Relevant bibliographies by topics / Insulin

Academic literature on the topic 'Insulin'

Author: Grafiati
Published: 4 June 2021
Last updated: 29 July 2024

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Journal articles on the topic "Insulin"

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Hansenne, Isabelle Sylvie, Chantal Renard, and Vincent Geenen. "Igf2 expression is required for complete tolerance to insulin (128.19)." Journal of Immunology 178, no. 1_Supplement (April 1, 2007): S213—S214. http://dx.doi.org/10.4049/jimmunol.178.supp.128.19.

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Abstract All members of insulin gene family are transcribed in human thymus according a hierarchy whereby IGF2 expression (thymic epithelial cells/TEC) exceeds IGF1 (macrophages), which exceeds INS (medullary TEC). Type 1 and type 2 IGF receptors are expressed by thymic T-cell populations. To further study the expression of IGF-2 in thymus, the dominance of this factor was compared to insulin, while ontogenesis of Igf2, insulin1 and insulin2 transcription was studied in Balb/c pancreas and thymus. In 4-wk old thymi, IGF-2 concentration is higher than insulin content. Ontogenesis of Igf2, insulin1 and insulin2 transcription from E13 to post-natal day 2 does not differ in Balb/c thymus and pancreas. In a second step, tolerance to IGF-2 and insulin was assessed by immunization of Igf2−/− mice. The profile of B-cell response in Igf2−/− mice immunized with IGF-2 evidenced a T-dependent profile of anti-IGF-2 antibodies that was absent in Igf2+/+ mice. This T-dependent isotype switch indicates the presence of specific anti-IGF-2 CD4+ T cells. Cloning of these T cells failed because Igf2−/− CD4+ T cells exhibit a low rate of proliferation in presence of IGF-2. After immunization with insulin, Igf2−/− mice developed a significantly higher humoral response against insulin, indicating that Igf2 expression is necessary for complete tolerance to insulin.
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Shestakova, Marina Vladimirovna, and Irina Vladimirovna Glinkina. "Insulin glargine does not increase the risk of malignancy.Synopsis of the article ?Combined randomised controlled trial experience of malignancies in studies using insulin glargine?byHome P.D. & Lagarenne P. (Diabetologia 2009, vol. 52 (12): 2499-2506)." Diabetes mellitus 13, no. 1 (March 15, 2010): 88–90. http://dx.doi.org/10.14341/2072-0351-6022.

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Results of 31 controlled randomized studies of insulin glargine given to patients with diabetes mellitus are reviewed to evaluate the frequency of malignantneoplasms. 52 tumours were diagnosed in 45 (0.8%) patients on insulin glargine therapy and 48 tumors in 46 (0.9%) patients using other insulins(mostly NPX insulin). The incidence of breast cancer was equal (0.1%) in both groups (4 and 6 cases respectively). These data indicate thatthe use of insuline glargine does not increase the risk of malignancy, e.g. breast cancer.
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Modi, K. D., Pradeep V. Gadge, Pradeep Jain, Sudhir Pawar, Ruchi D. Shah, Shahu A. Ingole, and Rishi Jain. "Clinical challenges with excipients in insulin formulations and role of concentrated insulin." International Journal of Basic & Clinical Pharmacology 8, no. 4 (March 23, 2019): 821. http://dx.doi.org/10.18203/2319-2003.ijbcp20191125.

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Most of the insulin formulations in clinical use contain phenol, meta-cresol or both as excipients. These excipients in insulin preparations provide stability and have antimicrobial properties. However, they are reported to be associated with undesirable side-effects especially localised allergic reactions. Amount of excipients injected per unit dose of insulin is a major determining factor in causation of these reactions. This review discusses the excipients in different insulin formulations available in India with potential of precipitating undesirable effects and the use of concentrated insulins to reduce these complications. To avoid the detrimental effects associated with excipients, removal of preservatives or use of insulin preparations devoid of excipients can be an option. Besides these approaches, one approach that can be considered is the use of concentrated insulin to reduce the volume of insulin dose and thereby the excipients. Concentrated insulins address the high insulin requirements of the growing population of patients with type 2 diabetes who require higher insulin doses. Concentrated insulins help in reduction of dose volume as well as amount of excipients injected per unit dose of insulin. U200 (concentrated r-DNA Human Insulin Premix 30/70-200 IU/ml) can be advantageous with better absorption from smaller quantity injected, lesser variability in absorption, lesser pain and discomfort due to smaller quantity, lesser chances of hypoglycaemia all of which can lead to better patient compliance. Thus, concentrated insulin U200 can be one of the alternatives to prevent/reduce clinical complications with excipients in insulins.
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Dąbrowski, Mariusz. "U kogo i dlaczego warto zastosować insulinę dwuanalogową aspart + degludec?" Medycyna Faktów 16, no. 2(59) (June 30, 2023): 227–33. http://dx.doi.org/10.24292/01.mf.0223.15.

