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Drug: Insulin

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Total 16 results found since Jan 2013.

Role of selenoprotein P expression in the function of pancreatic β cells: Prevention of ferroptosis-like cell death and stress-induced nascent granule degradation
Free Radic Biol Med. 2022 Mar 19:S0891-5849(22)00104-6. doi: 10.1016/j.freeradbiomed.2022.03.009. Online ahead of print.ABSTRACTSelenoprotein P (SELENOP) is a major selenium (Se)-containing protein (selenoprotein) in human plasma that is mainly synthesized in the liver. SELENOP transports Se to the cells, while SELENOP synthesized in peripheral tissues is incorporated in a paracrine/autocrine manner to maintain the levels of cellular selenoproteins, called the SELENOP cycle. Pancreatic β cells, responsible for the synthesis and secretion of insulin, are known to express SELENOP. Here, using MIN6 cells as a mouse model for...
Source: Free Radical Biology and Medicine - March 23, 2022 Category: Biology Authors: Nanako Kitabayashi Shohei Nakao Yuichiro Mita Kotoko Arisawa Takayuki Hoshi Takashi Toyama Kiyo-Aki Ishii Toshinari Takamura Noriko Noguchi Yoshiro Saito Source Type: research

NLRP3 inflammasome mediate palmitate-induced endothelial dysfunction
This study aimed to investigate the role of NLRP3 (NOD-like receptor pyrin domain containing-3) inflammasome in FFA induced endothelial dysfunction.Main methodsHUVECs were transfected with NLRP3 siRNA and then stimulated with LPS and palmitate. C57 BL/6J mice transfected with NLRP3 Lenti-Virus were fed with a high-fat diet (HFD). The levels of NLRP3 inflammasome, AMPKα (AMP-activated protein kinase), endothelial nitric oxide synthase (eNOS) and the activity of the insulin signal pathway, in endothelial cells were determined via Western blotting. Endothelial function was determined by measuring the level of endothelium-dep...
Source: Life Sciences - November 7, 2019 Category: Biology Source Type: research

FoxO6-mediated IL-1β induces hepatic insulin resistance and age-related inflammation via the TF/PAR2 pathway in aging and diabetic mice
Publication date: Available online 3 April 2019Source: Redox BiologyAuthor(s): Dae Hyun Kim, Bonggi Lee, Jaewon Lee, Mi Eun Kim, Jun Sik Lee, Jae Heun Chung, Byung Pal Yu, H. Henry Dong, Hae Young ChungAbstractFoxO has been proposed to play a role in the promotion of insulin resistance, and inflammation. FoxO is a pro-inflammatory transcription factor that is a key mediator of generation of inflammatory cytokines such as IL-1β in the liver. However, the detailed association of FoxO6 with insulin resistance and age-related inflammation has not been fully documented. Here, we showed that FoxO6 was elevated in the livers of ...
Source: Redox Biology - April 4, 2019 Category: Biology Source Type: research

High circulatory leptin mediated NOX-2-peroxynitrite-miR21 axis activate mesangial cells and promotes renal inflammatory pathology in nonalcoholic fatty liver disease
Publication date: July 2018Source: Redox Biology, Volume 17Author(s): Firas Alhasson, Ratanesh Kumar Seth, Sutapa Sarkar, Diana A. Kimono, Muayad S. Albadrani, Diptadip Dattaroy, Varun Chandrashekaran, Geoffrey I. Scott, Samir Raychoudhury, Mitzi Nagarkatti, Prakash Nagarkatti, Anna Mae Diehl, Saurabh ChatterjeeAbstractHigh circulatory insulin and leptin followed by underlying inflammation are often ascribed to the ectopic manifestations in non-alcoholic fatty liver disease (NAFLD) but the exact molecular pathways remain unclear. We have shown previously that CYP2E1-mediated oxidative stress and circulating leptin in NAFLD...
Source: Redox Biology - July 11, 2018 Category: Biology Source Type: research

SOCS2 exacerbates myocardial injury induced by ischemia/reperfusion in diabetic mice and H9c2 cells through inhibiting the JAK-STAT-IGF-1 pathway
This study aimed to investigate potential candidates and molecular mechanisms of myocardial ischemia/reperfusion (I/R) injury (MIRI) in type 2 diabetes mellitus. Main methods Type 2 diabetic and myocardial I/R mouse models were established with a high fat-diet (HFD) for 24weeks and subjecting to global ischemia/reperfusion for 1h/3h, respectively. Microarray analysis was applied to screen differentially expressed genes (DEGs) in the hearts of these mice. Moreover, H9c2 cells were treated with high glucose (HG) and/or hypoxia and reoxygenation (H/R). Subsequently, the expression of suppressor of cytokine signaling 2 (SOCS2)...
Source: Life Sciences - September 8, 2017 Category: Biology Source Type: research

Insulin receptor substrate-1 time-dependently regulates bone formation by controlling collagen I{alpha}2 expression via miR-342 Research
Insulin promotes bone formation via a well-studied canonical signaling pathway. An adapter in this pathway, insulin-receptor substrate (IRS)-1, has been implicated in the diabetic osteopathy provoked by impaired insulin signaling. To further investigate IRS-1’s role in the bone metabolism, we generated Irs-1-deficient Irs-1smla/smla mice. These null mice developed a spontaneous mutation that led to an increase in trabecular thickness (Tb.Th) in 12-mo-old, but not in 2-mo-old mice. Analyses of the bone marrow stromal cells (BMSCs) from these mice revealed their differential expression of osteogenesis-related genes and...
Source: FASEB Journal - November 29, 2016 Category: Biology Authors: Guo, Y., Tang, C.-Y., Man, X.-F., Tang, H.-N., Tang, J., Wang, F., Zhou, C.-L., Tan, S.-W., Feng, Y.-Z., Zhou, H.-D. Tags: Research Source Type: research

Effects of IGF-1 on neural differentiation of human umbilical cord derived mesenchymal stem cells
This study indicated that IGF-1 could improve neural differentiation of human UC-MSCs and provided a novel strategy to enhance astrocyte differentiation of NPCs from UC-MSCs.
Source: Life Sciences - March 3, 2016 Category: Biology Source Type: research

Beyond the brain: disrupted in schizophrenia 1 regulates pancreatic {beta}-cell function via glycogen synthase kinase-3{beta} Research Communication
Individuals with schizophrenia and their first-degree relatives have higher rates of type 2 diabetes (T2D) than the general population (18–30 vs. 1.2–6.3%), independent of body mass index and antipsychotic medication, suggesting shared genetic components may contribute to both diseases. The cause of this association remains unknown. Mutations in disrupted in schizophrenia 1 (DISC1) increase the risk of developing psychiatric disorders [logarithm (base 10) of odds = 7.1]. Here, we identified DISC1 as a major player controlling pancreatic β-cell proliferation and insulin secretion via regulation of glycogen ...
Source: FASEB Journal - February 1, 2016 Category: Biology Authors: Jurczyk, A., Nowosielska, A., Przewozniak, N., Aryee, K.-E., DiIorio, P., Blodgett, D., Yang, C., Campbell-Thompson, M., Atkinson, M., Shultz, L., Rittenhouse, A., Harlan, D., Greiner, D., Bortell, R. Tags: Research Communication Source Type: research

Analysis of the Role of Insulin Signaling in Bone Turnover Induced by Fluoride.
In conclusion, insulin played the important role in bone lesion induced by excessive amount of fluoride through mediating InR receptor signaling, and IGF1 signaling probably exerted action on bone turnover caused by overdose of fluoride. PMID: 26521058 [PubMed - as supplied by publisher]
Source: Biological Trace Element Research - October 31, 2015 Category: Biology Authors: Liu Q, Liu H, Yu X, Wang Y, Yang C, Xu H Tags: Biol Trace Elem Res Source Type: research

Activated Kupffer cells inhibit insulin sensitivity in obese mice Research Communication
Obesity promotes insulin resistance associated with liver inflammation, elevated glucose production, and type 2 diabetes. Although insulin resistance is attenuated in genetic mouse models that suppress systemic inflammation, it is not clear whether local resident macrophages in liver, denoted Kupffer cells (KCs), directly contribute to this syndrome. We addressed this question by selectively silencing the expression of the master regulator of inflammation, NF-B, in KCs in obese mice. We used glucan-encapsulated small interfering RNA particles (GeRPs) that selectively silence gene expression in macrophages in vivo. Followin...
Source: FASEB Journal - June 30, 2015 Category: Biology Authors: Tencerova, M., Aouadi, M., Vangala, P., Nicoloro, S. M., Yawe, J. C., Cohen, J. L., Shen, Y., Garcia-Menendez, L., Pedersen, D. J., Gallagher-Dorval, K., Perugini, R. A., Gupta, O. T., Czech, M. P. Tags: Research Communication Source Type: research

Adiponectin deletion impairs insulin signaling in insulin-sensitive but not insulin-resistant 3T3-L1 adipocytes
This study investigated regulatory effects of adiponectin on glucose transport and insulin signaling in insulin-sensitive or insulin-resistant 3T3-L1 adipocytes. Main methods 3T3-L1 fibroblasts were transfected with non-target or adiponectin (ADN) siRNA and differentiated. Chronic treatment with insulin (24 h, 100 nM) was employed to induce insulin resistance in differentiated adipocytes. Insulin-stimulated glucose transport was measured and protein and mRNA levels were assessed by Western blot and RT-PCR. Key findings Prolonged incubation with insulin significantly reduced insulin-stimulated glucose uptake, suggesting t...
Source: Life Sciences - May 7, 2015 Category: Biology Source Type: research

Dimerumic acid attenuates receptor for advanced glycation endproducts signal to inhibit inflammation and diabetes mediated by Nrf2 activation and promotes methylglyoxal metabolism into d-lactic acid.
This study was designed to evaluate the effects of dimerumic acid (DMA) on receptor for advanced glycation endproducts (RAGE) signal activation and THP-1 monocyte inflammation treated with S100b, a specific ligand of RAGE. We found that DMA inhibited inflammatory cytokine production via upregulation of nuclear factor-erythroid 2-related factor 2 (Nrf2) and alleviated oxidative stress through attenuation of p47phox translocation to the membrane of S100b-treated THP-1 monocytes. We found that DMA activated Nrf2 mediated by the p38 kinase pathway in THP-1 monocytes. However, anti-inflammatory activity of DMA was attenuated by...
Source: Free Radical Biology and Medicine - May 23, 2013 Category: Biology Authors: Lee BH, Hsu WH, Hsu YW, Pan TM Tags: Free Radic Biol Med Source Type: research