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Base de datos :	IBECS
Búsqueda :	"1138-7548" [ISSN]
Referencias encontradas :	970 [refinar]
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Id:	-580
Autor:	Xiang, Mengqi; Yuan, Xinmeng; Zhang, Nianyun; Zhang, Liumei; Liu, Yuting; Liu, Jingjing; Gao, Yaran; Xu, Ye; Sun, Wen; Tang, Qiang.
Título:	Effects of exercise, metformin, and combination treatments on type 2 diabetic mellitus-induced muscle atrophy in db/db mice: Crosstalk between autophagy and the proteasome
Fuente:	J. physiol. biochem;80(1):235-247, Feb. 2024. ilus, graf.
Idioma:	en.
doi:	10.1007/s13105-023-01001-y.
Resumen:	Both exercise and metformin are common effective clinical treatments of type 2 diabetic mellitus. This study investigated the functional role of exercise, metformin, and combination treatment on type 2 diabetic mellitusûinduced muscle atrophy. In this experiment, a total of 10 BKS mice were set as the control group. A total of 40 BKS-db/db mice were randomly divided into the control group (db/db); the exercise intervention group (db/db + Ex), which ran on a treadmill at 7û12 m/min, 30û40 min/day, 5 days/week; the metformin administration group (db/db + Met), which was administered 300 mg/kg of metformin solution by gavage daily; and the exercise combined with metformin administration group (db/db + Ex + Met). After 8 weeks of intervention, their tibialis anterior muscles were removed. The levels of insulin signaling pathway proteins, ubiquitin proteasome, and autophagic lysosomeûassociated proteins were detected using western blot, the expression of MuRF1 and Atrogin-1 was detected using immunohistochemical staining, and the degradation of autophagosomes was detected using double-labeled immunofluorescence. The db/db mice exhibited reduced insulin sensitivity and inhibition of the autophagicûlysosome system, the ubiquitinûproteasome system was activated, and protein degradation was exacerbated, leading to skeletal muscle atrophy. Exercise and metformin and their combined interventions can increase insulin sensitivity, whereas exercise alone showed more effective in inhibiting the ubiquitinûproteasome system, improving autophagy levels, and alleviating skeletal muscle atrophy. Compared with metformin, exercise demonstrated superior improvement of muscle atrophy by promoting the synthesis and degradation of autophagy through the AMPK/ULK1 pathway. However, the combination treatment exhibits no synergistic effect on muscle atrophy. (AU)
Descriptores:	diabetes mellitus tipo II/complicaciones atrofia muscular ejercicio físico metformina autofagia inhibidores del proteasoma
Límites:	animales ratones
Responsable:	ES15.1 - BNCS

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Id:	-579
Autor:	Guo, Liang; Wu, Di; Shen, Jianfen; Gao, Yuan.
Título:	ERG mediates the inhibition of NK cell cytotoxicity through the HLX/STAT4/Perforin signaling pathway, thereby promoting the progression of myocardial infarction
Fuente:	J. physiol. biochem;80(1):219-233, Feb. 2024. ilus, graf.
Idioma:	en.
doi:	10.1007/s13105-023-00999-5.
Resumen:	This study aimed to investigate the role of ERG in the HLX/STAT4/Perforin signaling axis, impacting natural killer (NK) cell cytotoxicity and myocardial infarction (MI) progression. NK cell cytotoxicity was assessed via co-culture and 51Cr release assays. Datasets GSE34198 and GSE97320 identified common differentially expressed genes in MI. NK cell gene expression was analyzed in MI patients and healthy individuals using qRT-PCR and Western blotting. ERG's regulation of HLX and STAT4's regulation of perforin were studied through computational tools (MEM) and ChIP experiments. HLX's influence on STAT4 was explored with the MG132 proteasome inhibitor. Findings were validated in a mouse MI model. ERG, a commonly upregulated gene, was identified in NK cells from MI patients and mice. ERG upregulated HLX, leading to STAT4 proteasomal degradation and reduced Perforin expression. Consequently, NK cell cytotoxicity decreased, promoting MI progression. ERG mediates the HLX/STAT4/Perforin axis to inhibit NK cell cytotoxicity, fostering MI progression. These results provide vital insights into MI's molecular mechanisms. (AU)
Descriptores:	oncogenes células asesinas naturales factor de transcripción STAT4 perforina infarto de miocardio
Límites:	seres humanos animales ratones
Responsable:	ES15.1 - BNCS

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Id:	-578
Autor:	Jagannath, Sanjana; Mallanna, Smitha Honnalagere; Nandini, C. D.
Título:	Diet-inducing hypercholesterolemia show decreased O-GlcNAcylation of liver proteins through modulation of AMPK
Fuente:	J. physiol. biochem;80(1):205-218, Feb. 2024. ilus, graf.
Idioma:	en.
doi:	10.1007/s13105-023-00997-7.
Resumen:	O-GlcNAcylation, a nutritionally driven, post-translational modification of proteins, is gaining importance because of its health implications. Changes in O-GlcNAcylation are observed in various disease conditions. Changes in O-GlcNAcylation by diet that causes hypercholesterolemia are not critically looked into in the liver. To address it, both in vitro and in vivo approaches were employed. Hypercholesterolemia was induced individually by feeding cholesterol (H)/high-fat (HF) diet. Global O-GlcNAcylation levels and modulation of AMPK activation in both preventive and curative approaches were looked into. Diet-induced hypercholesterolemia resulted in decreased O-GlcNAcylation of liver proteins which was associated with decreased O-linked N-acetylglucosaminyltransferase (OGT) and Glutamine fructose-6-phosphate amidotransferase-1 (GFAT1). Activation of AMPK by metformin in preventive mode restored the O-GlcNAcylation levels; however, metformin treatment of HepG2 cells in curative mode restored O-GlcNAcylation levels in HF but failed to in H condition (at 24 h). Further, maternal faulty diet resulted in decreased O-GlcNAcylation in pup liver despite feeding normal diet till adulthood. A faulty diet modulates global O-GlcNAcylation of liver proteins which is accompanied by decreased AMPK activation which could exacerbate metabolic syndromes through fat accumulation in the liver. (AU)
Descriptores:	hipercolesterolemia enfermedades metabólicas vías biosintéticas hexosaminas CINASAS DE LA PROTEINA-CINASA ACTIVADA POR EL AMP
Responsable:	ES15.1 - BNCS

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Id:	-576
Autor:	Shao, Zifei; Xu, Jinghao; Zhou, Yuxi; Wang, Yujing; Li, Yiyang; Zhao, Jianping; Li, Kun.
Título:	Exosomes derived from adipose tissues accelerate fibroblasts and keratinocytes proliferation and cutaneous wound healing via miR-92a/Hippo-YAP axis
Fuente:	J. physiol. biochem;80(1):189-204, Feb. 2024. ilus, graf.
Idioma:	en.
doi:	10.1007/s13105-023-00996-8.
Resumen:	Delayed wound healing is an urgent clinical issue. Cellular communication involving exosome-borne cargo such as miRNA is a critical mechanism involved in wound healing. This study isolated and identified human adipose tissue-derived exosomes (Exo-ATs). The specific effects of Exo-ATs on keratinocytes and fibroblasts were examined. Enriched miRNAs in Exo-ATs were analyzed, and miR-92a-3p was selected. The transfer of Exo-ATs-derived miR-92a-3p to keratinocytes and fibroblasts was verified. miR-92a-3p binding to LATS2 was examined and the dynamic effects of the miR-92a-3p/LATS2 axis were investigated. In a dorsal skin wound model, the in vivo effects of Exo-ATs on wound healing were examined. Exo-AT incubation increased keratinocytes and fibroblast proliferation, migration, and extracellular matrix (ECM) accumulation. miR-92a-3p, enriched in Exo-ATs, could be transferred to keratinocytes and fibroblasts, resulting in enhanced proliferation, migration, and ECM accumulation. Large tumor suppressor kinase 2 (LATS2) was a direct target of miR-92a-3p. miR-92a-3p inhibitor effects on keratinocytes and fibroblasts could be partially reversed by LATS2 knockdown. In a dorsal skin wound model, Exo-ATs accelerated wound healing through enhanced cell proliferation, collagen deposition, re-epithelialization, and YAP/TAZ activation. In conclusion, Exo-ATs improve skin wound healing by promoting keratinocyte and fibroblast migration and proliferation and collagen production by fibroblast, which could be partially eliminated by miR-92a inhibition through its downstream target LATS2 and the YAP/TAZ signaling. (AU)
Descriptores:	exosomas cicatrización de heridas proliferación celular PROTEINAS DE SENALIZACION YAP PROTEINAS COACTIVADORAS DE LA TRANSCRIPCION CON MOTIVO DE UNION A PDZ
Responsable:	ES15.1 - BNCS

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Id:	-575
Autor:	Zeng, Wen; Cai, Nan; Liu, Jia; Liu, Kunying; Lin, Shuo; Zeng, Longyi.
Título:	Caveolin-1 deficiency alleviates palmitate-induced intracellular lipid accumulation and inflammation in pancreatic β cells
Fuente:	J. physiol. biochem;80(1):175-188, Feb. 2024. ilus, graf.
Idioma:	en.
doi:	10.1007/s13105-023-00995-9.
Resumen:	Lipotoxicity-induced pancreatic β cell damage is a strong predictor of type 2 diabetes mellitus (T2DM). Our previous work showed that Caveolin-1 (Cav-1) depletion decreased β-cell apoptosis and improved β-cell viability. Further microarray analysis indicated significant changes in the expression of genes related to fatty acid metabolism and inflammation. The objective of this study was to explore the role of Cav-1 in intracellular lipid accumulation and inflammation in β cells under lipotoxic conditions. Here, we established a β-cell-specific Cav-1 knockout (β-Cav-1 KO) mouse model and a CAV-1 depleted β cell line (NIT-1). We found that Cav-1 silencing significantly reduced palmitate (PA)-induced intracellular triglyceride (TG) accumulation and decreased proinflammatory factor expression in both the mouse and cell models. Further mechanistic investigation revealed that amelioration of lipid metabolism was achieved through the downregulation of lipogenic markers (SREBP-1c, FAS and ACC) and upregulation of a fatty acid oxidation marker (CPT-1). Meanwhile, decrease of inflammatory cytokines (IL-6, TNF-α, and IL-1β) secretion was found with the involvement of the IKKβ/NF-κB signaling pathways. Our findings suggest that Cav-1 is of considerable importance in regulating lipotoxicity-induced β-cell intracellular lipid accumulation and inflammation. (AU)
Descriptores:	caveolina 1/deficiencia células secretoras de insulina inflamación palmitatos
Responsable:	ES15.1 - BNCS

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Id:	-574
Autor:	Muller, Carlos Henrique de Lemos; Schroeder, Helena Trevisan; Farinha, Juliano Boufleur; Lopez, Pedro; Reischak-Oliveira, Álvaro; Pinto, Ronei Silveira; Bittencourt Júnior, Paulo Ivo Homem de; Krause, Mauricio.
Título:	Effects of resistance training on heat shock response (HSR), HSP70 expression, oxidative stress, inflammation, and metabolism in middle-aged people
Fuente:	J. physiol. biochem;80(1):161-173, Feb. 2024. graf.
Idioma:	en.
doi:	10.1007/s13105-023-00994-w.
Resumen:	Resistance training (RT) can increase the heat shock response (HSR) in the elderly. As middle-aged subjects already suffer physiological declines related to aging, it is hypothesized that RT may increase the HSR in these people. To assess the effects of resistance training on heat shock response, intra and extracellular HSP70, oxidative stress, inflammation, body composition, and metabolism in middle-aged subjects. Sixteen volunteers (40 û 59 years) were allocated to two groups: the trained group (n = 7), which performed 12 weeks of RT; and the physically inactiveùcontrol group (n = 9), which did not perform any type of exercise. The RT program consisted of 9 whole-body exercises (using standard gym equipment) and functional exercises, carried out 3 times/week. Before and after the intervention, body composition, muscle mass, strength, functional capacity, and blood sample measurements (lipid profile, glucose, insulin, oxidative damage, TNF-α, the HSR, HSP70 expression in leukocytes, and HSP72 in plasma) were performed. The HSR analysis demonstrated that this response is maintained at normal levels in middle-aged people and that RT did not cause any improvement. Also, RT increases muscle mass, strength, and functional capacity. Despite no additional changes of RT on the antioxidant defenses (catalase, glutathione peroxidase, and reductase) or inflammation, lipid peroxidation was diminished by RT (group x time interaction, p = 0.009), indicating that other antioxidant defenses may be improved after RT. HSR is preserved in middle-aged subjects without metabolic complications. In addition, RT reduces lipid peroxidation and can retard muscle mass and strength loss related to the aging process. (AU)
Descriptores:	respuesta al choque por calor entrenamiento de fuerza proteínas de choque térmico HSP70 estrés oxidativo inflamación metabolismo
Límites:	seres humanos persona de mediana edad
Responsable:	ES15.1 - BNCS

