyze the impact of food supplementation on the repair of possible changes that may occur in this organ due to malnutrition. AIMS: To evaluate the effects of a low-cost supplementation derived from Buriti and dairy byproducts on liver recovery in malnourished mice, focusing on the expression of oxidative stressrelated genes, as well as biochemical and histological parameters. METHODS: Swiss mice were divided into six groups and submitted to two treatment phases: food restriction, for malnutrition onset; and renutrition, with mice being fed with different diets. RESULTS: Our results indicate that dietary supplementation was successful in recovering liver damage caused by malnutrition in animal models. The new supplement has been shown to recover liver damage with similar or superior results compared to the commercial reference supplement on the market. CONCLUSION: Our work presents a new composition of low cost food supplement based on buriti and dairy by-products, proven to be effective in the malnutrition treatment of malnutrition. The improvements were proven through the recovery of body weight, reduction of inflammation and oxidative stress.


Subject(s)
Arecaceae/metabolism , Dairy Products/analysis , Liver Diseases/diet therapy , Liver/injuries , Malnutrition/complications , Animals , Arecaceae/chemistry , Body Weight , Dietary Supplements/analysis , Fruit/chemistry , Fruit/metabolism , Humans , Liver Diseases/etiology , Liver Diseases/metabolism , Liver Diseases/physiopathology , Male , Mice , Oxidative Stress
2.
Protein Pept Lett ; 28(7): 781-787, 2021.
Article in English | MEDLINE | ID: mdl-33504292

ABSTRACT

BACKGROUND: Brazilian flora is rich in plants with medicinal properties, which though popular, has contributed to the development of a range of phytotherapic products that use plants to treat and cure diseases. However, studies that use Brazilian plants in the treatment of metabolic disorders are still scarce in the literature. OBJECTIVE: The aim of this study was to analyze the effect of hepatotoxicity Lafoensia pacari on the metabolism of mice with obesity induced by a high-fat diet and to verify the phytochemical difference between the Lafoensia pacari bark of the trunk, leaves, and branches. METHODS: The plant material was collected from April to May in the municipality of Bonito de Minas, MG, Brazil. Qualitative tests for the presence of secondary metabolite classes were performed for leaves, branches and bark of the trunk. Through histological analysis, we evaluated hepatocytes and cell lesions in the liver. RESULTS: The comparative phytochemical analysis of the plant did not reveal alterations between the different plant parts. The phytochemical test showed that is preferable to use the leaves to make the extract to be applied, aiming to reduce the plant aggression. After treatment, greater changes were observed in the animals that received the high-fat diet and the hydroethanolic extract; the levels of AST, ALT, albumin and creatinine that were increased, thus demonstrating a possible toxicity. There were no significant differences in body weight. In the histological analysis, the animals without plant treatment displayed decreased liver weight and reduction in the inflammatory infiltrate. CONCLUSION: We conclude that Lafoensia pacari should be better evaluated for oral consumption and may cause liver damage.


Subject(s)
Anti-Obesity Agents/toxicity , Liver/drug effects , Lythraceae/chemistry , Obesity/drug therapy , Plant Extracts/toxicity , Alanine Transaminase/metabolism , Albumins/metabolism , Alkaloids/isolation & purification , Alkaloids/toxicity , Animals , Anti-Obesity Agents/chemistry , Aspartate Aminotransferases/metabolism , Body Weight/drug effects , Brazil , Creatinine/metabolism , Diet, High-Fat/adverse effects , Flavonoids/isolation & purification , Flavonoids/toxicity , Glutathione Peroxidase/metabolism , Hepatocytes/drug effects , Hepatocytes/metabolism , Hepatocytes/pathology , Liver/metabolism , Liver/pathology , Male , Mice , Obesity/etiology , Obesity/metabolism , Obesity/pathology , Phenols/isolation & purification , Phenols/toxicity , Plant Bark/chemistry , Plant Extracts/chemistry , Plant Leaves/chemistry , Plant Stems/chemistry , Secondary Metabolism , Superoxide Dismutase/metabolism , Glutathione Peroxidase GPX1
3.
Metabolism ; 95: 36-45, 2019 06.
Article in English | MEDLINE | ID: mdl-30905634

ABSTRACT

Nowadays the adipose tissue is recognized as one of the most critical endocrine organs releasing many adipokines that regulate metabolism, inflammation and body homeostasis. There are several described adipokines, including the renin-angiotensin system (RAS) components that are especially activated in some diseases with increased production of angiotensin II and several pro-inflammatory hormones. On the other hand, RAS also expresses angiotensin-(1-7), which is now recognized as the main peptide on counteracting Ang II effects. New studies have shown that increased activation of ACE2/Ang-(1-7)/MasR arm can revert and prevent local and systemic dysfunctions improving lipid profile and insulin resistance by modulating insulin actions, and reducing inflammation. In this context, the present review shows the interaction and relevance of Ang-(1-7) effects on regulating adipokines, and as one adipokine itself, modulating body homeostasis, with emphasis on its anti-inflammatory properties, especially in the context of metabolic disorders with focus on obesity and type 2 diabetes mellitus pandemic.


Subject(s)
Adipokines/metabolism , Angiotensin I/metabolism , Inflammation/metabolism , Peptide Fragments/metabolism , Adipose Tissue/metabolism , Animals , Humans , Proto-Oncogene Mas
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