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Ostatnie lata przyniosły istotne zmiany paradygmatu terapii cukrzycy typu 2. Po ogłoszeniu wyników pierwszych i kolejnych badań bezpieczeństwa sercowo-naczyniowego leków przeciwcukrzycowych na pierwszą linię frontu wysunęły się leki nieinsulinowe, a szczególne miejsce zajęły inhibitory kotransportera sodowo-glukozowego typu 2 i agoniści receptora glukagonopodobnego peptydu-1 (te drugie są rekomendowane jako pierwsza terapia iniekcyjna w cukrzycy typu 2). Spowodowało to nieznaczny spadek liczby pacjentów leczonych insuliną. Niemniej należy pamiętać, że w populacji osób z cukrzycą typu 2 u wielu pacjentów wystąpi wcześniej lub później konieczność wdrożenia insulinoterapii. Zwykle jest ona inicjowana w postaci jednej iniekcji insuliny bazowej, przy czym w naszych warunkach zwykle jest to insulina NPH. Brak efektywności tej terapii wymaga dalszej intensyfikacji leczenia w postaci dołączania kolejnych iniekcji insuliny doposiłkowej. Jedną z takich opcji jest zastosowanie połączenia w jednym wstrzykiwaczu szybko działającego analogu – insuliny aspart (IAsp) oraz ultradługo działającego analogu – insuliny degludec (IDeg), z których każdy zachowuje swój profil farmakokinetyczny. Zaletą tej opcji jest mniejsza liczba iniekcji przy porównywalnej lub lepszej kontroli glikemii w porównaniu z innymi schematami terapii, a dodatkową korzyścią dla pacjenta jest mniejsza liczba hipoglikemii, szczególnie nocnych. Leczenie to umożliwia dalszą intensyfikację terapii poprzez dodanie drugiej iniekcji IDegAsp lub kolejnych iniekcji insuliny doposiłkowej. Insulina IDegAsp może być też użyta przy inicjowaniu insulinoterapii w warunkach znacznej hiperglikemii, przy zamianie terapii mieszankami insulin ludzkich bądź analogowych na jedną lub dwie iniekcje insuliny IDegAsp, a i to nie wyczerpuje pełnego spektrum jej możliwych zastosowań. Podsumowując, insulina IDegAsp jest wartościowym i bezpiecznym uzupełnieniem możliwości insulinoterapii u pacjentów z cukrzycą typu 2, ale też typu 1.
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Ray, Sumit. "Insulin infusion protocol (Human insulin®/Insugen®)." Current Medicine Research and Practice 4, no. 4 (July 2014): 186–87. http://dx.doi.org/10.1016/j.cmrp.2014.08.007.

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Kucera, Michelle L., and John P. Graham. "Insulin Lispro, a New Insulin Analog." Pharmacotherapy: The Journal of Human Pharmacology and Drug Therapy 18, no. 3 (May 6, 1998): 526–38. http://dx.doi.org/10.1002/j.1875-9114.1998.tb03116.x.

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Insulin lispro is a rapid‐acting insulin analog to regular insulin. Inversion of the proline‐lysine amino acid sequence at positions 28 and 29 on the B chain is responsible for its more rapid absorption, faster onset, and shorter duration of action compared with regular insulin. The fast onset of action allows for greater flexibility in dosing and mealtime scheduling. Insulin lispro provides equivalent or slightly improved glycemic control in patients with types I and II diabetes mellitus compared with regular insulin, without subsequent increases in hypoglycemic episodes. It also results in greater reduction in postprandial blood glucose excursion than regular insulin. Compared with other insulins, insulin lispro represents a more physiologic approach to exogenous insulin therapy.
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ZHANG, Zhou. "Protein engineering of insulin: Two novel fast-acting insulins [B16Ala]insulin and [B26Ala]insulin." Science in China Series C 46, no. 5 (2003): 474. http://dx.doi.org/10.1360/01yc0295.

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Harned, Leighton Kahle, and Edward Chin. "PSUN278 Factitious hypoglycemia, diagnostic delay due to insulin assay failure to detect insulin analogues." Journal of the Endocrine Society 6, Supplement_1 (November 1, 2022): A403. http://dx.doi.org/10.1210/jendso/bvac150.838.

