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Статті в журналах з теми "Insulin resistance diabete"
Feng, Jiayue, and Xiaoping Chen. "A9353 Assessing hip index as a marker for insulin resistance in the general Chinese population without diabete." Journal of Hypertension 36 (October 2018): e153. http://dx.doi.org/10.1097/01.hjh.0000548621.12493.c8.
Повний текст джерелаDruet, C., V. Baltaks??, M. Dabbas, G. Sebag, S. Dorgeret, R. Hankard, D. Chevenne, M. Polak, and C. Levy-Marchal. "O0057 OBESE CHILDREN WITH HIGH RISK OF DIABETE HAVE A REAL INSULIN RESISTANCE (IR) BUT NO DETERIORATION OF GLUCOSE TOLERANCE." Journal of Pediatric Gastroenterology and Nutrition 39, Supplement 1 (June 2004): S29. http://dx.doi.org/10.1097/00005176-200406001-00059.
Повний текст джерелаAdiga, Usha, Kathyayani P, and Nandith P.B. "Association of Insulin Based Insulin Resistance with Liver Biomarkers in Type 2 Diabetes mellitus." Journal of Pure and Applied Microbiology 13, no. 2 (June 30, 2019): 1199–205. http://dx.doi.org/10.22207/jpam.13.2.60.
Повний текст джерелаMaqbool, Mudasir. "Role of Insulin Resistance in Gestational Diabetes Mellitus: A Literature Review." Chettinad Health City Medical Journal 11, no. 02 (June 30, 2022): 69–74. http://dx.doi.org/10.24321/2278.2044.202218.
Повний текст джерелаPremkumar, Daivasikamani. "The Role of Obesity in Producing Type 2 Diabetes by Insulin Resistance." Diabetes & Obesity International Journal 5, no. 2 (2020): 1–9. http://dx.doi.org/10.23880/doij-16000227.
Повний текст джерелаMcClain, D. A., and E. D. Crook. "Hexosamines and insulin resistance." Diabetes 45, no. 8 (August 1, 1996): 1003–9. http://dx.doi.org/10.2337/diabetes.45.8.1003.
Повний текст джерелаCoghlan, M. P., and D. M. Smith. "Introduction to the Kinases in Diabetes Biochemical Society focused meeting: are protein kinases good targets for antidiabetic drugs?" Biochemical Society Transactions 33, no. 2 (April 1, 2005): 339–42. http://dx.doi.org/10.1042/bst0330339.
Повний текст джерелаKraegen, E. W., P. W. Clark, A. B. Jenkins, E. A. Daley, D. J. Chisholm, and L. H. Storlien. "Development of muscle insulin resistance after liver insulin resistance in high-fat-fed rats." Diabetes 40, no. 11 (November 1, 1991): 1397–403. http://dx.doi.org/10.2337/diabetes.40.11.1397.
Повний текст джерелаMykkanen, L., D. J. Zaccaro, L. E. Wagenknecht, D. C. Robbins, M. Gabriel, and S. M. Haffner. "Microalbuminuria is associated with insulin resistance in nondiabetic subjects: the insulin resistance atherosclerosis study." Diabetes 47, no. 5 (May 1, 1998): 793–800. http://dx.doi.org/10.2337/diabetes.47.5.793.
Повний текст джерелаGokcen, Pinar, and Kamil zdil. "A Risk Factor In The Development of Hepatocellular Carcinoma: Insulin Analogues Running Title: Insulin Analogues as a Risk Factor for Liver Cancer." Annals of Medical Research 29, no. 11 (2022): 1. http://dx.doi.org/10.5455/annalsmedres.2022.02.051.
Повний текст джерелаДисертації з теми "Insulin resistance diabete"
Capetini, Vinícius Cooper. "Efeito da suplementação com zinco na evolução da resistência à insulina induzida por dieta hiperlipídica em camundongos." Universidade de São Paulo, 2016. http://www.teses.usp.br/teses/disponiveis/42/42137/tde-10082016-154401/.
