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Добірка наукової літератури з теми "Insulin resistance diabete"

Автор: Grafiati
Опубліковано: 9 червня 2023

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  1. Статті в журналах
  2. Дисертації
  3. Книги
  4. Частини книг
  5. Тези доповідей конференцій
  6. Звіти організацій

Статті в журналах з теми "Insulin resistance diabete":

1

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.

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2

Druet, 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.

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3

Adiga, 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.

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4

Maqbool, 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.

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Several physiologic, hormonal, and molecular processes contribute to the emergence of hyperglycaemia during pregnancy. Increased insulin resistance is seen during the course of a healthy pregnancy. During the early stages of normal pregnancies, the pancreatic β-cells secrete more insulin, which slows the rise in plasma glucose levels. This regulation explains the abnormally modest increases in plasma glucose levels brought on by elevated insulin resistance. The aim of this review was to evaluate the role of insulin resistance in gestational diabetes mellitus (GDM). The authors extensively searched various electronic databases like PubMed, Scopus, and Google Scholar for the collection of material regarding the role of insulin resistance in GDM. It was seen that hyperglycaemia results from the combination of the pregnancy’s increased insulin tolerance and pancreatic beta-cell insufficiency. Scientific studies have revealed that individuals who present with GDM are more likely to acquire chronic insulin resistance because of the superimposition of lower insulin production by the cells in that condition (GDM). Due to their significance in the development of postpartum diabetes mellitus, inflammation markers in GDM have been widely researched. Inflammation during GDM induces adaptive reactions in the placenta, which can have a substantial effect on the programming of foetal development.
5

Premkumar, 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.

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Obesity is a common condition due wrong eating habits and less physical activity. But it can produce serious illness like type 2 diabetes. In Malaysia 18 years and above 33.3% (5.4 million) are pre-obese and 27.2% (4.4 million) are obese. 7.2% are known to have diabetes and 8.0% are previously undiagnosed with diabetes. There is a strong relationship between obesity and diabetes mellitus. We must understand the mechanism by which obesity causes diabetes through and insulin resistance. When the fat distribution is more peripheral have more insulin sensitivity than whose fat distribution is more in the waist. The insulin resistance is caused by variety of substances like non-esterified fatty acids, glycerol, hormones, cytokines, proinflammatory markers which leads to the development of insulin resistance. The development of diabetes is a combination of the failure of β-islet cells of the pancreas and insulin resistance. There is a rising incidence of type 1 and type 2 diabetes due to obesity and weight gain. The obesity is more common in females. Obesity increases with age. Similarly, the incidence of diabetes also increases with and in male sex. Out of 219 persons 77 had normal BMI (less than 25), 83 were overweight (BMI 25 to 30) and 59 were obese (more than 30). The incidence of overweight (37.8%) and obese (26%). People who are overweight (BMI 25- 30) below 40 years are 8, between 40-60 years are 36 and above 60 years are 39. The people who are obese in the 40 years age group 6, 40-60 years 23 and above 60 years 30. Incidence of overweight and obese is more in the females 72.7% and males 58.4%. Incidence of overweight among female is 42% and obese are 30%. Comparatively among male 34.4% are overweight and 24% are obese.
6

McClain, 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.

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7

Coghlan, 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.

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Insulin regulates whole-body glucose homoeostasis by modulating the activities of protein kinases in its target tissues: muscle, liver and fat. Defects in insulin's ability to modulate protein kinase activity lead to ‘insulin resistance’ or impaired insulin action. Insulin resistance in combination with defective insulin secretion from the pancreas results in the elevated blood glucose levels that are characteristic of diabetes mellitus. Pharmacological agents that selectively modulate protein kinase activities in insulin-resistant tissues may act either as insulin-sensitizing or insulin-mimetic drugs. Consistent with this, small molecule modulators of a number of protein kinases have demonstrated efficacy in animal models of insulin resistance and diabetes. Moreover, emerging data in humans suggest that marketed anti-diabetic agents may also act in part through modulating protein kinase activities. This meeting was convened to consider the potential to treat insulin resistance and Type II diabetes by modulating protein kinase activity.
8

Kraegen, 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.

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9

Mykkanen, 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.

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10

Gokcen, 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.