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Abstract Factitious hypoglycemia may be difficult to diagnose clinically. Hypoglycemia due to insulin self-administration is established by the presence of a low c-peptide and elevated plasma insulin levels. Commercial insulin assays often fail to detect insulin analogs and can create confusion among providers investigating causes of hypoglycemia. A 20 year old female with no significant past medical history presented to an Emergency Room (ER) with hypoglycemia. She was treated with a single dose of octreotide 150 mcg, dexamethasone 10 mg PO and started on a D10W drip at 100ml/hr prior to transfer. Laboratory studies on transfer reported plasma glucose 52ng/dL (RR: 70-100), low C-peptide 0.02 (RR: 0.78-5.19), low insulin level <0.087 uIU/mL, normal IGF-I level 122 ng/mL (RR: 85-370). Normal IGF-II level 401 ng/mL (RR: 333-967), and low Pro-insulin level 1.8 pmol/L (RR: 3.6-22 pmol/L). Sulfonylurea Screen was negative. The patient and her mother both denied exogenous insulin use. The patient and her mother both work in healthcare. The patient's boyfriend has type 1 diabetes mellitus and the patient stated she keeps insulin in her purse for him. The patient was admitted for a 72 hour fast and remained normoglycemic. An aliquot of the admission ER insulin blood sample was sent to second laboratory utilizing an assay able to detect analog insulins. The patient's sample previously reporting an undetectable insulin level (<0.087 uIU/mL) now reported an insulin level 8 uIU/mL. Factitious hypoglycemia is a challenging clinical diagnosis. The term factitious implies an attempt to deceive and creates mistrust between the physician and patient. However, hypoglycemia may be the result of medication errors or administered by a second party with the intent to harm. Analog insulins (glargine, aspart, lispro, glulisine, etc) are genetically modified insulins developed to mimic the physiologic pattern of pancreatic beta cell insulin secretion. The amino acid modifications in analog insulins result in structural variations which alters the ability of highly specific commercial automated immunoassays to accurately quantitate these analog insulins. The variation in lab assay detection may cause confusion when interpreting the results. The DiaSorin Liaison XL platform in our hospital utilizes a chemiluminescence immunoassay which does not detect insulin analogs, but detects regular and NPH insulin as they are structurally identical to endogenous human insulin. The second laboratory uses the Siemens Advia Centaur platform, an immunoassay which reacts with insulin analogs "on a nearly equimolar basis with the analogs insulin aspart, insulin glargine, and insulin lispro. Insulin detemir exhibits approximately 50 percent cross-reactivity. Test reactivity with insulin glulisine is negligible (< 3 percent)". Many commercial insulin assays do not detect analog insulins and none qualitatively distinguish between different insulins. Failure to recognize this detection flaw may result in misdiagnosis, patient safety issues and costly unneeded additional studies Presentation: Sunday, June 12, 2022 12:30 p.m. - 2:30 p.m.
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Gargiulo, P., U. Di Mario, O. Zuccarini, F. Troili, C. Tiberti, U. Nicolini, A. Pachi, G. Gerlini, and F. Fallucca. "Treatment of diabetic pregnant women with monocomponent insulins." Acta Endocrinologica 113, no. 3_Suppl (August 1986): S60—S65. http://dx.doi.org/10.1530/acta.0.111s0060.

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Abstract. Very little immunological research has been undertaken in pregnant diabetic women in relation to insulin therapy. We investigated the relations between treatment with insulins of varied immunogenic character and the presence of immune factors such as insulin antibodies, immune complexes and insulin antiinsulin complexes as well as some maternal and neonatal complications of diabetic pregnancy. 128 insulin treated diabetic pregnant women and 121 of their newborns were included in the study. The incidence of insulin antibodies, immune complexes and insulin antiinsulin complexes was lower in patients treated with highly purified insulins than in those treated with conventional insulins. The insulin antibody levels were significantly related to the occurrence of maternal and neonatal morbibity. The presence of insulin antiinsulin complexes in the cord blood of infants of diabetic mothers was related to the presence of these complexes in their mothers. Our results seem to indicate that the use of highly purified insulin could favour the outcome of diabetic pregnancy.
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Mbanya, Jean Claude, Juergen Sandow, Wolfgang Landgraf, and David R. Owens. "Recombinant Human Insulin in Global Diabetes Management – Focus on Clinical Efficacy." European Endocrinology 13, no. 01 (2017): 21. http://dx.doi.org/10.17925/ee.2017.13.01.21.

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Biosynthetic human insulin and insulin analogues are the mainstay of insulin therapy for both type 1 and type 2 diabetes although access to human insulin at affordable prices remains a global issue. The world is experiencing an exponential rise in the prevalence of diabetes presenting an urgent need to establish effective diabetes therapy in countries burdened by inadequate health care budgets, malnutrition and infectious diseases. Recombinant human insulin has replaced animal insulins and animal-based semisynthetic human insulin thereby available in sufficient quantities and at affordable prices able to provide global access to insulin therapy. In many patients, analog insulins can offer additional clinical benefit, although at a considerably higher price thus severely restricting availability in low income countries. The approval process for recombinant human insulins (i.e. biosimilars) and analogue insulins is highly variable in the developing countries in contrast to Europe and in North America, where it is well established within a strict regulatory framework. This review aims to discuss the future access to human insulin therapy in a global context with an ever increasing burden of diabetes and significant economic implications.
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Dissertations / Theses on the topic "Insulin"

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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
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2

Aili, Fagerholm Siri. "Insulin signaling in primary adipocytes in insulin sensitive and insulin resistant states." Doctoral thesis, Linköpings universitet, Avdelningen för cellbiologi, 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-95562.

