El objetivo de este trabajo es evaluar la función de un microscopio de origami Foldscope como herramienta de apoyo en la identificación taxonómica de garrapatas Rhipicephalus sanguineus. Se recolectaron 257 muestras de garrapatas en cinco colonias de la ciudad de Chihuahua, México. Se analizaron las estructuras morfológicas más representativas para su identificación taxonómica con un estereoscopio y Foldscope. Con el microscopio de papel fue posible identificar palpos, base del gnatosoma, ojos, surco anal, festones, primera coxa, placa estigmatal y escudo en especímenes menores a 7 mm de longitud. El Foldscope es una herramienta que permite la identificación de garrapatas en campo, útil para estudios de vigilancia epidemiológica y potenciales campañas de concientización ciudadana en enfermedades transmitidas por vector.
Poor dietary habits such as overconsumption of hypercaloric diets characterized by a high content of fructose and fat are related to metabolic abnormalities development such as obesity, diabetes, and dyslipidemia. Accumulating evidence supports the hypothesis that if energy intake gradually exceeds the body's ability to store fat in adipose tissue, the prolonged metabolic imbalance of circulating lipids from endogenous and exogenous sources leads to ectopic fat distribution in the peripheral organs, especially in the heart, liver, and kidney. The kidney is easily affected by dyslipidemia which induces lipid accumulation and reflects an imbalance between fatty acid supply and fatty acid utilization. This derives on tissue lipotoxicity, oxidative stress, fibrosis, and inflammation that results in structural and functional changes that lead to glomerular and tubule-interstitial damage. Some authors indicate that a lipid-lowering pharmacological approach combined with a substantial lifestyle change should be considered as part of the treatment of chronic kidney disease (CKD). Also, the new therapeutic targets identification and the development of new drugs targeting metabolic pathways involved with kidney lipotoxicity could constitute an additional alternative to combat the complex mechanisms involved in impaired kidney function. In this review article, we first provide the pathophysiological evidence regarding the impact of hypercaloric diets, such as high-fat diets and high-fructose diets, on the development of metabolic disorders associated with impaired renal function and the molecular mechanisms underlying tissue lipid deposition. In addition, we present the current progress regarding translational strategies to prevent and/or treat kidney injury related to the consumption of hypercaloric diets.
Background: It has been proposed that curcumin modulates the gene expression of different signaling pathways, improve the fatty acids metabolism and exerts a potential beneficial effect on cardiometabolic disease, but this has not been thoroughly demonstrated. In the present study, we evaluated the effect of curcumin upon the expression of PPARα, CPT1, MCAD, VLCAD and ACAA2 in heart of mice fed a high-fructose diet (HFD).Methods: Twenty-four mice C57BL/6 were divided into four groups (n=6) and treated for 15 weeks. Control group (C) received standard diet (SD), Curcumin group (C+Cur), Fructose group (F) and Fructose with Curcumin group (F+Cur). The groups were treated with 0.75% w/w curcumin mixed in the SD and 30% w/v fructose in water, respectively. Heart proteins expression were analyzed by Western Blot.Results: Curcumin supplementation increased PPARα and ACAA2 expression and decreased CPT1 and MCAD expression in heart of mice fed a HFD. However, it did not modify the VLCAD expression.Conclusions: Curcumin regulated PPARα, CPT1 and MCAD expression and increased ACAA2 expression; suggesting a therapeutic potential in the prevention of alterations in mitochondrial fatty acids metabolism in heart of mice fed a HFD.
Background: Dyslipidemia and obesity hypercaloric diet-induced lead to kidney damage. We investigated the effect of curcumin on the expression of proteins related to inflammation, fibrosis, fatty acids metabolism, kidney damage, and morphological changes in the kidney of mice hypercaloric diets-fed. Methods: Groups of 5-week-old C57BL/6 mice (n=6) were formed: Control (C), High-fructose diet (F), High-fructose diet and curcumin (F+Cur), High-fat diet (HFD), High-fat diet and curcumin (HFD+Cur), High-fat diet and fructose (HFD+F), High-fat diet, fructose and curcumin (HFD+F+Cur), treated for 16 weeks with 30% (w/v) fructose, 60% (w/w) fat and 0.75% (w/w) curcumin. Kidneys were obtained for histomorphological and Western Blot analysis. Results: Curcumin prevented TNF-α overexpression in the F and HFD+F groups. VLCAD expression was higher in the F, HFD, and HFD+F groups. PPARγ expression was lower in the F+Cur, HFD+Cur, and HFD+F+Cur groups. Curcumin prevented overexpression of CPT1 and KIM1 in the HFD+F and HFD groups. Curcumin prevented morphological lesions, fibrosis, and lipid deposition hypercaloric diet-induced. Conclusion: Chronic consumption of hypercaloric diets causes inflammation, fibrosis, and lipid deposition in the kidney. It is suggested that curcumin differentially modulates kidney injury as a function of the damage induced by the high-fat/high-fructose diet.
Background: the consumption of a high-fructose diet (HFD) contributes to obesity, dyslipidemia, and cardiovascular diseases. It has been proposed that curcumin modulates lipid metabolism and it has a potential beneficial effect in the context of the cardiometabolic diseases, although it has not been clearly demonstrated Objective: to evaluate the effect of curcumin on the expression of the PPARα, CPT1, MCAD, VLCAD, and ACAA2 genes in the hearts of mice fed with a HFD. k (F), and 4) standard diet + 0.75% (w/w) curcumin + 30% (w/v) fructose (F+Cur). The gain of body weight, glucose, and the overall serum cholesterol levels were measured after the respective treatment. The expression of PPARα, MCAD, VLCAD, ACAA2, and CPT1 was assessed by Western blot in mice hearts. Results: our data showed that a curcumin treatment induced a higher expression of PPARα and ACAA2 whereas it decreased CPT1 and MCAD expression in the hearts of mice fed with a HFD. However, it had no effect on VLCAD expression Conclusion: curcumin regulates PPARα, CPT1, and MCAD expression and increased that of ACAA2. This suggests a possible therapeutic use to prevent the alterations of mitochondrial fatty acid metabolism in the hearts of mice fed with a HFD.
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