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Aim: The most important mechanisms in the pathogenesis of the relationship between diabetes mellitus and cancer; hyperglycemia, insulin resistance and the inflammation resulting from the activation of insulin receptors. Apart from insulin resistance, hyperinsulinemia may also occur with the use of exogenous insulin. We aimed to investigate the effect of diabetes mellitus and insulin use as a risk factor for hepatocellular carcinoma development in a large patient population with chronic hepatitis B cirrhosis. Materials and Methods: 493 chronic hepatitis B-associated cirrhotic patients were included in the study. The patients were evaluated at 3-6month intervals during follow-up for hepatocellular carcinoma screening. Demographic and laboratory variables, presence of diabetes mellitus, insülin usage, and hepatocellular carcinoma occurrence were recorded. Results: The mean age of patients was 53.5±13.9 years, and 66.2% were male. 18.7% of the patients had a diagnosis of diabetes mellitus and 12% of the patients had insulin use. 68 patients (13.8%) were decompensated cirrhotic. The mean follow-up period was 50.6±33.6 months, during which 43 patients (8.7%) developed hepatocellular carcinoma. In the multivariable analysis, older age, male gender, presence of decompensation, use of exogenous insulin were associated with HCC occurrence (all p<0.05) Conclusion: Diabetes mellitus and insulin resistance have been associated with many cancers due to insulins’ mitogenic effects. We showed that insulin use is a risk factor for hepatocellular carcinoma development in our chronic hepatitis B-associated cirrhotic patients. Further studies including antidiabetic treatment subgroups are needed.
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Статті в журналах Дисертації Книги

Дисертації з теми "Insulin resistance diabete":

1

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/.

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O aumento da prevalência do diabete melito do tipo 2 (DM2) é intenso e implica ampla busca pela prevenção e tratamento da doença. Estudos têm mostrado a participação do zinco na síntese, secreção e via de sinalização da insulina e sobre o controle glicêmico. Este trabalho objetivou analisar o mecanismo de ação do zinco no controle da secreção de insulina e no controle glicêmico, de modo a entender se a suplementação com o zinco previne ou retarda a manifestação do DM2. O projeto foi aprovado pela CEUA-ICB (USP). Camundongos machos C57BL/6 foram divididos em 4 grupos experimentais: dieta controle (NFD); dieta controle suplementada com ZnCl2 (NFDZ); dieta hiperlipídica (HFD); e dieta hiperlipídica suplementada com ZnCl2 (HFDZ). A massa corporal, a ingestão de ração e água e a glicemia foram acompanhados semanalmente. Testes intraperitoneais de tolerância à glicose (ipGTT) e à insulina (ipITT) foram realizados na 14ª semana de tratamento. Completado as 15 semanas de tratamento a glicemia, a insulinemia e a zincemia foram analisadas, sendo aplicados os testes de HOMA-IR e HOMA-β. Em ilhotas pancreáticas isoladas foi analisada a secreção estática de insulina em diferentes concentrações de glicose. O teste de captação e metabolismo de glicose foi feito no músculo sóleo e a análise do conteúdo das proteínas AKT e GSK3-β foi feita no músculo sóleo e no fígado. Os dados (média±SEM) foram analisados por Two-way ANOVA com pós-teste Bonferoni ou por teste t de Student (P 0,05). A suplementação com zinco melhorou a disfunção glicêmica induzida por dieta hiperlipídica, sem no entanto afetar a resistência à insulina ou a secreção de insulina por ilhotas isoladas.
The 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.
2

Napolitano, Tiziana. "Confidentiel." Thesis, Université Côte d'Azur (ComUE), 2017. http://www.theses.fr/2017AZUR4141.

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3

GRANCINI, 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.

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BACKGROUND & AIMS: Diabetes occurring as a direct consequence of loss of liver function is usually characterized by non-diabetic fasting plasma glucose (FPG) and haemoglobin A1c (HbA1c) levels and should regress after orthotopic liver transplantation (OLT). This observational, longitudinal study investigated the relationship between the time-courses of changes in all 3 direct determinants of glucose regulation, i.e., β-cell function, insulin clearance and insulin sensitivity, and diabetes regression after OLT. METHODS: Eighty cirrhotic patients with non-diabetic FPG and HbA1c levels underwent an extended oral glucose tolerance test (OGTT) before and 3, 6, 12 and 24 months after OLT. The OGTT data were analysed with a mathematical model to estimate derivative control (DC) and proportional control (PC) of β-cell function and insulin clearance (which determine insulin bioavailability), and with the Oral Glucose Insulin Sensitivity (OGIS)-2 h index to estimate insulin sensitivity. RESULTS: At baseline, 36 patients were diabetic (45%) and 44 were non-diabetic (55%). Over the 2-year follow-up, 23 diabetic patients (63.9%) regressed to non-diabetic glucose regulation, whereas 13 did not (36.1%); moreover, 4 non-diabetic individuals progressed to diabetes (9.1%), whereas 40 did not (90.9%). Both DC and PC increased in regressors (from month 3 and 24, respectively) and decreased in progressors, whereas they remained stable in non-regressors and only PC decreased in non-progressors. Insulin clearance increased in all groups, apart from progressors. Likewise, OGIS-2 h improved at month 3 in all groups, but thereafter it continued to improve only in regressors, whereas it returned to baseline values in the other groups. CONCLUSIONS: Increased insulin bioavailability driven by improved β-cell function plays a central role in favouring diabetes regression after OLT, in the presence of a sustained improvement of insulin sensitivity.
4

Pappalardo, 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.

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Il GABA o acido gamma-aminobutirrico è il principale neurotrasmettitore inibitorio del sistema nervoso centrale (SNC) dei mammiferi. Circa il 20 - 50% di tutte le sinapsi utilizzano questo neurotrasmettitore. Esso è presente in quantità elevate, anche nello spazio interstiziale delle isole pancreatiche e nelle beta cellule pancreatiche dalle quali viene secreto. Il GABA oltre ad avere funzione trofica sulle beta cellule, attraverso il suo recettore (GABAA) controlla la riduzione della secrezione di glucagone insieme con lâ insulina. Nel nostro lavoro abbiamo studiato gli effetti dell'esposizione cronica al palmitato sul signaling del GABA e sulla pathway dellâ insulina in un modello di alfa cellule pancreatiche. Le cellule alfa-TC1-C6 sono state coltivate in presenza o in assenza di palmitato (0,5 mmol / l) per 48 h. Al termine del trattamento si osservava un aumento della secrezione basale di glucagone, induzione di uno stato di insulino-resistenza (diminuzione della fosforilazione di IRS-1 e Akt), e riduzione dellâ effetto inibitorio del GABA sulla secrezione di glucagone; inoltre anche la fosforilazione del canale GABAA indotta dal GABA era notevolmente ridotta dopo l'esposizione a palmitato. Nella seconda parte di questo lavoro abbiamo studiato la possibilità di prevenire i danni causati dell'esposizione cronica al palmitato sul nostro sistema co-trattando le nostre cellule con GLP-1 (100 nmol /l ). Nei gruppi trattati con GLP-1, la secrezione basale di glucagone non risultava aumentata e l'effetto inibitorio del GABA sulla secrezione di glucagone non era ridotto. Questi risultati indicano che il clone alfa-TC1 6, una linea cellulare di cellule pancreatiche alfa, coltivate per 48 ore in presenza di elevate concentrazioni di palmitato (0,5 mmol / l) sviluppano insulino resistenza attraverso la riduzione della fosforilazione di IRS-1 e Akt; questo percorso controlla la secrezione di glucagone ed è critico per la traslocazione del recettore GABAA sulle membrane cellulari e quindi per la polarizzazione della membrana delle alfa cellule. Il GLP-1 sembra in grado di prevenire tali alterazioni. Questi risultati supportano l'ipotesi che l'esposizione cronica agli acidi grassi può contribuire alla alterazione della secrezione di glucagone; e il GLP-1 mostra un effetto positivo sulla prevenzione dell'insulino-resistenza e sull'attivazione del canale GABA.
5

Leança, 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/.