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Increasing numbers of people world-wide develops the disease type 2 diabetes. Development of type 2 diabetes is characterized by a shift from an insulin sensitive state to an insulin resistant state in peripheral insulin responding organs, which originates from the development of insulin resistance in the adipose tissue. Insulin resistance in combination with reduced pancreatic insulin secretion lead to overt type 2 diabetes. In this thesis, the insulin signaling network in primary adipocytes was analyzed. Key proteins and mechanisms were studied to gain deeper knowledge of signaling both in the insulin sensitive state and in the insulin resistant state produced by rapid weight gain as well as in type 2 diabetes. The surface of the adipocyte is dotted with invaginations in the cell membrane called caveolae that act as important metabolic and signaling platforms in adipocytes, and also harbor the insulin receptor. In paper I we show that insulin stimulation of primary adipocytes results in a rapid phosphorylation of the insulin receptor and caveolin-1, and that internalization of the proteins is mediated by endocytosis of caveolae. Weight gain due to overfeeding and obesity has been associated with the development of insulin resistance in insulin sensitive tissues such as the adipose tissue. In paper II we show that short-term overfeeding for one month of lean subjects results in an insulin resistant state. At the end of the study, the subjects had developed a mild systemic insulin resistance. Moreover, in isolated subcutaneous adipocytes we found several alterations of the insulin signaling pathway that mimicked alterations found in isolated subcutaneous adipocytes from subjects with type 2 diabetes. In paper III we present a first dynamic mathematical model of the insulin signaling network in human adipocytes that are based on experimental data acquired in a consistent fashion. The model takes account of insulin signaling in both the healthy, insulin sensitive state and in the insulin resistant state of type 2 diabetes. We show that attenuated mTORC1-mediated positive feedback to control of phosphorylation of IRS1 at Ser307 is an essential component of the insulin resistant state of type 2 diabetes. A future application of the model is the identification and evaluation of drug targets for the treatment of insulin resistance and type 2 diabetes. In paper IV we examine the protein kinase that catalyzes the insulin stimulated mTORC1- mediated feedback to IRS1. We find that the phosphorylation of IRS1 at Ser307 is not likely to be catalyzed by the kinases S6K1, mTOR or PKB. However, a catalyzing protein kinase for the in vitro phosphorylation of IRS1 at Ser307 was found to be associated with the complex mTORC1. In conclusion, this thesis provide new insights and characterize mechanisms of the intrinsically complex insulin signaling network of primary adipocytes, both in insulin sensitive and insulin resistant states.
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Protzek, André Otavio Peres 1984. "Increased insulin secretion and decreased insulin clearance contributes to the hyperinsulinemia in rats and mice treated with glucocorticoid = Aumento da secreção e redução do clearance de insulina contribuem para a hiperinsulinemia compensatória em ratos e camundongos tratados com glicocorticoide." [s.n.], 2013. http://repositorio.unicamp.br/jspui/handle/REPOSIP/313949.

