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1.
Br J Nutr ; 127(3): 321-334, 2022 02 14.
Artículo en Inglés | MEDLINE | ID: mdl-33749571

RESUMEN

A12-week experiment was conducted to evaluate the influences of thiamine ongrowth performance, and intestinal mitochondrial biogenesis and function of Megalobramaamblycephala fed a high-carbohydrate (HC) diet. Fish (24·73 (sem 0·45) g) were randomly assigned to one of four diets: two carbohydrate (CHO) levels (30 and 45 %) and two thiamine levels (0 and 1·5 mg/kg). HC diets significantly decreased DGC, GRMBW, FIMBW, intestinal activities of amylase, lipase, Na+, K+-ATPase, CK, complexes I, III and IV, intestinal ML, number of mitochondrial per field, ΔΨm, the P-AMPK: T-AMPK ratio, PGC-1ß protein expression as well as the transcriptions of AMPKα1, AMPKα2, PGC-1ß, mitochondrial transcription factor A, Opa-1, ND-1 and COX-1 and 2, while the opposite was true for ATP, AMP and reactive oxygen species, and the transcriptions of dynamin-related protein-1, fission-1 and mitochondrial fission factor. Dietarythiamine concentrations significantly increased DGC, GRMBW, intestinal activities of amylase, Na+, K+-ATPase, CK, complexes I and IV, intestinal ML, number of mitochondrial per field, ΔΨm, the P-AMPK:T-AMPK ratio, PGC-1ß protein expression as well as the transcriptions of AMPKα1, AMPKα2, PGC-1ß, Opa-1, ND-1, COX-1 and 2, SGLT-1 and GLUT-2. Furthermore, a significant interaction between dietary CHO and thiamine was observed in DGC, GRMBW, intestinal activities of amylase, CK, complexes I and IV, ΔΨm, the AMP:ATP ratio, the P-AMPK:T-AMPK ratio, PGC-1ß protein expression as well as the transcriptions of AMPKα1, AMPKα2, PGC-1ß, Opa-1, COX-1 and 2, SGLT-1 and GLUT-2. Overall, thiamine supplementation improved growth performance, and intestinal mitochondrial biogenesis and function of M. amblycephala fed HC diets.


Asunto(s)
Carbohidratos de la Dieta , Biogénesis de Organelos , Proteínas Quinasas Activadas por AMP/metabolismo , Adenosina Monofosfato , Adenosina Trifosfatasas/metabolismo , Adenosina Trifosfato/metabolismo , Amilasas/metabolismo , Animales , Carbohidratos de la Dieta/metabolismo , Carbohidratos de la Dieta/farmacología , Coactivador 1-alfa del Receptor Activado por Proliferadores de Peroxisomas gamma/metabolismo , Tiamina/farmacología
2.
J Clin Lab Anal ; 33(4): e22831, 2019 May.
Artículo en Inglés | MEDLINE | ID: mdl-30666727

RESUMEN

BACKGROUND: To explore the correlations between SAA, CRP, and clinical indices of patients with acutely exacerbated chronic obstructive pulmonary disease (AECOPD). METHODS: A total of 120 patients with AECOPD and another 120 with remitted COPD were enrolled in an AECOPD group and a COPD remission group, respectively. Meanwhile, 120 healthy subjects were included as a control group. SAA, CRP, PCT, Fbg, IL-8, IL-6, TNF-α, and IP-10 levels were detected. FEV1 and FEV1 /FVC were measured. RESULTS: Compared with control group, the serum levels of SAA, CRP, PCT, Fbg, IL-8, IL-6, TNF-α, and IP-10 significantly increased in COPD remission group (P < 0.05). The levels of AECOPD group significantly exceeded those of COPD remission group (P < 0.05). The levels of AECOPD patients with different GOLD grades were significantly different (P < 0.05). AECOPD group had significantly lower FEV1 and FEV1 /FVC than those of COPD remission group (P < 0.05). The CAT score of AECOPD patients was (18.41 ± 2.55) points. The levels of SAA, CRP, PCT, Fbg, IL-8, IL-6, TNF-α, and IP-10 were negatively correlated with FEV1 and FEV1 /FVC, and positively correlated with CAT score. The area under receiver operating characteristic curve of SAA was largest (0.931). The cutoff values for SAA, CRP, PCT and Fbg were 18.68 mg/L, 14.70 mg/L, 0.39 µg/L, 3.91 g/L, 0.46 µg/L, 24.17 µg/L, 7.18 mg/L, and 83.19 ng/L, respectively. CONCLUSIONS: Serum levels of SAA, CRP, PCT, Fbg, IL-8, IL-6, TNF-α, and IP-10 in AECOPD patients were elevated, which may undermine pulmonary functions. SAA can be used as an effective index for AECOPD diagnosis and treatment.


Asunto(s)
Proteína C-Reactiva/análisis , Enfermedad Pulmonar Obstructiva Crónica/etiología , Proteína Amiloide A Sérica/análisis , Adulto , Anciano , Biomarcadores/sangre , Estudios de Casos y Controles , Quimiocina CXCL10/sangre , Femenino , Humanos , Interleucina-6/sangre , Interleucina-8/sangre , Masculino , Persona de Mediana Edad , Polipéptido alfa Relacionado con Calcitonina/sangre , Pruebas de Función Respiratoria , Factor de Necrosis Tumoral alfa/sangre
3.
Int J Biol Macromol ; 188: 460-472, 2021 Oct 01.
Artículo en Inglés | MEDLINE | ID: mdl-34391784

RESUMEN

This study aimed to characterize the full-length cDNA of thioredoxin-interacting protein (TXNIP) from Megalobrama amblycephala, and investigate its roles in high glucose (HC)-induced inflammatory response. The cDNA obtained covered 2706-bp with an open reading frame of 1203-bp encoding 400 amino acids, compared to Cyprinus carpio, it showed 89.96% homology. The highest expression of txnip was observed in head kidney followed by spleen and liver. After a 12-week feeding trial, high-carbohydrate diet remarkably increased txnip expression in liver and white muscle. Glucose administration resulted in a remarkably increased liver txnip expression, which peaked at 1 h. Thereafter, the expression decreased remarkably to the basal value at 12 h. However, insulin injection resulted in a significant decrease in txnip expression with minimum values attained at 2 h. Subsequently, it gradually increased to the normal values. Moreover, in the in-vitro study, over-expression of txnip along with remarkably increased il-1ß and il-6 expression in hepatocytes, and its knockdown led to remarkably reduced il-1ß expression. Furthermore, metformin treatment remarkably increased the cell viability and trx expression of hepatocytes under high glucose, while the opposite was true for ROS levels, LDH activity, the ALT/AST ratio, Txnip protein content and the transcriptions of txnip, tnfα and il-1ß.


Asunto(s)
Proteínas Portadoras/genética , Cipriniformes/genética , Hígado/metabolismo , Tiorredoxinas/genética , Animales , Proteínas Portadoras/química , ADN Complementario/genética , Glucosa/efectos adversos , Hepatocitos/metabolismo , Humanos , Inflamación/genética , Inflamación/metabolismo , Insulina/genética , Interleucina-6/genética , Hígado/efectos de los fármacos , Tiorredoxinas/metabolismo
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