Повний текст джерелаThe increase in prevalence of type 2 diabetes mellitus (DM2) is intense and implies broad quest for prevention and treatment of disease. Studies have shown the participation of zinc in the synthesis, secretion and signaling pathway of insulin and the glucose control. This study aimed to analyze the mechanism of action of zinc in the control of insulin secretion and glucose control in order to understand whether supplementation with zinc prevents or delays the manifestation of DM2. The project was approved by CEUA-ICB (USP). Male mice C57BL/6 were divided en 4 groups: control diet (NFD); control diet supplemented with ZnCl2 (NFDZ); high fat diet (HFD); and high fat diet supplemented with ZnCl2 (HFDZ). Body weight, feed intake and water and the glucose levels were monitored weekly. Intraperitoneal glucose tolerance test (ipGTT) and insulin (ipITT) were performed at the 14th week of treatment. Completing the 15 weeks of the treatment glycemia, insulinemia and zincemia were analyzed, being applied HOMA-IR and HOMA-β tests. In isolated islets was assessed the static insulin secretion at different glucose concentrations. The uptake and glucose metabolism test was done in the soleus muscle and the content analysis of the AKT and GSK3-β protein was made in the soleus muscle and liver. The data (mean ± SEM) were analyzed by two-way ANOVA with Bonferoni post-test or Student\'s t test (P < 0,05). Zinc supplementation improves glucose dysfunction induced by high fat diet, without nonetheless affecting insulin resistance and insulin secretion by isolated islets.
Napolitano, Tiziana. "Confidentiel." Thesis, Université Côte d'Azur (ComUE), 2017. http://www.theses.fr/2017AZUR4141.
Повний текст джерелаGRANCINI, VALERIA. "RUOLO CENTRALE DELLA BETA-CELLULA NEL PROMUOVERE LA REGRESSIONE DEL DIABETE DOPO TRAPIANTO DI FEGATO IN PAZIENTI CON CIRROSI EPATICA." Doctoral thesis, Università degli Studi di Milano, 2019. http://hdl.handle.net/2434/658515.
Повний текст джерелаPappalardo, Alessandro Orazio Giovanni. "Ruolo del recettore Gabaa nelle cellule alfa pancreatiche e suo coinvolgimento nelle fasi di desensibilizzazione indotta dalla lipotossicità nel diabete di tipo II." Doctoral thesis, Università di Catania, 2016. http://hdl.handle.net/10761/3991.
Повний текст джерелаLeança, Camila Canteiro. "O metabolismo de lipoproteínas e a sensibilidade à insulina são distintamente modulados em indivíduos saudáveis com concentração alta ou baixa de HDL-colesterol." Universidade de São Paulo, 2012. http://www.teses.usp.br/teses/disponiveis/5/5135/tde-27072012-143556/.
Повний текст джерелаThe metabolic syndrome (MS) and the diabetes mellitus (DM) are characterized for a series of alterations in lipoprotein metabolism as hypertriglyceridemia and reduced HDL-cholesterol (HDL-C) concentration. In previous study we demonstrated that healthy non obese subjects with HDL-C concentration below 40mg/dL, when compared with those with HDL-C above 60mg/dL, present low plasma sterol markers of alimentary cholesterol intestinal absorption and high plasma sterol markers of cholesterol synthesis. Similar findings have been described by others in subjects with MS and DM, suggesting that insulin resistance participates in the origin of the disorder, although by unknown mechanisms. Considering our previous findings, the objectives of this study are to investigate the molecular mechanisms involved in alterations of cholesterol metabolism in subjects with high HDL-C (HYPERALPHA, HDL-C > 60mg/dL, n = 36) or low HDL-C (HYPOALPHA, HDL-C < 40mg/dL, n = 37) concentration by means of measuring: 1) cellular cholesterol content and gene expression of critical enzymes and receptors involved in the intracellular cholesterol regulation, having peripheral blood mononuclear cells as model; 2) parameters that regulate the plasma lipoproteins metabolism and that are influenced by insulin, such as lecithin: cholesterol acyltransferase (LCAT), post-heparin hepatic (HL) and lipoprotein lipase (LPL), cholesteryl ester transfer protein (CETP), phospholipid transfer protein (PLTP) and pre-beta1 HDL. The exclusion criteria were: diabetes mellitus, body mass index 30Kg/m2, smoking, heavy drinking and use of medications that interfere with lipoprotein metabolism. We demonstrated that, as compared with HYPERALPHA, the HYPOALPHA group presented higher insulin, triglycerides and alanine aminotransferase concentrations, HOMA index, LCAT and HL activities and lower LPL activity and pre-beta1 HDL concentration. There was no difference between the groups in the cellular cholesterol content, expression of genes (ABCA1, ABCG1, SR-BI, LDLR, HMG CoA reductase, SREBP-1c and LXR alpha), plasma CETP and PLTP activities and carotid ultrasonography. Our results show that subjects with high or low plasma HDL-C concentration differ in relation to insulin sensitivity and in parameters involved in lipoprotein metabolism regulation. These findings were not related to the cellular cholesterol metabolism in the studied model, but they suggest that this metabolic disturbance, whose origin is unknown, precedes the appearance, in the course of the human life of other typical alterations of metabolic syndrome in the low HDL-C concentration group
Kergoat, Micheline. "Secretion et mode d'action de l'insuline dans un modele de diabete non-insulinodependant chez le rat." Paris 7, 1988. http://www.theses.fr/1988PA077085.
Повний текст джерелаPickavance, Lucy Cecilia. "Thiazolidinedione treatment in models of insulin resistance." Thesis, University of Liverpool, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.367553.
Повний текст джерелаGALLI, ANGELICA. "Ruolo dei PUFA OMEGA-3 nella regolazione della funzione endoteliale in parenti di primo grado di pazienti affetti da diabete mellito di tipo 2." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2007. http://hdl.handle.net/2108/377.
Повний текст джерелаObjective: Endothelial dysfunction is the early and fundamental step in the pathogenesis of atherosclerosis. It has been indicated as one of the precocious vascular abnormalities in apparently healthy first-degree relatives of type 2 diabetic patients.(FDR). N-3 polyunsaturated fatty acids (PUFA n-3), such as eicosapentaenoic acid (EPA) and docosahexaenoico acid (DHA), have a wide range of anti-inflammatory properties. The aim of this study is that a supplementation of n3-PUFA might be effective to improve the endothelial dysfunction in FDR subjects at higher risk of developing atherosclerosis. RESEARCH DESIGN AND METHODS: We carried out a randomized, controlled with placebo, double blind, parallel-groups clinical trial. The study included 70 subjects (age 30.5 ± 5.2 years, 30 women e 40 men), all first-degree relatives of type 2 diabetic patients. The subjects were randomly assigned to assume placebo (n = 34) or n-3 PUFA (n= 36) for 12 weeks. Endothelial function was assessed by brachial artery reactivity test (BART), measuring the flow-mediated dilatation (FMD). Weight, BMI, systolic and diastolic blood pressure, and laboratory parameters (lipid profile, fasting plasma glucose, insulin, and C-peptide, TNF-α, adiponectin, hs-PCR) were assessed at baseline and after treatment. At the beginning of the study, each subject underwent a standard oral glucose tolerance test (OGTT). RESULTS: Upon OGTT we identified 53 normoglycemic subjects (NGT) and 17 subjects with impaired glucose tolerance (IGT). At baseline, the subjects IGT were older and presented significant higher levels of BMI, triglycerides, and fasting insulin, as well an increased insulin resistance, and a worse endothelial function, compared with NGT individuals. After treatment, we found only little if any change in metabolic and biomarkers levels of the participants of the placebo group (NGT and IGT); on the contrary, the n-3 PUFA group showed some difference respect to the baseline characteristics: the triglycerides and the TNF-α levels were significantly decrease, the adiponectin was increase, and the endothelial function showed a significant improvement. The changing of TNF-α levels emerged as the unique independent and significant predictor of the improvement of the FMD after the period of assumption of n-3 PUFA. CONCLUSIONS: We concluded that the N-3 PUFA oral supplementation is associated with an improvement of endothelial function via decreasing TNF-alpha in NGT and IGT subjects offspring of patients with Type 2 Diabetes.