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Orientadores: Antonio Carlos Boschiero, Alex Rafacho
Tese (doutorado) - Universidade Estadual de Campinas, Instituto de Biologia
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Resumo: Os glicocorticoides (GC) são amplamente utilizados devido aos seus efeitos anti-inflamatórios. Porém, o tratamento com GC pode induzir efeitos deletérios sobre a homeostase glicêmica como a resistência à insulina (RI), intolerância à glicose e, dependendo do tempo e dose, pode levar a instalação do Diabetes mellitus tipo 2 (DM2). Neste sentido, ratos têm sido vastamente utilizados como modelo animal para elucidar as compensações pancreáticas envolvidas na hiperinsulinemia induzida por GC e, poucos estudos enfocando os efeitos do tratamento com GC foram realizados em camundongos. Além disso, não é completamente elucidado se a hiperinsulinemia compensatória induzida pelo tratamento com GC esta associada com alteração do clearance de insulina. Assim, nossos objetivos foram avaliar se: as compensações do pâncreas endócrino em resposta ao tratamento com GC são similares entre camundongos e ratos e, identificar possíveis mecanismos que as expliquem; e se a hiperinsulinemia compensatória induzida pelo tratamento com GC em camundongos e ratos esta associada com alterações do clearance de insulina e a expressão da proteína insuling degrading enzyme (IDE) no fígado. Para isto, camundongos Swiss e ratos Wistar machos foram tratados com o glicocorticoide sintético dexametasona (1 mg/kg p.c.; 5 dias consecutivos). O tratamento com GC induziu RI, hiperinsulinemia e dislipidemia em ambas as espécies, embora mais pronunciado em ratos, que também apresentaram intolerância à glicose e hiperglicemia no jejum. Ambas as espécies tratadas com GC apresentaram incremento da secreção de insulina ex vivo estimulada com glicose, massa e proliferação de células ?, que foram associados com aumento da sinalização da via Ir-?/AKT/mTOR e redução da via AMPK/ACC/AS160 em ilhotas isoladas. O clearance de insulina reduziu em camundongos e ratos tratados com GC, o que foi associado com redução da expressão de IDE no fígado. Desta forma, nossos resultados indicam que camundongos são menos sensíveis aos efeitos deletérios do tratamento com GC sobre a homeostase glicêmica, quando comparado com ratos. Ainda, camundongos e ratos apresentam compensações pancreáticas semelhantes (incremento da função e massa de células ?) em resposta ao tratamento com GC, que foi associado com aumento da sinalização da via canônica de insulina e redução da via não canônica em ilhotas isoladas. Além disso, a redução do clearance de insulina foi, ao menos em parte, devido a redução da expressão de IDE no fígado, o que contribuiu para a hiperinsulinemia compensatória em ambas as espécies tratadas com GC. Em conclusão, estes resultados corroboram a hipótese de que fármacos que inibam a expressão ou atividade da IDE no fígado podem ser uma intervenção anti-diabetogênica que auxilie na manutenção da homeostase glicêmica sem sobrecarregar as células ?
Abstract: Glucocorticoids (GCs) are widely used as anti-inflammatory agent, but they may induce adverse metabolic effects such as insulin resistance (IR), glucose intolerance, and occasionally, diabetes mellitus type 2. Healthy rats have been used as animal models to elucidate the islet compensatory mechanisms involved in these metabolic disturbances, and only a few studies, which have focused on the in vivo effects of GCs, have been conducted in mice models. Yet, whether the reduced insulin clearance also contributes to the compensatory hyperinsulinemia in GC-treated rodents is not fully understood. Here, we aimed to elucidate whether mice and rats share the pancreatic compensations that result in response to dexamethasone (DEX) treatment and also to identify the possible mechanisms that can explain its effects. Yet, we investigated whether the hyperinsulinemia induced by GC treatment in mice and rats is associated with altered hepatic insulin degrading enzyme (IDE) expression and insulin clearance. For this, male Swiss mice and Wistar rats were treated with the synthetic GC dexamethasone (1 mg/kg b.w.; 5 days). DEX treatment induced IR, hyperinsulinemia and dyslipidemia in both species (there was a higher magnitude in rats), but treatment had a greater effect in rats that had glucose intolerance and increased basal blood glucose compared to the control group. Ex vivo insulin secretion at different glucose concentrations was higher in both groups of DEX-treated rodents compared to their controls. Mice and rats showed a significant increase in ?-cell mass due to increased ?-cell proliferation, which was associated with upregulation of the Ir-?/AKT/mTOR and downregulation of AMPK/ACC/AS160 signaling. Insulin clearance reduced in GC-treated mice and rats, which were associated with reduced hepatic IDE expression. Thus, mice are less vulnerable than rats to the deleterious effect of GCs on glucose homeostasis. In addition, rats and mice share common islet compensations (increased ?-cell function and mass) in response to GC treatment, which were associated with increased canonical and decreased non-canonical insulin signaling. Farther, the reduced insulin clearance in GC-treated rodents was, at least in part, due to reduced hepatic IDE expression, which contributed to the compensatory hyperinsulinemia. These findings corroborate the idea that pharmacological interventions that inhibit hepatic IDE may be an alternative anti-diabetic agent that helps to maintain glucose homeostasis due to hyperinsulinemia instead of hypoglycemic agent, which increase the overload in the ?-cells and may lead to ?-cell failure and DM2
Doutorado
Fisiologia
Doutor em Biologia Funcional e Molecular
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4

Tavare, J. M. "The insulin receptor and insulin stimulated protein kinase : Their role in insulin action." Thesis, University of Bristol, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.370675.

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Moraes, Keila Aziz Chehoud de [UNESP]. "Efeitos decorrentes da ingestão do fluoreto na sensibilidade à insulina e transdução do sinal insulínico." Universidade Estadual Paulista (UNESP), 2006. http://hdl.handle.net/11449/95423.