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	Texto Completo

Id:	-573
Autor:	Becerril, Sara; Cienfuegos, Javier A; Rodríguez, Amaia; Catalán, Victoria; Ramírez, Beatriz; Valentí, Víctor; Moncada, Rafael; Unamuno, Xabier; Gómez-Ambrosi, Javier; Frühbeck, Gema.
Título:	Single anastomosis duodeno-ileal bypass with sleeve gastrectomy generates sustained improvement of glycemic control compared with sleeve gastrectomy in the diet-induced obese rat model
Fuente:	J. physiol. biochem;80(1):149-160, Feb. 2024. ilus, graf.
Idioma:	en.
doi:	10.1007/s13105-023-00993-x.
Resumen:	Bariatric surgery has become a recognized and effective procedure for treating obesity and type 2 diabetes (T2D). Our objective was to directly compare the caloric intake-independent effects of sleeve gastrectomy (SG) and single anastomosis duodenoileal bypass with SG (SADI-S) on glucose tolerance in rats with diet-induced obesity (DIO) and to elucidate the differences between bariatric surgery and caloric restriction. A total of 120 adult male Wistar rats with DIO and insulin resistance were randomly assigned to surgical (sham operation, SG, and SADI-S) and dietary (pair-feeding the amount of food eaten by animals undergoing the SG or SADI-S surgeries) interventions. Body weight and food intake were weekly monitored, and 6 weeks after interventions, fasting plasma glucose, oral glucose and insulin tolerance tests, plasma insulin, adiponectin, GIP, GLP-1, and ghrelin levels were determined. The body weight of SADI-S rats was significantly (p < 0.001) lower as compared to the sham-operated, SG, and pair-fed groups. Furthermore, SADI-S rats exhibited decreased whole body fat mass (p < 0.001), lower food efficiency rates (p < 0.001), and increased insulin sensitivity, as well as improved glucose and lipid metabolism compared to that of the SG and pair-fed rats. SADI-S was more effective than SG, or caloric restriction, in improving glycemic control and metabolic profile, with a higher remission of insulin resistance as well as long-term weight loss. (AU)
Descriptores:	obesidad gastrectomía anastomosis quirúrgica CONTROL GLUCEMICO
Límites:	animales ratas
Responsable:	BNCS

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Id:	-572
Autor:	Li, Rui; Wang, Guiping; Liu, Ruitong; Luo, Lan; Zhang, Ying; Wan, Zhongxiao.
Título:	Quercetin improved hepatic circadian rhythm dysfunction in middle-aged mice fed with vitamin D-deficient diet
Fuente:	J. physiol. biochem;80(1):137-147, Feb. 2024. graf.
Idioma:	en.
doi:	10.1007/s13105-023-00990-0.
Resumen:	We aimed to determine whether quercetin is capable of improving circadian rhythm and metabolism disorder under vitamin D-deficient condition. Middle-aged mice were randomly divided into four groups, namely, control (CON), vitamin D-deficient diet (VDD), quercetin (Q), and quercetin intervention in vitamin D-deficient diet (VDQ), with a total of 12 weeks' intervention. Mice were sacrificed at zeitgeber time1 (ZT1) and ZT13 time points. At ZT1, circadian locomotor output cycle kaput (CLOCK) protein expression from VDD, Q, and VDQ groups; CRY1 from Q group; and CRY2 from VDD group were significantly lower compared to CON group. The mRNA expression of Sirt1, Bmal1, Clock, Cry1, and Cry2 in VDQ groups, also Bmal1, Clock, and Cry1 from Q group, were significantly decreased compared to CON group. At ZT13, compared to CON group, fasting insulin and homeostasis model assessment-insulin resistance (HOMA-IR) were higher in VDD group; BMAL1 was significantly increased, while CLOCK and CRY1 protein were significantly decreased from VDD group; CLOCK protein from VDQ group was significantly higher compared to CON, VDD, and Q groups, and also, BMAL1 protein expression from VDQ group was elevated compared to CON group. The mRNA expression of Bmal1, Clock, Per2, Cry1, and Cry2 in VDQ groups were significantly increased compared to CON groups. The mRNA expression of Bmal1 from VDQ group was decreased compared to both VDD and Q group. In conclusion, vitamin D-deficient diet resulted in a disordered liver circadian rhythm, and quercetin improved the hepatic circadian desynchronization. Quercetin supplementation might be effective for balancing circadian rhythm under vitamin D-deficient condition. (AU)
Descriptores:	deficiencia de vitamina D quercetina/farmacología ritmo circadiano/efectos de los fármacos resistencia a la insulina
Límites:	animales ratones
Responsable:	ES15.1 - BNCS

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Id:	-571
Autor:	Gu, Qiang; Xiao, Ying-Bin; Wang, Yong.
Título:	Silencing suppressor of cytokine signaling 3 induces apoptosis and activates the p-STAT3/NF-κ B pathway in hypoxic cultivated H9c2 cells
Fuente:	J. physiol. biochem;80(1):127-136, Feb. 2024. ilus, graf.
Idioma:	en.
doi:	10.1007/s13105-023-00989-7.
Resumen:	Suppressor of cytokine signaling 3 (SOCS3) plays a significant role in the process of myocardial adaptation to chronic hypoxia. SOCS3 finely regulates cell signaling cross-talk that occurs between NF-κB and STAT3 during the compensatory protective response. However, the role and mechanism of SOCS3 in hypoxic cardiomyocytes are not fully understood. In the study, we investigated the effect of SOCS3 on the p65 and STAT3 signaling pathways and further examined the potential molecular mechanism involved in regulating apoptosis. Our data showed that SOCS3 silencing could upregulate Ac-p65, p-p65, and p-STAT3 expression in nuclear extracts of H9c2 cells that received hypoxic treatment for 24, 48, and 72 h. SOCS3 silencing also remarkably increased the DNA-binding activity of the p65 motif in hypoxic cultivated H9c2 cells. We also found that SOCS3 knockdown increased cleaved-caspase-3, Bax, and PUMA expression and decreased cleaved PARP and Bcl-2 in expression in hypoxic H9c2 cells. Silencing of SOCS3 caused an increase in LDH leakage from injured cardiomyocytes and reduced cell viability under conditions of hypoxic stress. Furthermore, SOCS3 silencing enhanced the apoptosis of H9c2 cells at 72 h of hypoxia. These findings suggest that knockdown of SOCS3 leads to excessive activation of the NF-κB pathway, which, in turn, might promote apoptosis under conditions of chronic hypoxia. (AU)
Descriptores:	proteína 3 supresora de la señalización de citocinas apoptosis factor de transcripción STAT3 hipoxia miocardio
Responsable:	ES15.1 - BNCS

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Id:	-570
Autor:	Wei, Pengfei; Li, Lixuan; Ran, Chenqiu; Jin, Mingyue; Zhao, Huijuan; Yang, Kelaier; Wang, Yu; He, Huaqiu; Jia, Mengyang; Pan, Hongyan.
Título:	High fat diet-induced downregulation of TRPV2 mediates hepatic steatosis via p21 signalling
Fuente:	J. physiol. biochem;80(1):113-126, Feb. 2024. ilus, graf.
Idioma:	en.
doi:	10.1007/s13105-023-00988-8.
Resumen:	The global prevalence and incidence of non-alcoholic fatty liver disease (NAFLD) are exhibiting an increasing trend. NAFLD is characterized by a significant accumulation of lipids, though its underlying mechanism is still unknown. Here we report that high-fat diet (HFD) feeding induced hepatic steatosis in mice, which was accompanied by a reduction in the expression and function of hepatic TRPV2. Moreover, conditional knockout of TRPV2 in hepatocytes exacerbated HFD-induced hepatic steatosis. In an in vitro model of NAFLD, TRPV2 regulated lipid accumulation in HepG2 cells, and TRPV2 activation inhibited the expression of the cellular senescence markers p21 and p16, all of which were mediated by AMPK phosphorylation. Finally, we found that administration of probenecid, a TRPV2 agonist, impaired HFD-induced hepatic steatosis and suppressed HFD-induced elevation in p21 and p16. Collectively, our findings imply that hepatic TRPV2 protects against the accumulation of lipids by modulating p21 signalling. (AU)
Descriptores:	hígado graso esteatosis hepática no alcohólica alimentación rica en grasa
Responsable:	ES15.1 - BNCS

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