Guarilha, Alessandra Lia Gasparetti. "Transdução do sinal da insulina em animais expostos ao frio : o papel do cross-talk entre o receptor 'beta' 3 - adrenergico e o receptor de insulina em tecido adiposo marrom." [s.n.], 2004. http://repositorio.unicamp.br/jspui/handle/REPOSIP/310365.
Повний текст джерелаTese (doutorado) - Universidade Estadual de Campinas, Faculdade de Ciencias Medicas
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Resumo: A exposição de animais homeotérmicos ao mo é utilizada como um método reprodutível para se obter um modelo animal de hipoinsulinemiaacompanhada por elevada mobilização periférica de glicose. No presente estudo, avaliaram-se as etapas iniciais e intermediárias da via de sinalização da insulina em tecidos periféricos de ratos expostos ao mo. Avaliou-se ainda, a comunicação intracelular entre o receptor (33-adrenérgicoe as vias de sinalização da insulina em tecido adiposo marrom de ratos expostos ao mo e tratados, ou não, com compostos agonista ou antagonista (33-adrenérgicos.A exposição de ratos ao mo promoveu a redução da secreção de insulina, acompanhada de um elevado clearance de glicose e maior captação de glicose por tecido muscular esquelético, adiposo branco e adiposo marrom. Tais fenômenos foram acompanhados por inibição da ativação da maior parte dos componentes da via de sinalização da insulina em tecido muscular esquelético e adiposo branco; por estimulação da maior parte dos componentes da via de sinalização da insulina em tecido adiposo marrom; e por efeitos variados (estímulo, inibição e não-modulação) de componentes da via de sinalização da insulina em figado. Por fim, este estudo demonstrou que a exposição ao mo ativa a sinalização (33-adrenérgicaem tecido adiposo marrom. Tal ativação leva à modulação da atividade de vários componentes da via de sinalização da insulina neste tecido. Entretanto, fatores independentes da sinalização (33-adrenérgica parecem contribuir para a complexa regulação do sinal da insulina obseIVada em tecido adiposo marrom de ratos expostos ao mo. Em conclusão, o presente estudo revelou alguns dos intrincados mecanismos pelos quais a exposição ao mo controla a atividade da insulina em animais homeotérmicos, podendo favorecer a identificação de potenciais alvos para a ação terapêutica em doenças onde a resistência à insulina desempenha papel central
Abstract: Cold exposure provides a reproducible model of improved glucose turnover accompanied by reduced blood levels of insulin. In the present study, the initial and intermediate steps of the insulin-signaling pathway in peripheral tissues of rats exposed to cold environment were evaluated. Also, the intracellular connection between insulin and ~3-adrenergic signaling in brown adipose tissue of cold exposed rats treated, or not, with ~3-adrenergic agonist or antagonist compounds were evaluated. During cold exposure, insulin secretion was significantly impaired, while whole body glucose clearance rates were significantly improved. This was accompanied by an increased glucose uptake by skeletal muscle, white adipose tissue and brown adipose tissue. These phenomena were paralleled by an apparent molecular resistance to insulin in skeletal muscle and white adipose tissue; by improved molecular response to insulin in brown adipose tissue; and by ambiguous effects (stimulation, inhibition and not modulation) of regulation of the insulin-signaling pathway in liver. Finally, cold exposure activated the ~3-adrenergic signaling in brown adipose tissue. It leads to modulation of activity of several components of the insulin signal transduction pathway in this tissue. However, ~3-adrenergic receptor independent mechanisms seem to contribute to the complex regulation of the insulin signaling observed in brown adipose tissue of rats exposed to cold. In conclusion, the present study revealed some of the complex mechanisms that participate in the cold-exposure-induced control of the insulin action in homeothermic animals. These results may favour the identification of novel potential targets for therapeutics in diabetes and related disorders
Doutorado
Medicina Experimental
Doutor em Fisiopatologia Medica
Lalli, Cristina Alba. "Efeito da rosiglitazona e da lovastatina na resistencia insulinica da dieta hiperlipidica." [s.n.], 2007. http://repositorio.unicamp.br/jspui/handle/REPOSIP/311224.
Повний текст джерелаTese (doutorado) - Universidade Estadual de Campinas, Faculdade de Ciencias Medicas
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Resumo: A insulina é o principal hormônio anabólico, que atua através da ativação de transportadores, regulação de enzimas e expressão de genes que codificam enzimas envolvidas na captação e armazenamento de substratos. Para exercer suas ações, a insulina emprega duas vias principais de sinalização intracelular: a via da PI 3-quinase e a via da MAPK. A regulação da ação do hormônio se faz por meio de vários mecanismos. O modelo animal de dieta hiperlipídica apresenta alterações metabólicas e de sinalização semelhantes aos encontrados na resistência insulínica de humanos com obesidade induzida por dieta. O objetivo de nosso trabalho foi estudar em ratos alimentados com dieta hiperlipídica, etapas da sinalização insulínica e também algumas vias de regulação da sinalização, após o uso de duas drogas: a rosiglitazona, uma tiazolidinediona usada para o tratamento do diabetes melito tipo 2 como sensibilizadora de insulina e a lovastatina, droga inibidora da HMGCoA redutase, que diminui a síntese de colesterol, mas que também tem apresentado efeito de aumentar a sensibilidade à insulina, tanto em modelos animais como em humanos. Ratos alimentados com dieta hiperlipídica por quatro semanas e tratados na última semana com as drogas, isoladamente, foram submetidos à extração de tecidos hepático e muscular e os fragmentos obtidos foram submetidos à análise de concentração protéica ou de grau de fosforilação de proteínas através de técnicas de imunoprecipitação e immunoblotting. A sensibilidade à insulina foi avaliada pelo teste de tolerância à insulina e cálculo da constante de decaimento da glicose (Kitt). No estudo. da rosiglitazona, foi observada diminuição significativa da sensibilidade à insulina expressa por diminuição no Kitt, nos animais que receberam a dieta e recuperação da sensibilidade após o uso da droga. A fosforilação do IRS-l, associação do substrato com a enzima PI3K e a ativação da Akt no tecido hepático e muscular também se mostraram diminuídas pela dieta e recuperadas com o uso da rosiglitazona. O estudo da lovastatina demonstrou efeito positivo da droga sobre a sensibilidade insulínica, revertendo a resistência induzida pela dieta hiperlipídica, expressa por valor de Kitt semelhante ao dos animais controle. Na via de sinalização da PI3K: fosforilação do IR e do IRS-I, associação do IRS-l à PI3k e ativação da Akt, tanto no tecido hepático como muscular, a lovastatina reverteu as alterações da dieta, com recuperação a valores semelhantes aos do grupo controle. Também nas vias de regulação, a dieta induziu maior fosforilação do IR em serina, maior fosforila do IRS-I em serina307, maior atividade da JNK e da proteína fosfatase PTPIB e menor ativação do IKB, efeitos que podem explicar a resistência desse modelo. A lovastatina reverteu todas essas alterações. Concluindo, a rosiglitazona reverteu as alterações causadas pela dieta hiperlipídica sobre as etapas iniciais da sinalização insulínica na via da PI3K. A lovastatina recuperou as alterações induzidas pela dieta hiperlipídica na transmissão do sinal insulínico, agindo sobre as vias de regulação da sinalização: ação da PTPIB, fosforilação do IR e do IRS-l em serina induzidos pela JNK e PTPIB e ativação da via inflamatória
Abstract: Insulin is the major anabolic hormone and acts through transporter activation, enzymes regulation and gene expression. This hormone uses' two main signaling pathways: the PI3K pathway, involved in its metabolic effects and the MAPK pathway, responsible for cell growth and differentiation. There are many mechanisms of regulation of insulin signaling. The use of a high- fat diet is a known model of insulin resistance with metabolic and signaling changes similar to those of human insulin resistance syndrome observed in diet induced obesity. Rosiglitazone is an agent of the class of thiazolidinediones, insulin-sensitizing agents whose effects are mainly due to the activation of PP ARy and are used to treat type 2 diabetes. Lovastatin is one of a class of a class of cholesterol synthesis inhibitors; recent studies have shown that this agent might have relevant effects on insulin resistance in both animal models and humans. The aim of this study was to evaluate the effects of two different drugs independent1y, rosiglitazone and lovastatin, on insulin signaling in liver and muscle of rats fed on a hígh-fat diet. We used four week old male Wistar rats, fed on a high- fat diet during four weeks and treated with rosiglitazone or lovastatin during the last week, compared to rats fed on standard chow. Fragments of liver and muscle tis sues were extracted from anesthetized animaIs and protein concentrations and phosphorylation degree were studied through immunoprecipitation and immunoblotting techniques. Insulin sensitivity was evaluated by insulin tolerance test and calculation of the disappearance rate constant (KitD. We observed that high-fat fed diet rats presented a significant decrease in Kitt compared to control rats. The animaIs that were fed with the high-fat diet and were treated with either one ofthe drugs presented a reversal ofthis effect. In the study of rosiglitazone, the high-fat model demonstrated a decrease in the IRS-I phosphorylation, IRS-l/PI3K association and activation of Akt and rosiglitazone administration resulted in the reversion of all the effects in liver and muscle. In addition to the effect on insulin sensitivity, the use of lovastatin was also associated with an increase in insulin-induced IR tyrosine phosphorylation and, in parallel, a decrease in IR serine phosphorylation and association with PTPIB. Our data also show that lovastatin treatment was associated with an increase in the insulin-stimulated IR/IRS-l/PI3KJ Akt pathway in the liver and musc1e of high-fat fed rats, in parallel with a decrease in the inflammatory pathway (JNK and IKKI3/IKB/NFKB) related to insulin resistance. In conclusion, rosiglitazone and lovastatin improved the altera_s in insulin signaling pathways presented by the high-fat model of insulin resistance
Doutorado
Clinica Medica
Doutor em Clínica Médica
Книги з теми "Insulin resistance diabete"
David, Moller, ed. Insulin resistance. Chichester: Wiley, 1993.
Знайти повний текст джерелаNational Diabetes Information Clearinghouse (U.S.), ed. Insulin resistance and pre-diabetes. [Bethesda, MD]: National diabetes Information Clearinghouse, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, U.S. Dept. of Health and Human Services, 2003.
Знайти повний текст джерелаB, Yao E., ed. Insulin resistance: New research. Hauppauge, NY: Nova Science, 2009.
Знайти повний текст джерелаBum, Huh Kap, Shinn Soon Hyun, and Kaneko Toshio, eds. Insulin resistance in human disease: Proceedings of the 7th Korea-Japan Symposium on Diabetes Mellitus, Seoul, Korea, 13-14 April 1993. Amsterdam: Excerpta Medica, 1993.
Знайти повний текст джерелаM, Reaven Gerald, and Laws Ami, eds. Insulin resistance: The metabolic syndrome X. Totowa, N.J: Humana Press, 1999.
Знайти повний текст джерелаConquering diabetes: A cutting-edge, comprehensive program for prevention and treatment. New York, N.Y: Hudson Street Press, 2005.
Знайти повний текст джерелаVernon, Mary C. Atkins Diabetes Revolution. New York: HarperCollins, 2005.
Знайти повний текст джерелаGaetano, Crepaldi, Tiengo Antonio, and Manzato E, eds. Diabetes, obesity, and hyperlipidemias, V: The plurimetabolic syndrome : proceedings of the European Symposium on Metabolism, Padova, 24-26 May 1993. Amsterdam: Excerpta Medica, 1993.
Знайти повний текст джерелаR, Zierath Juleen, and Wallberg-Henriksson Harriet, eds. Muscle metabolism. London: Taylor & Francis, 2002.
Знайти повний текст джерелаC, Atkins Robert, and Eberstein Jacqueline A, eds. Atkins diabetes revolution: The groundbreaking approach to preventing and controlling diabetes. New York: William Morrow, 2004.
Знайти повний текст джерелаЧастини книг з теми "Insulin resistance diabete"
Bell, Patrick M. "Insulin Resistance." In Diabetes and Atherosclerosis, 27–51. Dordrecht: Springer Netherlands, 1992. http://dx.doi.org/10.1007/978-94-011-2734-9_3.
Повний текст джерелаMcKeigue, Paul M. "Ethnic Variation in Insulin Resistance and Risk of Type 2 Diabetes." In Insulin Resistance, 19–33. Totowa, NJ: Humana Press, 1999. http://dx.doi.org/10.1007/978-1-59259-716-1_2.
Повний текст джерелаBeck-Nielsen, Henning, Frank Alford, and Ole Hother-Nielsen. "Insulin Resistance in Glucose Disposal and Production in Man with Specific Reference to Metabolic Syndrome and Type 2 Diabetes." In Insulin Resistance, 155–78. Chichester, UK: John Wiley & Sons, Ltd, 2005. http://dx.doi.org/10.1002/0470011327.ch6.
Повний текст джерелаSingh, Kamalpreet, and Vasudevan A. Raghavan. "Insulin Resistance and Atherosclerosis." In Contemporary Diabetes, 41–54. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-7554-5_3.
Повний текст джерелаMoore, Lisa E. "Pathophysiology of Insulin Resistance." In Diabetes in Pregnancy, 1–5. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-65518-5_1.
Повний текст джерелаWieringa, Tj. "Cellular insulin resistance." In Pathogenesis and Treatment of Diabetes Mellitus, 75–82. Dordrecht: Springer Netherlands, 1986. http://dx.doi.org/10.1007/978-94-009-4301-8_9.
Повний текст джерелаCarlberg, Carsten, Stine Marie Ulven, and Ferdinand Molnár. "Insulin Resistance and Diabetes." In Nutrigenomics: How Science Works, 131–51. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-36948-4_9.
Повний текст джерелаRaffel, Leslie J., Tamar Shohat, and Jerome I. Rotter. "Diabetes and Insulin Resistance." In Genetic factors in coronary heart disease, 203–15. Dordrecht: Springer Netherlands, 1994. http://dx.doi.org/10.1007/978-94-011-1130-0_14.
Повний текст джерелаGartler, Stanley M., R. Scott Hansen, Vinzenz Oji, Heiko Traupe, Julia Horn, Bodo Grimbacher, Srijita Sen-Chowdhry, et al. "Insulin Resistance Related Diabetes." In Encyclopedia of Molecular Mechanisms of Disease, 1060. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_6449.
Повний текст джерелаCarlberg, Carsten, Eunike Velleuer, and Ferdinand Molnár. "Insulin Resistance and Diabetes." In Molecular Medicine, 633–51. Cham: Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-031-27133-5_40.
Повний текст джерелаТези доповідей конференцій з теми "Insulin resistance diabete"
Al-Jaber, Hend Sultan, Layla Jadea Al-Mansoori, and Mohamed Aghar Elrayess. "The Role of GATA3 in Adipogenesis & Insulin Resistance." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0143.
Повний текст джерелаAldali, Sara Haitham, and Sownd Sankaralingam. "Induction of Glyoxalase 1 to prevent Methylglyoxal-Induced Insulin Resistance in Cardiomyocytes." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0230.
Повний текст джерелаElcin, Huseyn. "EARLY IDENTIFICATION OF THE NEUROLOGICAL COMPLICATIONS OF DIABETES MELLITUS." In International Trends in Science and Technology. RS Global Sp. z O.O., 2021. http://dx.doi.org/10.31435/rsglobal_conf/30032021/7474.
Повний текст джерелаNogueira, Fábio Dias, Ana Klara Rodrigues Alves, Barbara Beatriz Lira da Silva, Ana Kamila Rodrigues Alves, Marlilia Moura Coelho Sousa, Ana Karla Rodrigues Alves, Wanderson da Silva Nery, Breno Carvalho de Almeida, Flávia Dias Nogueira, and Leiz Maria Costa Véras. "The relationship of diabetes mellitus with Alzheimer’s disease: a literature review." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.280.
Повний текст джерела"Understanding Mechanisms of Insulin Resistance in Diabetes and Obesity." In International Conference on Agricultural, Ecological and Medical Sciences. International Institute of Chemical, Biological & Environmental Engineering, 2015. http://dx.doi.org/10.15242/iicbe.c0415038.
Повний текст джерелаLeboucher, A., M. Rath, and A. Kleinridders. "Increased uremic toxins in cerebrospinal fluid of obese mice cause insulin resistance." In Diabetes Kongress 2018 – 53. Jahrestagung der DDG. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1641817.
Повний текст джерелаNikolic, A. "Genetic variation in a patient with a rare syndrome of severe insulin resistance." In Diabetes Kongress 2021 – 55. Jahrestagung der DDG. Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1727543.
Повний текст джерелаTabei, S., L. Scheffler, R. Chakaroun, S. Ziesche, A. Crane, M. Stumvoll, A. Dietrich, M. Blüher, M. Gericke, and P. Kovacs. "Low-grade inflammation in insulin resistance associates with bacterial load in adipose tissue." In Diabetes Kongress 2019 – 54. Jahrestagung der DDG. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1688193.
Повний текст джерелаAlkhateeb, H. "Oleuropein ameliorates palmitate-induced insulin resistance by increasing Glut4 translocation through activation of AMPK." In Diabetes Kongress 2018 – 53. Jahrestagung der DDG. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1641812.
Повний текст джерелаGeißler, C., C. Krause, M. Kähler, I. Cascorbi, and H. Kirchner. "Longitudinal analysis of the development of hepatic insulin resistance in diet-induced obese mice." In Diabetes Kongress 2018 – 53. Jahrestagung der DDG. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1641822.
Повний текст джерелаЗвіти організацій з теми "Insulin resistance diabete"
Chen, Jiankun, Yingming Gu, Lihong Yin, Minyi He, Na Liu, Yue Lu, Changcai Xie, Jiqiang Li, and Yu Chen. Network meta-analysis of curative efficacy of different acupuncture methods on obesity combined with insulin resistance. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, August 2022. http://dx.doi.org/10.37766/inplasy2022.8.0075.
Повний текст джерелаyu, luyou, jinping yang, xi meng, and yanhua lin. Effectiveness of the gut microbiota-bile acid pathway (BAS) in the treatment of Type 2 diabetes: A protocol for systematic review and meta analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, July 2022. http://dx.doi.org/10.37766/inplasy2022.7.0117.
Повний текст джерелаHung, Hsuan-Yu, and Chung-Yu Chen. The impact of Sofosbuvir/Velpatasvir/Voxilaprevir treatment on serum hyperglycemia in HCV infections: A Systematic Review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, December 2021. http://dx.doi.org/10.37766/inplasy2021.12.0109.
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