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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
Nos últimos anos tem ocorrido uma redução acentuada nos índices de cárie dentária em diversas regiões do planeta, fato que tem se atribuído ao consumo de produtos fluoretados. Entretanto, o flúor, quando ingerido em excesso, causa intoxicação crônica ou aguda, como a fluorose dentária e distúrbios na homeostase da glicose. As crianças se tornam foco de preocupação, principalmente às portadoras de diabetes mellitus (DM), pois geralmente ingerem grandes quantidades de dentifrício fluoretado durante a escovação, ultrapassando a dose preconizada como limite de ingestão diária de flúor de 0,05 a 0,07mg/F/kg de peso corpóreo. Este trabalho, que foi dividido em duas partes, pretende realizar uma breve revisão de literatura sobre os efeitos decorrentes da ingestão de NaF no metabolismo de carboidratos e avaliar os efeitos da ingestão do fluoreto na sensibilidade à insulina e na transdução do sinal insulínico. A primeira parte, baseada em artigos científicos publicados, procura discorrer sobre os efeitos da ingestão de flúor no metabolismo de carboidratos, na tolerância à glicose e no sinal insulínico, e algumas considerações sobre o diabetes mellitus e sobre as possíveis complicações que a ingestão de NaF pode ocasionar às crianças portadoras desta doença. Estes trabalhos demonstraram que o tratamento agudo ou prolongado com altas doses de fluoreto de sódio interfere na homeostase da glicose. Convém salientar que esta alteração é similar à observada em casos de diabetes mellitus. Além do mais, o flúor quando ingerido em excesso, também ocasiona diminuição da secreção de insulina, inibição da glicólise e depleção de glicogênio. Muitas dessas respostas sugerem que o NaF pode promover resistência à insulina. Portanto, a ingestão em excesso de NaF pode prejudicar a saúde, principalmente de crianças portadora de DM.
Over the last few years there has been a significant reduction in the incidence of dental caries in several regions of the world. This has been attributed to the consumption of fluoridated products. However, excess of fluoride intake can cause chronic or acute intoxication, such as dental fluorosis and impaired glucose homeostasis. Concern is focused on children, especially those with diabetes mellitus, because children usually swallow large amounts of fluoridated dentifrice during tooth brushing, in excess of the maximum recommended daily fluoride dose of 0.05 to 0.07 mg/F/kg of body weight. This report, divided into two parts, intends to make a brief literature review about effects of NAF intake on glucose metabolism, and to determine the effects of this intake on insulin sensitivity and insulin signal transduction. The first part, based on published scientific articles, endeavors to describe the effects of NaF intake on glucose metabolism, glucose tolerance and insulin signal, and put forward considerations concerning diabetes mellitus (DM), and the possible complications that NaF intake could cause in children with DM. These reports demonstrated that the acute or chronic treatment with high sodium fluoride dose interferes in glucose homeostasis, resulting in conditions such as hyperglycemia. This alteration is similar to that observed in DM. Furthermore, NaF ingestion in high doses can produce abnormalities in insulin secretion, glycolysis inhibition, and glycogen depletion. Many of these evidences suggest that NaF can induce insulin resistance. Thus, excessive fluoride consumption could worsen health, particularly of diabetic children. Based on that fluoride can interfere in the glucose metabolism, it is important for the second part of this report to determine the acute effect of fluoride on insulin sensitivity and pp185 (IRS-1/IRS-2) phosphorylation in insulin sensitive tissues.
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Bertelli, Daniela Faleiros. "Mecanismos moleculares envolvidos no controle da ingestão alimentar e do peso corporal : participação da 5PTASE IV." [s.n.], 2006. http://repositorio.unicamp.br/jspui/handle/REPOSIP/312921.

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Orientador: Licio Augusto Velloso
Tese (doutorado) - Universidade Estadual de Campinas, Faculdade de Ciencias Medicas
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Resumo: A enzima fosfatidilinositol 3-quinase (PI3-kinase) exerce uma importante função na transdução dos sinais anorexigênicos e termogênicos enviados pela insulina e leptina em primeira ordem aos neurônios do núcleo arqueado no hipotálamo. A cascata de sinais intracelulares gerados pela ativação da PI3-kinase depende da atividade coordenada de inositol-fosfatases específicas. Neste trabalho, mostramos que a phosphoinositide-specific inositol polyphosphate 5-phosphatase IV (5ptase IV) está altamente expressa em neurônios do núcleo arqueado e lateral do hipotálamo. Submetido ao tratamento intracerebroventricular (ICV) com insulina, a 5ptase IV sofre fosforilação em tirosina de acordo com um padrão tempo-dependente, a qual segue os mesmos moldes da sinalização da insulina através do seu receptor (IR), seu substrato-2 (IRS2) e da PI3-kinase. Para avaliar a participação da 5ptase IV na ação da insulina no hipotálamo, trabalhamos com um oligonucleotídeo antisense específico para esta enzima. O tratamento dos ratos com este oligonucleotídeo durante quatro dias reduziu a expressão hipotalâmica da 5ptase IV em aproximadamente 80%. Tal fato foi acompanhado pela redução de 70% na sua fosforilação induzida pela insulina, e ainda pelo aumento na quantidade basal dos inositóis fosforilados no hipotálamo. Finalmente, a inibição da expressão da 5ptase IV no hipotálamo pelo oligonucleotídeo antisense, resultou na redução da ingestão média diária de alimentos, na perda de massa corporal e ainda na redução da ingestão alimentar em 12 horas. Desta forma, a 5ptase IV é um potente regulador da sinalização através da PI3kinase no hipotálamo e pode tornar-se um alvo interessante para a terapêutica da obesidade e para as desordens relacionadas
Abstract: The enzyme phosphatidylinositol 3-kinase (PI 3-kinase) exerts an important role in the transduction of the anorexigenic and thermogenic signals delivered by insulin and leptin to first-order neurons of the arcuate nucleus in the hypothalamus. The termination of the intracellular signals generated by the activation of PI 3-kinase depends on the coordinated activity of specific inositol phosphatases. Here, we show that phosphoinositide-specific inositol polyphosphate 5-phosphatase IV (5ptase IV) is highly expressed in neurons of the arcuate and lateral nuclei of the hypothalamus. Upon intracerebroventicular (ICV) treatment with insulin, 5ptase IV undergoes a time-dependent tyrosine phosphorylation, which follows the same patterns of canonical insulin signaling through the insulin receptor, IRS-2, and PI 3-kinase. To evaluate the participation of 5ptase IV in insulin action in hypothalamus, we employed a phosphorthioate modified antisense oligonucleotide specific for this enzyme. The treatment of rats with this oligonucleotide for four days reduced the hypothalamic expression of 5ptase IV by ~80%. This was accompanied by a ~70% reduction of insulin-induced tyrosine phosphorylation of 5ptase IV and by an increase in basal accumulation of phosphorylated inositols in the hypothalamus. Finally, inhibition of hypothalamic 5ptase IV expression by the antisense approach resulted in reduced daily food intake, body weight loss and decreased 12 h spontaneous food intake. Thus, 5ptase IV is a powerful regulator of signaling through PI 3-kinase in hypothalamus and may become an interesting target for therapeutics of obesity and related disorders
Doutorado
Biologia Estrutural, Celular, Molecular e do Desenvolvimento
Doutor em Fisiopatologia Medica
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Hagihara, Graziela Neves. "Resposta à angiotensina II em artérias mesentéricas de resistência na obesidade: participação das MAPKs." Universidade de São Paulo, 2012. http://www.teses.usp.br/teses/disponiveis/42/42136/tde-18092012-095317/.

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A angiotensina II (AngII) pode ativar as vias de sinalização das proteínas quinases ativadas por mitógenos (MAPKs). Investigamos o papel da obesidade e das MAPKs na resposta à AngII em ratos obesos por injeção de glutamato monossódico (Ob). Artérias mesentéricas de resistência com endotélio intacto e não as artérias sem endotélio, isoladas de Ob, respondem menos à AngII. As respostas à noradrenalina e ao cloreto de potássio estavam inalteradas. Aumento da expressão do receptor AT2 (AT2R), da óxido nítrico sintase (eNOS) e da ERK1/2 podem estar envolvidos na menor resposta pois a inibição do AT2R, da eNOS e da ERK1/2 corrigiram-na. A maior ativação da ERK1/2 nos Ob levou à maior ativação da eNOS e maior geração de NO, diminuindo a resposta à Ang II. Concluímos que na obesidade, a resposta contrátil à Ang II é menor, como possível mecanismo adaptativo frente ao aumento da ativação do sistema renina-angiotensina. Esse mecanismo envolve a participação do endotélio com maior liberação de NO, aumento do número de AT2R, e da fosforilação da eNOS e da ERK1/2.
Angiotensin II (AngII) can activate mitogen-activated protein kinases (MAPKs) pathways. We investigated the role of obesity and MAPKs in AngII response in monosodium glutamate-induced obese rats (Ob). Endothelium-intact but not endothelium-denuded mesenteric resistance arteries isolated from Ob exhibited a lower response to AngII. The response to nordrenaline and potassium chloride were unaltered. Increased expression of AT2 receptor, nitric oxide synthase (eNOS) and ERK1/2 might be involved in the reduced response since inhibition of AT2R, eNOS and ERK1/2 corrected it. Increased activation of ERK 1/2 in Ob might activate eNOS, generating more NO and vasodilation that contributed to reduce the contraction to AngII. We concluded that, in obesity, the lower response to AngII might be an adaptive mechanism against the increased activation of the renin-angiotensin system. This mechanism involves the participation of the endothelium through a greater release of NO, increased AT2R, eNOS and ERK1/2 expressions.
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Pacheco, Calderón Javier, Fernández Paloma Salas, and Rigo-Righi Carla Galli. "Vanadium Insulin mimetic activity." Revista de Química, 2012. http://repositorio.pucp.edu.pe/index/handle/123456789/100049.

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La diabetes mellitus es un serio desorden metabólicocrónico que se caracteriza por el incremento anormal de laglucosa en la sangre y por complicaciones vasculares yneurológicas. La diabetes mellitus es causada por una falta oun defecto en la acción de la insulina. Si bien actualmenteexisten varios medicamentos orales además de la insulina oanálogos de la insulina, ninguno de estos es el ideal.El vanadio es capaz de imitar los efectos mostrados por lainsulina tanto in vitro como in vivo y se estudia la posibilidadde usar compuestos de vanadio como agentes antidiabéticos. Eneste artículo se revisará la acción insulino-mimética del vanadioy sus posibles mecanismos en comparación con la insulina.
Diabetes mellitus is a serious chronic metabolic disordercharacterized by an increased plasma glucose concentrationand vascular and neurologic complications as well. Diabetesmellitus results from relative or absolute deficiency of insulinsecretion or insulin deficient action. Although there are anumber of oral antidiabetic agents besides insulin or insulinanalogues, none of them is optimal.Vanadium can mimic insulin effects in vitro and in vivoand the possibility of using vanadium compounds asantidiabetic agents is under study. This review will summarizethe insulin mimetic action of vanadium and its possiblemechanisms in comparison with insulin.
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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.
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Gormley, M. J. J. "Aspects of insulin treatment of non-insulin-dependent diabetes." Thesis, Queen's University Belfast, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.373006.

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Books on the topic "Insulin"

1

Cuatrecasas, Pedro, and Steven Jacobs, eds. Insulin. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-74098-5.

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Brian, Kahn. Insulin. Cambridge: Cambridge Micro Software, 1987.

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United States. Food and Drug Administration. Office of Women's Health. Insulin. Washington, D.C.]: Dept. of Health and Human Services, FDA, Office of Women's Health, 2010.

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Pedro, Cuatrecasas, Jacobs Steven 1946-, and Avruch J, eds. Insulin. Berlin: Springer-Verlag, 1990.

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Eleazar, Shafrir, and Hansen Barbara C, eds. Insulin resistance and insulin resistance syndrome. London: Taylor & Francis, 2002.

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Zeitler, Philip S., and Kristen J. Nadeau, eds. Insulin Resistance. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-25057-7.

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Srivastava, Ashok K., and Barry I. Posner, eds. Insulin Action. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-5647-3.

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Reaven, Gerald M., and Ami Laws, eds. Insulin Resistance. Totowa, NJ: Humana Press, 1999. http://dx.doi.org/10.1007/978-1-59259-716-1.

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Strachan, Mark W. J., and Brian M. Frier. Insulin Therapy. London: Springer London, 2013. http://dx.doi.org/10.1007/978-1-4471-4760-2.

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Zeitler, Philip Scott, and Kristen J. Nadeau, eds. Insulin Resistance. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-59745-192-5.

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Book chapters on the topic "Insulin"

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Titchener, Janet. "Insulins and insulin management." In Diabetes Management, 25–37. First edition. | Boca Raton: CRC Press, 2020.: CRC Press, 2020. http://dx.doi.org/10.1201/9780429326196-6.

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Titchener, Janet. "Insulins and insulin management." In Diabetes Management, 25–37. First edition. | Boca Raton: CRC Press, 2020.: CRC Press, 2020. http://dx.doi.org/10.4324/9780429326196-6.

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Brandenburg, D. "Insulin Chemistry." In Insulin, 3–22. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-74098-5_1.

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Hollenberg, M. D. "Insulin Receptor-Mediated Transmembrane Signalling." In Insulin, 183–207. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-74098-5_10.

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Rothenberg, P., M. F. White, and C. R. Kahn. "The Insulin Receptor Tyrosine Kinase." In Insulin, 209–36. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-74098-5_11.

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Levy, J. R., and J. M. Olefsky. "Receptor-Mediated Internalization and Turnover." In Insulin, 237–66. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-74098-5_12.

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Jacobs, S. "Insulin-like Growth Factor I Receptors." In Insulin, 267–86. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-74098-5_13.

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Saltiel, A. R., and P. Cuatrecasas. "Second Messengers of Insulin Action." In Insulin, 289–311. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-74098-5_14.

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Avruch, J., H. E. Tornqvist, J. R. Gunsalus, E. J. Yurkow, J. M. Kyriakis, and D. J. Price. "Insulin Regulation of Protein Phosphorylation." In Insulin, 313–66. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-74098-5_15.

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Larner, J. "Effects of Insulin on Glycogen Metabolism." In Insulin, 367–84. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-74098-5_16.

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Conference papers on the topic "Insulin"

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Goodwin, P. "Obesity, Insulin Resistance and Insulin." In Abstracts: Thirty-Second Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 10‐13, 2009; San Antonio, TX. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-09-ms2-1.

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Lin, J., P. Docherty, A. