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Pesquisa : D12.644.360.024.301 [Categoria DeCS]
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  1 / 3793 MEDLINE  
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[PMID]:29364977
[Au] Autor:Ono K; Igata M; Kondo T; Kitano S; Takaki Y; Hanatani S; Sakaguchi M; Goto R; Senokuchi T; Kawashima J; Furukawa N; Motoshima H; Araki E
[Ad] Endereço:Department of Metabolic Medicine, Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan.
[Ti] Título:Identification of microRNA that represses IRS-1 expression in liver.
[So] Source:PLoS One;13(1):e0191553, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:MicroRNAs (miRNAs) are short, non-coding RNAs that post-transcriptionally regulate gene expression and have been shown to participate in almost every cellular process. Several miRNAs have recently been implicated in glucose metabolism, but the roles of miRNAs in insulin-resistant conditions, such as obesity or type 2 diabetes, are largely unknown. Herein, we focused on miR-222, the expression of which was increased in the livers of high fat/high sucrose diet-fed mice injected with gold thioglucose (G+HFHSD). Overexpression of miR-222 in primary mouse hepatocytes attenuated Akt phosphorylation induced by insulin, indicating that miR-222 negatively regulates insulin signaling. As per in silico analysis, miR-222 potentially binds to the 3' untranslated region (3' UTR) of the IRS-1 gene, a key insulin signaling molecule. In fact, IRS-1 protein expression was decreased in the livers of G+HFHSD-fed mice. We further confirmed a direct interaction between miR-222 and the 3' UTR of IRS-1 via luciferase assays. Our findings suggest that up-regulation of miR-222 followed by reduction in IRS-1 expression may be a viable mechanism of insulin resistance in the liver.
[Mh] Termos MeSH primário: Proteínas Substratos do Receptor de Insulina/metabolismo
Fígado/metabolismo
MicroRNAs/metabolismo
[Mh] Termos MeSH secundário: Regiões 3' não Traduzidas
Animais
Gluconeogênese/genética
Insulina/metabolismo
Proteínas Substratos do Receptor de Insulina/genética
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Fosforilação
Proteínas Proto-Oncogênicas c-akt/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (3' Untranslated Regions); 0 (Insulin); 0 (Insulin Receptor Substrate Proteins); 0 (Irs1 protein, mouse); 0 (MIRN222 microRNA, mouse); 0 (MicroRNAs); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180125
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191553


  2 / 3793 MEDLINE  
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[PMID]:28460125
[Au] Autor:Law NC; Donaubauer EM; Zeleznik AJ; Hunzicker-Dunn M
[Ad] Endereço:School of Molecular Biosciences, College of Veterinary Medicine, Washington State University, Pullman, Washington 99164.
[Ti] Título:How Protein Kinase A Activates Canonical Tyrosine Kinase Signaling Pathways To Promote Granulosa Cell Differentiation.
[So] Source:Endocrinology;158(7):2043-2051, 2017 07 01.
[Is] ISSN:1945-7170
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Protein kinase A (PKA) has recently been shown to mimic the actions of follicle-stimulating hormone (FSH) by activating signaling pathways that promote granulosa cell (GC) differentiation, such as phosphatidylinositol 3-kinase (PI3K) and mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK). We sought to elucidate the mechanism by which PKA, a Ser/Thr kinase, intersected the PI3K/AKT and MAPK/ERK pathways that are canonically activated by receptor tyrosine kinases (RTKs). Our results show that for both of these pathways, the RTK is active in the absence of FSH yet signaling down the pathways to commence transcriptional responses requires FSH-stimulated PKA activation. For both pathways, PKA initiates signaling by regulating the activity of a protein phosphatase (PP). For the PI3K/AKT pathway, PKA activates the Ser/Thr PP1 complexed with the insulinlike growth factor 1 receptor (IGF-1R) and insulin receptor substrate 1 (IRS1) to dephosphorylate Ser residues on IRS1, authorizing phosphorylation of IRS1 by the IGF-1R to activate PI3K. Treatment of GCs with FSH and exogenous IGF-1 initiates synergistic IRS1 Tyr phosphorylation and resulting gene activation. The mechanism by which PKA activates PI3K is conserved in preovulatory GCs, MCF7 breast cancer cells, and FRTL thyroid cells. For the MAPK/ERK pathway, PKA promotes inactivation of the MAPK phosphatase (MKP) dual specificity phosphatase (DUSP) MKP3/DUSP6 to permit MEK-phosphorylated ERK to accumulate downstream of the epidermal growth factor receptor. Thus, for the two central signaling pathways that regulate gene expression in GCs, FSH via PKA intersects canonical RTK-regulated signaling by modulating the activity of PPs.