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A síndrome metabólica (SM) e o diabete melito (DM) caracterizam-se por uma série de alterações no metabolismo de lipoproteínas, entre elas a hipertrigliceridemia e a redução nas concentrações de HDL-colesterol (HDL-C). Em estudo prévio demonstramos que indivíduos saudáveis, não obesos, com concentração de HDL-C abaixo de 40mg/dL, quando comparados àqueles com concentração de HDL-C acima de 60mg/dL, apresentam, no plasma, esteróis marcadores de absorção intestinal de colesterol alimentar diminuídos, e de síntese de colesterol aumentados. Achados semelhantes foram descritos por outros autores em portadores de SM e DM, sugerindo que a resistência à insulina participa na origem do distúrbio, embora não se saiba por quais mecanismos. Considerando nossos achados prévios, os objetivos deste estudo são investigar quais os mecanismos moleculares envolvidos nas alterações do metabolismo de colesterol presentes em indivíduos com concentrações alta (HIPERALFA, HDL-C > 60mg/dL, n = 36) ou baixa (HIPOALFA, HDL-C < 40mg/dL, n = 37) de HDL-C por meio de medida de: 1) conteúdo celular de colesterol e expressão gênica de enzimas e receptores críticos para a regulação intracelular de colesterol, tendo como modelo células linfomononucleares de sangue periférico; 2) parâmetros que regulam o metabolismo de lipoproteínas no plasma e que são influenciados pela insulina, tais como lecitina-colesterol aciltransferase (LCAT), lipoproteína lipase (LPL) e lipase hepática (LH) pós-heparina, proteína de transferência de colesterol esterificado (CETP), proteína de transferência de fosfolípides (PLTP) e pré- beta1 HDL. Os critérios de exclusão foram: diabete melito, IMC 30Kg/m2, tabagismo, consumo elevado de álcool e uso de fármacos capazes de interferir no metabolismo de lipoproteínas. Mostramos que, quando comparado ao grupo HIPERALFA, o grupo HIPOALFA apresentou maiores concentrações de insulina, triglicérides, ALT(TGP), índice HOMA, atividade de LCAT e LH, e menor atividade de LPL e concentração de pré-beta1 HDL. Não houve diferença entre os grupos com relação ao conteúdo celular de colesterol, à expressão dos genes estudados (ABCA1, ABCG1, SR-BI, LDLR, HMG CoA redutase, SREBP-1c e LXR alfa), às atividades de CETP e PLTP no plasma e à ultrassonografia de carótidas. Nossos resultados mostram que indivíduos com concentração alta ou baixa de HDL-C no plasma diferem com relação à sensibilidade à insulina, além de parâmetros envolvidos na regulação do metabolismo de lipoproteínas. Estes achados não se relacionaram com o metabolismo celular de colesterol no modelo estudado, mas sugerem que este quadro metabólico, cuja origem é desconhecida, precede o aparecimento, no decorrer da idade, de outras alterações típicas da síndrome metabólica no grupo com baixas concentrações de HDL-C no plasma
The 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
6

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.

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7

Pickavance, 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.

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8

GALLI, 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.

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Obiettivi: La disfunzione endoteliale è il meccanismo iniziale nella patogenesi dell’aterosclerosi. Costituisce una delle alterazioni vascolari presenti in soggetti apparentemente sani parenti di primo grado di pazienti affetti da Diabete Mellito Tipo 2 (FDR). Gli acidi grassi polinsaturi n-3 (PUFA n-3), come l’acido eicosapentaenoico (EPA) e l’acido docosaesaenoico (DHA), hanno un’ampia serie di proprietà antinfiammatorie. Noi abbiamo voluto testare l’ipotesi che la somministrazione di PUFA n-3 potesse migliorare la funzione endoteliale in soggetti FDR, ad elevato rischio di sviluppare precocemente aterosclerosi. DISEGNO DELLO STUDIO E METODI: Abbiamo condotto uno studio monocentrico, randomizzato, controllato con placebo, in doppio cieco, a gruppi paralleli. Sono stati inclusi 70 soggetti (età 30.5 ± 5.2 anni, 30 donne e 40 uomini) con un parente di primo grado affetto da Diabete di Tipo 2. I soggetti sono stati assegnati per randomizzazione ad assumere placebo (n = 34) o PUFA n-3 (n= 36) per 12 settimane. La funzione endoteliale è stata esaminata attraverso la tecnica del brachial artery reactivity test (BART) misurando la dilatazione flusso-mediata (FMD). Peso, BMI, pressione sisto-diastolica, e parametri di laboratorio (profilo lipidico, glicemia, insulinemia e C-peptide a digiuno, TNF-α, adiponectina, hs-PCR) sono stati misurati prima e dopo il trattamento. All’inizio dello studio, ciascun soggetto è stato sottoposto a una curva da carico orale di glucosio (OGTT). RISULTATI: Dopo OGTT abbiamo identificato 53 soggetti normoglicmici (NGT) e 17 soggetti con alterata tolleranza ai carboidrati (IGT). Al baseline i soggetti IGT presentavano un’età maggiore, un livello significativamente più alto di BMI, trigliceridi ed insulinemia a digiuno, un aumento dell’insulino-resistenza, e una funzione endoteliale peggiore rispetto ai soggetti NGT. Dopo trattamento, il braccio placebo, non ha mostrato significative modificazioni dei parametri valutati rispetto alle misurazioni basali; viceversa, il gruppo PUFA n-3 ha mostrato livelli significativamente ridotti di trigliceridi e TNF-α, un aumento dell’adiponectina circolante e un significativo miglioramento della funzione endoteliale. Il cambiamento dei livelli di TNF-α emergeva come unico e significativo predittore indipendente dell’aumento della FMD. CONCLUSIONI: La somministrazione di PUFA n-3 in soggetti NGT ed IGT parenti di primo grado di pazienti affetti da Diabete Mellito Tipo 2 determina un miglioramento della funzione endoteliale che si accompagna ad una diminuzione dei livelli circolanti TNF-α.
Objective: 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.
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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.

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Orientador: Licio Augusto Velloso
Tese (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
10

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.

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Orientador: Mario Jose Abdalla Saad
Tese (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
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Книги з теми "Insulin resistance diabete":

1

David, Moller, ed. Insulin resistance. Chichester: Wiley, 1993.

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2

National 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.

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3

B, Yao E., ed. Insulin resistance: New research. Hauppauge, NY: Nova Science, 2009.

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4

Korea-Japan Symposium on Diabetes Mellitus (7th 1993 Seoul, Korea). Insulin resistance in human disease: Proceedings of the 7th Korea-Japan Symposium on Diabetes Mellitus, Seoul, Korea, 13-14 April 1993. Edited by Huh Kap Bum, Shinn Soon Hyun, and Kaneko Toshio. Amsterdam: Excerpta Medica, 1993.

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5

M, Reaven Gerald, and Laws Ami, eds. Insulin resistance: The metabolic syndrome X. Totowa, N.J: Humana Press, 1999.

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6

Peters, Anne L. Conquering diabetes: A cutting-edge, comprehensive program for prevention and treatment. New York, N.Y: Hudson Street Press, 2005.

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7

Vernon, Mary C. Atkins Diabetes Revolution. New York: HarperCollins, 2005.

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8

European Symposium on Metabolism (6th 1993 Padua, Italy). Diabetes, obesity, and hyperlipidemias, V: The plurimetabolic syndrome : proceedings of the European Symposium on Metabolism, Padova, 24-26 May 1993. Edited by Crepaldi Gaetano, Tiengo Antonio, and Manzato E. Amsterdam: Excerpta Medica, 1993.

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9

R, Zierath Juleen, and Wallberg-Henriksson Harriet, eds. Muscle metabolism. London: Taylor & Francis, 2002.

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10

Vernon, Mary C. Atkins diabetes revolution: The groundbreaking approach to preventing and controlling diabetes. New York: William Morrow, 2004.

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Частини книг з теми "Insulin resistance diabete":

1

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.

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2

McKeigue, 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.

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3

Beck-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.

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4

Singh, 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.

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5

Moore, 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.

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6

Wieringa, 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.

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7

Carlberg, 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.

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8

Raffel, 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.

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9

Gartler, 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.

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10

Carlberg, 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.

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Тези доповідей конференцій з теми "Insulin resistance diabete":

1

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.

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Background: Impaired adipogenesis plays an important role in the development of obesityassociated insulin resistance and type 2 diabetes. Adipose tissue inflammation is a crucial mediator of this process. In hyperglycemia, immune system is activated partially through upregulation of GATA3, causing exacerbation of the inflammatory state associated with obesity. GATA3 also plays a role as a gatekeeper of terminal adipocyte differentiation. Here we are examining the impact of GATA3 inhibition in adipose tissue on restoring adipogenesis, reversing insulin resistance and potentially lowering the risk of type 2 diabetes. Results: GATA-3 expression was higher in insulin resistant obese individuals compared to their insulin sensitive counterparts. Targeting GATA-3 with GATA-3 specific inhibitors reversed impaired adipogenesis and induced changes in the expression of a number insulin signaling-related genes, including up-regulation of insulin sensitivity-related gene and down-regulation of insulin resistance-related genes. Conclusion: GATA3 expression is higher in differentiating adipocytes from obese insulin resistant. Inhibiting GATA3 improves adipocytes differentiation and rescues insulin sensitivity in insulin resistant cells
2

Aldali, 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.

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Background: Type 2 Diabetes mellitus is characterized by hyperglycemia and insulin resistance. Methylglyoxal (MG) a highly reactive dicarbonyl compound is also increased in diabetes. MG is detoxified by glyoxalase 1 (Glo-1) enzyme using reduced glutathione (GSH) as a co-factor. MG has been shown to have deleterious effects on cardiovascular cells and impairs insulin signaling. Insulin resistance is associated with diabetic cardiomyopathy. Trans-resveratrol (tRES) and Hesperetin (HES) combination has been shown to increase Glo-1 and improve insulin signaling in obese patients. Aim(s): The aim of this study is to investigate whether tRES-HES combination prevents MG-induced cardiac insulin resistance and the underlying mechanisms in cardiomyocytes in culture. Methodology: (H9C2) rat cardiomyocytes were treated with MG (100 µM) for 24 hours in the presence or absence of tRES-HES (10 µM). Glo-1 activity was determined by the formation of S-D lactoylglutathione; protein expression of P-Akt and P-GSK3b was determined using Western blot. In some experiments, cells were stimulated with insulin (100 nM) for 10 minutes to test insulin sensitivity. Results: MG reduced Glo-1 activity by ~25%, blunted insulin-induced phosphorylation of Akt and Gsk3b and increased the expression of beta-myosin heavy chain by ~50% (a marker of cardiac dysfunction) significantly (P˂0.05) compared to untreated control group of cells. Co-administration of tRES-HES combination restored Glo1 activity, maintained insulin-induced phosphorylation of Akt and GSK3b and prevented the increase in beta myosin heavy chain significantly (P<0.05). Conclusion: Induction of Glo1 prevents MG-induced cardiac insulin resistance and the increase in marker of cardiac dysfunction. This strategy could be helpful in preventing cardiovascular complications associated with diabetes.
3

Elcin, 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.

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Diabetes mellitus is still a very common disease in the world and affects the daily lives of patients negatively. Diabetes is also known to be associated with neurological diseases such as peripheral nerve diseases, stroke and dementia. Among these, the most common disease is a peripheral nerve disease, and it has been reported that poor diabetic control increases the risk of development and can be prevented by education of the patients. Vascular dementia is more common in patients with diabetes than Alzheimer's disease, and it is thought that cerebrovascular diseases may berelated to cognitive impairment in diabetes. Although the mechanisms by which diabetes affects the brain are not clearly revealed, it is thought that changes in vascular structure, insulin resistance, glucose toxicity, oxidative stress, accumulation of glycation end products, hypoglycemic episodes and amyloid metabolism are effective.The aim of this article is to describe the neurological complications of diabetes and to emphasize the importance of patient education, good diabetes control and early diagnosis in preventing these complications.
4

Nogueira, 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.

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Introduction: Alzheimer’s disease (AD) is closely related to diabetes mellitus (DM), and AD is also considered to be type 3 diabetes (T3D). Glycogen synthase kinase-3β (GSK-3β) may be the potential link between DM and AD. GSK-3β is one of the main factors that lead to insulin deficiency and insulin resistance, and insulin resistance is a characteristic of the development of DM. In AD, GSK-3β plays an important role in hyperphosphorylation of the tau protein (tau) associated with microtubules, which is one of the pathological features in AD. Objective: To analyze DM as a factor for the development of AD. METHODOLOGY: This is an integrative review of the literature, which is a construction of a comprehensive analysis of the literature with pre-defined steps, carried out through PubMed, 1.501 articles were found, of which 10 were selected, through the simultaneous crossing between the descriptors “Diabetes mellitus”, “Alzheimer “. Articles written in Portuguese and English published between 2016 and 2021 were inserted. Results: DM associated with insulin resistance affects psychomotor efficiency, attention, learning memory, mental flexibility, speed and executive function of the brain, thus being an independent risk factor for cognitive impairment and damage to the central nervous system, hyperglycemia, which can cause increased oxidative stress leading to progressive functional and structural abnormalities in the brain. Conclusion:The risk of dementia in patients with DM is higher than in nondiabetic patients and it is also well known that DM2 / insulin resistance is involved in AD.
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"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.

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Leboucher, 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.

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Nikolic, 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.

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Tabei, 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.

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Alkhateeb, 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.

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Geißler, 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.

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Звіти організацій з теми "Insulin resistance diabete":

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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.

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Review question / Objective: Population：Patients diagnosed as obesity with insulin resistance. Obesity reference: Consensus of experts on the Prevention and treatment of adult obesity in China in 2011 and Consensus of Chinese experts on medical nutrition therapy for overweight/obesity in 2016 were developed by the Obesity Group of Chinese Society of Endocrinology(CSE); BMI≥28. IR reference: According to the Expert opinions on insulin resistance evaluation published by Chinese Diabetes Society, HOMA-IR≥2.68 is regarded as the standard for the diagnosis of IR. Regardless of age, gender and course of disease. Patients diagnosed as obesity with insulin resistance. Intervention：Any kind of acupuncture, moxibustion, acupuncture+moxibustion, warm acupuncture, electropuncture, auricular point, acupoint application and acupoint catgut embedding. Comparison：Other acupuncture treatments, Drug therapy or blank control. Outcome：Primary outcomes: ①Fasting blood-glucose (FBG); ②Fasting serum insulin (FINS); ③Homeostasis model assessment-IR (HOMA-IR); ④Body Mass Index (BMI). Secondary outcomes: ①Waistline; ②Waist-hip ratio;③Triglyceride (TG); ④Total cholesterol (TC); ⑤High-density lipoprotein (HDL); ⑥Low-density lipoprotein (LDL). Study: Randomized controlled trials (RCTs) of different acupuncture methods in the treatment on obesity with insulin resistance, blind method and language are not limited. Randomized controlled trials (RCTs).
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yu, 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.

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Review question / Objective: To systematically evaluate the efficacy of the intestinal microbiome - bile acid pathway (BAS) in the treatment of T2DM. Condition being studied: Bile acids (BAs), an important component of bile, are also metabolites derived from cholesterol and promote intestinal absorption and transportation of dietary lipids . Studies have shown that bile acid receptor agonists can promote glP-1 secretion and improve glucose metabolism in preclinical mouse models of obesity and insulin resistance , which may become a new therapeutic target for Type 2 diabetes. However, no systematic review and meta-analysis has been found on the treatment of type 2 diabetes by intestinal microbiome - bile acid pathway. Therefore, we conducted a systematic review and meta-analysis to evaluate the safety and effectiveness of intestinal microbiome-bile acid pathway in the treatment of type 2 diabetes.
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Hung, 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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Review question / Objective: To assess the possible cause of events, the incidence of grade 3 hyperglycemia after treating Sofosbuvir/Velpatasvir/Voxilaprevir in HCV infections. Condition being studied: Sofosbuvir, velpatasvir, and voxilaprevir (SOF/VEL/VOX) is an effective, safe rescue therapy regimen for patients have previously been treated failure. Initiating Direct-Acting Antiviral (DAA) treatment for HCV infection with diabetes have experienced hypoglycemia, it could improve insulin resistance due to clean HCV. However, some studies shown that SOF/VEL/VOX has Grade 3 hyperglycemia adverse events. This finding contradicts that other DAAs studies. Information sources: Conducting a comprehensive literature search on the pubmed, Cochrane, clinicalkey, Embase, and MEDLINE electronic databases.

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