[Mh] Termos MeSH primário: Diferenciação Celular
Proteínas Quinases Dependentes de AMP Cíclico/fisiologia
Células da Granulosa/fisiologia
Proteínas Tirosina Quinases/metabolismo
[Mh] Termos MeSH secundário: Animais
Diferenciação Celular/genética
Células Cultivadas
Proteínas Quinases Dependentes de AMP Cíclico/genética
Proteínas Quinases Dependentes de AMP Cíclico/metabolismo
Ativação Enzimática
Feminino
Seres Humanos
Proteínas Substratos do Receptor de Insulina/metabolismo
Sistema de Sinalização das MAP Quinases/genética
Células MCF-7
Fosforilação
Ratos
Transdução de Sinais/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (IRS1 protein, human); 0 (Insulin Receptor Substrate Proteins); EC 2.7.10.1 (Protein-Tyrosine Kinases); EC 2.7.11.11 (Cyclic AMP-Dependent Protein Kinases)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180203
[Lr] Data última revisão:
180203
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE
[do] DOI:10.1210/en.2017-00163


  3 / 3793 MEDLINE  
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[PMID]:29240812
[Au] Autor:Liu S; Li X; Wu Y; Duan R; Zhang J; Du F; Zhang Q; Li Y; Li N
[Ad] Endereço:Department of Endocrinology, Shanxi DAYI Hospital, Shanxi Medical University, Taiyuan, China.
[Ti] Título:Effects of vaspin on pancreatic ß cell secretion via PI3K/Akt and NF-κB signaling pathways.
[So] Source:PLoS One;12(12):e0189722, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Vaspin (visceral adipose tissue-derived serine protease inhibitor) is a recently discovered adipokine that has been implicated in diabetes mellitus and other metabolic disorders. However, the effects of vaspin on pancreatic ß cell function and related mechanisms are not fully understood. Thus, the present study was performed to investigate the effects of vaspin on pancreatic ß cell function and the potential underlying mechanisms. Both in vitro (rat insulinoma cells, INS-1) and in vivo (high fat diet fed rats) experiments were conducted. The results showed that vaspin significantly increased INS-1 cell secretory function. Potential mechanisms were explored using inhibitors, western blot and real-time PCR techniques. We found that vaspin increased the levels of IRS-2 mRNA and IRS-2 total protein, while decreased the serine phosphorylation level of IRS-2 protein. Moreover, vaspin increased the Akt phosphorylation protein level which was reversed by PI3K inhibitor ly294002. In addition, vaspin increased the phosphorylation levels of mTOR and p70S6K, which was inhibited by rapamycin. Meanwhile, we found that the NF-κB mRNA and protein levels were reduced after vaspin treatment, similar to the effect of NF-κB inhibitor TPCK. Furthermore, vaspin increased the glucose stimulated insulin secretion (GSIS) level, lowered blood glucose level and improved the glucose tolerance and insulin sensitivity of high fat diet fed rats. Hyperglycemic clamp test manifested that vaspin improved islet ß cell function. Together, these findings provide a new understanding of the function of vaspin on pancreatic ß cell and suggest that it may serve as a potential agent for the prevention and treatment of type 2 diabetes.
[Mh] Termos MeSH primário: Ilhotas Pancreáticas/secreção
NF-kappa B/metabolismo
Fosfatidilinositol 3-Quinases/metabolismo
Proteínas Proto-Oncogênicas c-akt/metabolismo
Serpinas/fisiologia
Transdução de Sinais
[Mh] Termos MeSH secundário: Animais
Glicemia/metabolismo
Linhagem Celular Tumoral
Teste de Tolerância a Glucose
Proteínas Substratos do Receptor de Insulina/genética
Proteínas Substratos do Receptor de Insulina/metabolismo
Resistência à Insulina
Ilhotas Pancreáticas/enzimologia
Ilhotas Pancreáticas/metabolismo
Masculino
Fosforilação
RNA Mensageiro/genética
Ratos
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Blood Glucose); 0 (Insulin Receptor Substrate Proteins); 0 (Irs2 protein, rat); 0 (NF-kappa B); 0 (RNA, Messenger); 0 (Serpins); 0 (vaspin protein, rat); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171229
[Lr] Data última revisão:
171229
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171215
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0189722


  4 / 3793 MEDLINE  
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[PMID]:28886131
[Au] Autor:Kawada Y; Asahara SI; Sugiura Y; Sato A; Furubayashi A; Kawamura M; Bartolome A; Terashi-Suzuki E; Takai T; Kanno A; Koyanagi-Kimura M; Matsuda T; Hashimoto N; Kido Y
[Ad] Endereço:Division of Metabolism and Disease, Department of Biophysics, Kobe University Graduate School of Health Sciences, Kobe, Japan.
[Ti] Título:Histone deacetylase regulates insulin signaling via two pathways in pancreatic ß cells.
[So] Source:PLoS One;12(9):e0184435, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Recent studies demonstrated that insulin signaling plays important roles in the regulation of pancreatic ß cell mass, the reduction of which is known to be involved in the development of diabetes. However, the mechanism underlying the alteration of insulin signaling in pancreatic ß cells remains unclear. The involvement of epigenetic control in the onset of diabetes has also been reported. Thus, we analyzed the epigenetic control of insulin receptor substrate 2 (IRS2) expression in the MIN6 mouse insulinoma cell line. We found concomitant IRS2 up-regulation and enhanced insulin signaling in MIN6 cells, which resulted in an increase in cell proliferation. The H3K9 acetylation status of the Irs2 promoter was positively associated with IRS2 expression. Treatment of MIN6 cells with histone deacetylase inhibitors led to increased IRS2 expression, but this occurred in concert with low insulin signaling. We observed increased IRS2 lysine acetylation as a consequence of histone deacetylase inhibition, a modification that was coupled with a decrease in IRS2 tyrosine phosphorylation. These results suggest that insulin signaling in pancreatic ß cells is regulated by histone deacetylases through two novel pathways affecting IRS2: the epigenetic control of IRS2 expression by H3K9 promoter acetylation, and the regulation of IRS2 activity through protein modification. The identification of the histone deacetylase isoform(s) involved in these mechanisms would be a valuable approach for the treatment of type 2 diabetes.
[Mh] Termos MeSH primário: Histona Desacetilases/metabolismo
Células Secretoras de Insulina/metabolismo
Insulina/metabolismo
Transdução de Sinais
[Mh] Termos MeSH secundário: Acetilação
Animais
Linhagem Celular Tumoral
Proliferação Celular
Diabetes Mellitus Tipo 2/genética
Diabetes Mellitus Tipo 2/metabolismo
Modelos Animais de Doenças
Expressão Gênica
Regulação da Expressão Gênica/efeitos dos fármacos
Inibidores de Histona Desacetilases/farmacologia
Histonas/metabolismo
Proteínas Substratos do Receptor de Insulina/genética
Proteínas Substratos do Receptor de Insulina/metabolismo
Camundongos
Camundongos Knockout
Modelos Biológicos
Fosforilação
Regiões Promotoras Genéticas
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Histone Deacetylase Inhibitors); 0 (Histones); 0 (Insulin); 0 (Insulin Receptor Substrate Proteins); EC 3.5.1.98 (Histone Deacetylases)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171018
[Lr] Data última revisão:
171018
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170909
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0184435


  5 / 3793 MEDLINE  
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[PMID]:28859155
[Au] Autor:Yoshitomi H; Tsuru R; Li L; Zhou J; Kudo M; Liu T; Gao M
[Ad] Endereço:School of Pharmaceutical Sciences, Mukogawa Women's University, Hyogo, Japan.
[Ti] Título:Cyclocarya paliurus extract activates insulin signaling via Sirtuin1 in C2C12 myotubes and decreases blood glucose level in mice with impaired insulin secretion.
[So] Source:PLoS One;12(8):e0183988, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Diabetes is caused by the lack of release or action of insulin. Some foods and supplements can compensate for this deficiency; thus, they can aid in the prevention or treatment of diabetes. The aim of this study was to investigate the effects of Cyclocarya paliurus extract (CPE) on insulin signaling and its capacity to correct hyperglycemia in the absence of insulin. To investigate the hypoglycemic effects of CPE, C2C12 cells were exposed to CPE (50 and 100 µg/mL). CPE promoted 2-(N-(7-Nitrobenz-2-oxa-1,3-diazol-4-yl)Amino)-2-Deoxyglucose (2NBDG) uptake into the cells via translocation of glucose transporter 4 (Glut4) to the plasma membrane. In addition, CPE enhanced tyrosine phosphorylation of insulin receptor substrate and activated phosphatidylinositol 3-kinase and protein kinase B (Akt) via sirtuin1 in C2C12 cells. Moreover, we found that oral administration of CPE (1 g/kg) to streptozotocin-induced hyperglycemic mice produced a progressive decrease in plasma glucose levels at 1 h after single dosing. At that point, CPE significantly increased the expression of skeletal muscle membrane Glut4 and enhanced the phosphorylation of Akt. These results suggest that CPE exerts antidiabetic effects similar to those of insulin, and may be an oral therapeutic alternative for the management of diabetes.
[Mh] Termos MeSH primário: Diabetes Mellitus Experimental/tratamento farmacológico
Medicamentos de Ervas Chinesas/farmacologia
Fagaceae/química
Hipoglicemiantes/farmacologia
Insulina/agonistas
Transdução de Sinais/efeitos dos fármacos
Sirtuína 1/genética
[Mh] Termos MeSH secundário: 4-Cloro-7-nitrobenzofurazano/análogos & derivados
4-Cloro-7-nitrobenzofurazano/metabolismo
Animais
Transporte Biológico/efeitos dos fármacos
Linhagem Celular
Desoxiglucose/análogos & derivados
Desoxiglucose/metabolismo
Diabetes Mellitus Experimental/genética
Diabetes Mellitus Experimental/metabolismo
Diabetes Mellitus Experimental/patologia
Medicamentos de Ervas Chinesas/isolamento & purificação
Regulação da Expressão Gênica
Transportador de Glucose Tipo 4/genética
Transportador de Glucose Tipo 4/metabolismo
Hipoglicemiantes/isolamento & purificação
Insulina/metabolismo
Proteínas Substratos do Receptor de Insulina/genética
Proteínas Substratos do Receptor de Insulina/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos ICR
Fibras Musculares Esqueléticas/citologia
Fibras Musculares Esqueléticas/efeitos dos fármacos
Fibras Musculares Esqueléticas/metabolismo
Músculo Esquelético/efeitos dos fármacos
Músculo Esquelético/metabolismo
Fosfatidilinositol 3-Quinase/genética
Fosfatidilinositol 3-Quinase/metabolismo
Fosforilação/efeitos dos fármacos
Transporte Proteico
Proteínas Proto-Oncogênicas c-akt/genética
Proteínas Proto-Oncogênicas c-akt/metabolismo
Sirtuína 1/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Drugs, Chinese Herbal); 0 (Glucose Transporter Type 4); 0 (Hypoglycemic Agents); 0 (Insulin); 0 (Insulin Receptor Substrate Proteins); 0 (Irs1 protein, mouse); 0 (Slc2a4 protein, mouse); 9G2MP84A8W (Deoxyglucose); EC 2.7.1.137 (Phosphatidylinositol 3-Kinase); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); EC 3.5.1.- (Sirt1 protein, mouse); EC 3.5.1.- (Sirtuin 1); EQF2794IRE (4-Chloro-7-nitrobenzofurazan); JE4F4P486R (2-(N-(7-nitrobenz-2-oxa-1,3-diazol-4-yl)amino)-2-deoxyglucose)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170901
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0183988


  6 / 3793 MEDLINE  
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[PMID]:28793771
[Au] Autor:Man S; Ma J; Yao J; Cui J; Wang C; Li Y; Ma L; Lu F
[Ad] Endereço:Tianjin Key Laboratory of Industry Microbiology, Key Laboratory of Industrial Microbiology, Ministry of Education, College of Biotechnology, Tianjin University of Science & Technology , Tianjin 300457, China.
[Ti] Título:Systemic Perturbations of Key Metabolites in Type 2 Diabetic Rats Treated by Polyphenol Extracts from Litchi chinensis Seeds.
[So] Source:J Agric Food Chem;65(35):7698-7704, 2017 Sep 06.
[Is] ISSN:1520-5118
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Our previous research obtained Litchi chinensis Sonn. seeds extract (LSE) which showed hypoglycaemic effects on type 2 diabetes (T2D) rats. In order to understand the detailed pathogenesis of diabetes intervened by LSE, the metabonomics strategy was used. As a result, LSE decreased the insulin resistance index and the levels of glucose in urine through elevating the mRNA level of insulin, while decreasing the expression of glucagon to enhance the function of the pancreas. Meanwhile, LSE regulated the glucose and fatty acid metabolisms via increasing the expression of glucose transporter (Glu) 2, Glu4, insulin receptor (IR), and IR substrate-2 (IRS2). LSE effectively restored the impairment of the IRS2/PI3K/Akt/mTOR insulin signaling in the livers. All in all, LSE played a pivotal role in the treatment of T2D through regulation of broad-spectrum metabolic changes and inhibition of the glycogenesis, proteolysis, and lipogenesis in T2D rats.
[Mh] Termos MeSH primário: Diabetes Mellitus Tipo 2/tratamento farmacológico
Litchi/química
Extratos Vegetais/administração & dosagem
Sementes/química
[Mh] Termos MeSH secundário: Animais
Glicemia/metabolismo
Diabetes Mellitus Tipo 2/genética
Diabetes Mellitus Tipo 2/metabolismo
Transportador de Glucose Tipo 2/genética
Transportador de Glucose Tipo 2/metabolismo
Transportador de Glucose Tipo 4/genética
Transportador de Glucose Tipo 4/metabolismo
Seres Humanos
Insulina/genética
Insulina/metabolismo
Proteínas Substratos do Receptor de Insulina/genética
Proteínas Substratos do Receptor de Insulina/metabolismo
Masculino
Ratos
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Blood Glucose); 0 (Glucose Transporter Type 2); 0 (Glucose Transporter Type 4); 0 (Insulin); 0 (Insulin Receptor Substrate Proteins); 0 (Plant Extracts)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170915
[Lr] Data última revisão:
170915
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170811
[St] Status:MEDLINE
[do] DOI:10.1021/acs.jafc.7b02206


  7 / 3793 MEDLINE  
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[PMID]:28655716
[Au] Autor:Ohlsson C; Hammarstedt A; Vandenput L; Saarinen N; Ryberg H; Windahl SH; Farman HH; Jansson JO; Movérare-Skrtic S; Smith U; Zhang FP; Poutanen M; Hedjazifar S; Sjögren K
[Ad] Endereço:Centre for Bone and Arthritis Research at Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
[Ti] Título:Increased adipose tissue aromatase activity improves insulin sensitivity and reduces adipose tissue inflammation in male mice.
[So] Source:Am J Physiol Endocrinol Metab;313(4):E450-E462, 2017 Oct 01.
[Is] ISSN:1522-1555
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Females are, in general, more insulin sensitive than males. To investigate whether this is a direct effect of sex-steroids (SS) in white adipose tissue (WAT), we developed a male mouse model overexpressing the aromatase enzyme, converting testosterone (T) to estradiol (E ), specifically in WAT (Ap2-arom mice). Adipose tissue E levels were increased while circulating SS levels were unaffected in male Ap2-arom mice. Importantly, male Ap2-arom mice were more insulin sensitive compared with WT mice and exhibited increased serum adiponectin levels and upregulated expression of and in WAT. The expression of markers of macrophages and immune cell infiltration was markedly decreased in WAT of male Ap2-arom mice. The adipogenesis was enhanced in male Ap2-arom mice, supported by elevated expression in WAT and enhanced differentiation of preadipocyte into mature adipocytes. In summary, increased adipose tissue aromatase activity reduces adipose tissue inflammation and improves insulin sensitivity in male mice. We propose that estrogen increases insulin sensitivity via a local effect in WAT on adiponectin expression, adipose tissue inflammation, and adipogenesis.
[Mh] Termos MeSH primário: Tecido Adiposo Branco/metabolismo
Aromatase/genética
Estradiol/metabolismo
Resistência à Insulina/genética
Testosterona/metabolismo
[Mh] Termos MeSH secundário: Adipócitos
Adipogenia/genética
Adiponectina/metabolismo
Tecido Adiposo Branco/imunologia
Animais
Técnicas de Introdução de Genes
Transportador de Glucose Tipo 4/metabolismo
Inflamação
Proteínas Substratos do Receptor de Insulina/metabolismo
Macrófagos/imunologia
Masculino
Camundongos
PPAR gama/metabolismo
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adiponectin); 0 (Adipoq protein, mouse); 0 (Glucose Transporter Type 4); 0 (Insulin Receptor Substrate Proteins); 0 (Irs1 protein, mouse); 0 (PPAR gamma); 0 (Slc2a4 protein, mouse); 3XMK78S47O (Testosterone); 4TI98Z838E (Estradiol); EC 1.14.14.1 (Aromatase)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171108
[Lr] Data última revisão:
171108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170629
[St] Status:MEDLINE
[do] DOI:10.1152/ajpendo.00093.2017


  8 / 3793 MEDLINE  
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[PMID]:28638873
[Au] Autor:Mansour AA; Nassan MA; Saleh OM; Soliman MM
[Ad] Endereço:Medical Biotechnology Department, Faculty of Applied Medical Sciences (Turbah), Taif Univ., KSA.
[Ti] Título:PROTECTIVE EFFECT OF CAMEL MILK AS ANTI-DIABETIC SUPPLEMENT: BIOCHEMICAL, MOLECULAR AND IMMUNOHISTOCHEMICAL STUDY.
[So] Source:Afr J Tradit Complement Altern Med;14(4):108-119, 2017.
[Is] ISSN:2505-0044
[Cp] País de publicação:Nigeria
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Diabetes is a serious disease affects human health. Diabetes in advanced stages is accompanied by general weakness and alteration in fats and carbohydrates metabolism. Recently there are some scientific trends about the usage of camel milk (CM) in the treatment of diabetes and its associated alterations. CM contains vital active particles with insulin like action that cure diabetes and its complications but how these effects occur, still unclear. MATERIALS AND METHODS: Seventy-five adult male rats of the albino type divided into five equal groups. Group 1 served as a negative control (C). Group 2 was supplemented with camel milk (CM). Diabetes was induced in the remaining groups (3, 4 and 5). Group 3 served as positive diabetic control (D). Group 4 served as diabetic and administered metformin (D+MET). Group 5 served as diabetes and supplemented with camel milk (D+CM). Camel milk was supplemented for two consecutive months. Serum glucose, leptin, insulin, liver, kidney, antioxidants, MDA and lipid profiles were assayed. Tissues from liver and adipose tissues were examined using RT-PCR analysis for the changes in mRNA expression of genes of carbohydrates and lipid metabolism. Pancreas and liver were used for immunohistochemical examination using specific antibodies. RESULTS: Camel milk supplementation ameliorated serum biochemical measurements that altered after diabetes induction. CM supplementation up-regulated mRNA expression of , , and genes, while down-regulated the expression of to control mRNA expression level. CM did not affect the expression of gene. On the other hand, metformin failed to reduce the expression of compared to camel milk administered rats. Immunohistochemical findings revealed that CM administration restored the immunostaining reactivity of insulin and GLUT-4 in the pancreas of diabetic rats. CONCLUSION: CM administration is of medical importance and helps physicians in the treatment of diabetes mellitus.
[Mh] Termos MeSH primário: Diabetes Mellitus Tipo 1/dietoterapia
Hipoglicemiantes/metabolismo
Leite/química
Leite/metabolismo
[Mh] Termos MeSH secundário: Animais
Glicemia/metabolismo
Camelus
Diabetes Mellitus Tipo 1/genética
Diabetes Mellitus Tipo 1/metabolismo
Seres Humanos
Insulina/metabolismo
Proteínas Substratos do Receptor de Insulina/genética
Proteínas Substratos do Receptor de Insulina/metabolismo
Peptídeos e Proteínas de Sinalização Intracelular/genética
Peptídeos e Proteínas de Sinalização Intracelular/metabolismo
Rim/metabolismo
Leptina/metabolismo
Fígado/metabolismo
Masculino
Fosfoenolpiruvato Carboxiquinase (GTP)/genética
Fosfoenolpiruvato Carboxiquinase (GTP)/metabolismo
Ratos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Blood Glucose); 0 (Hypoglycemic Agents); 0 (Insulin); 0 (Insulin Receptor Substrate Proteins); 0 (Intracellular Signaling Peptides and Proteins); 0 (Leptin); EC 4.1.1.32 (Phosphoenolpyruvate Carboxykinase (GTP)); EC 4.1.1.32 (phosphoenolpyruvate carboxykinase 1 (soluble) protein, rat)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170623
[St] Status:MEDLINE
[do] DOI:10.21010/ajtcam.v14i4.13


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[PMID]:28633482
[Au] Autor:Matulewicz N; Stefanowicz M; Nikolajuk A; Karczewska-Kupczewska M
[Ad] Endereço:Department of Metabolic Diseases, Medical University of Bialystok, Poland.
[Ti] Título:Markers of Adipogenesis, but Not Inflammation, in Adipose Tissue Are Independently Related to Insulin Sensitivity.
[So] Source:J Clin Endocrinol Metab;102(8):3040-3049, 2017 Aug 01.
[Is] ISSN:1945-7197
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Context: In obesity, adipose tissue (AT) undergoes dynamic remodeling, including an alternation in adipogenesis, AT-resident cell content, angiogenesis, and turnover of extracellular matrix (ECM) components. Studies of AT in humans have been carried out mostly in people with severe metabolic abnormalities, like type 2 diabetes or morbid obesity. Objective: The purpose of this study was to investigate subcutaneous AT gene expression of markers of adipogenesis, ECM remodeling, and inflammation in young, healthy, overweight or obese subjects. Design: The study group comprised 83 normal-weight, 48 overweight, and 19 obese subjects. Euglycemic hyperinsulinemic clamp, biopsy of subcutaneous AT, and isolation of peripheral blood mononuclear cells (PBMCs) were performed. Gene expression was measured with real-time polymerase chain reaction. Results: Overweight/obese subjects had lower AT expression of markers of adipogenesis, insulin signaling, and angiogenesis; higher expression of markers of ECM remodeling; altered expression of genes of the nuclear factor-κ-B (NFκB), but not c-Jun NH2-terminal kinase, pathway; and higher expression of macrophage markers but not markers of other immune cells. In multiple regression analysis, the expression of CEBPA, ADIPOQ, IRS1, IRS2, SLC2A4, and MMP9 was associated with insulin sensitivity independently of body mass index. No differences were found in inflammatory-gene PBMC expression. Conclusion: Overweight/obesity is associated with altered expression of genes of adipogenesis, insulin signaling, ECM remodeling, and inflammation. NFκB seems to be the earliest inflammatory pathway altered at the transcriptional level in AT. Macrophages seem to be the first immune cells to infiltrate AT. Adipogenesis and ECM remodeling are the initial processes in AT that are independently associated with insulin sensitivity.
[Mh] Termos MeSH primário: Adipogenia/genética
Resistência à Insulina/genética
Obesidade/genética
Gordura Subcutânea/metabolismo
[Mh] Termos MeSH secundário: Adiponectina/genética
Tecido Adiposo/imunologia
Tecido Adiposo/metabolismo
Adulto
Biomarcadores/metabolismo
Proteínas Estimuladoras de Ligação a CCAAT/genética
Estudos de Casos e Controles
Matriz Extracelular/metabolismo
Feminino
Técnica Clamp de Glucose
Transportador de Glucose Tipo 4/genética
Seres Humanos
Inflamação
Proteínas Substratos do Receptor de Insulina/genética
Proteínas Quinases JNK Ativadas por Mitógeno/genética
Leucócitos Mononucleares
Masculino
Metaloproteinase 9 da Matriz/genética
NF-kappa B/genética
Obesidade/imunologia
Obesidade/metabolismo
Sobrepeso/genética
Sobrepeso/imunologia
Sobrepeso/metabolismo
Análise de Regressão
Transdução de Sinais
Gordura Subcutânea/imunologia
Transcriptoma
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ADIPOQ protein, human); 0 (Adiponectin); 0 (Biomarkers); 0 (CCAAT-Enhancer-Binding Proteins); 0 (CEBPA protein, human); 0 (Glucose Transporter Type 4); 0 (IRS1 protein, human); 0 (IRS2 protein, human); 0 (Insulin Receptor Substrate Proteins); 0 (NF-kappa B); 0 (SLC2A4 protein, human); EC 2.7.11.24 (JNK Mitogen-Activated Protein Kinases); EC 3.4.24.35 (MMP9 protein, human); EC 3.4.24.35 (Matrix Metalloproteinase 9)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170920
[Lr] Data última revisão:
170920
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170622
[St] Status:MEDLINE
[do] DOI:10.1210/jc.2017-00597


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[PMID]:28630133
[Au] Autor:Sasaki M; Sasako T; Kubota N; Sakurai Y; Takamoto I; Kubota T; Inagi R; Seki G; Goto M; Ueki K; Nangaku M; Jomori T; Kadowaki T
[Ad] Endereço:Department of Diabetes and Metabolic Diseases, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
[Ti] Título:Dual Regulation of Gluconeogenesis by Insulin and Glucose in the Proximal Tubules of the Kidney.
[So] Source:Diabetes;66(9):2339-2350, 2017 Sep.
[Is] ISSN:1939-327X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Growing attention has been focused on the roles of the proximal tubules (PTs) of the kidney in glucose metabolism, including the mechanism of regulation of gluconeogenesis. In this study, we found that PT-specific insulin receptor substrate 1/2 double-knockout mice, established by using the newly generated sodium-glucose cotransporter 2 (SGLT2)-Cre transgenic mice, exhibited impaired insulin signaling and upregulated gluconeogenic gene expression and renal gluconeogenesis, resulting in systemic insulin resistance. In contrast, in streptozotocin-treated mice, although insulin action was impaired in the PTs, the gluconeogenic gene expression was unexpectedly downregulated in the renal cortex, which was restored by administration of an SGLT1/2 inhibitor. In the HK-2 cells, the gluconeogenic gene expression was suppressed by insulin, accompanied by phosphorylation and inactivation of forkhead box transcription factor 1 (FoxO1). In contrast, glucose deacetylated peroxisome proliferator-activated receptor γ coactivator 1-α (PGC1α), a coactivator of FoxO1, via sirtuin 1, suppressing the gluconeogenic gene expression, which was reversed by inhibition of glucose reabsorption. These data suggest that both insulin signaling and glucose reabsorption suppress the gluconeogenic gene expression by inactivation of FoxO1 and PGC1α, respectively, providing insight into novel mechanisms underlying the regulation of gluconeogenesis in the PTs.
[Mh] Termos MeSH primário: Gluconeogênese/fisiologia
Glucose/metabolismo
Insulina/metabolismo
Túbulos Renais Proximais/fisiologia
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Diabetes Mellitus Experimental/metabolismo
Proteína Forkhead Box O1/genética
Proteína Forkhead Box O1/metabolismo
Regulação da Expressão Gênica/fisiologia
Seres Humanos
Proteínas Substratos do Receptor de Insulina/genética
Proteínas Substratos do Receptor de Insulina/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Camundongos Obesos
Camundongos Transgênicos
Transdução de Sinais/fisiologia
Sirtuína 1/genética
Sirtuína 1/metabolismo
Transportador 2 de Glucose-Sódio/genética
Transportador 2 de Glucose-Sódio/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (FOXO1 protein, human); 0 (Forkhead Box Protein O1); 0 (Insulin); 0 (Insulin Receptor Substrate Proteins); 0 (Irs1 protein, mouse); 0 (Irs2 protein, mouse); 0 (Slc5a2 protein, mouse); 0 (Sodium-Glucose Transporter 2); EC 3.5.1.- (SIRT1 protein, human); EC 3.5.1.- (Sirtuin 1); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171017
[Lr] Data última revisão:
171017
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170621
[St] Status:MEDLINE
[do] DOI:10.2337/db16-1602



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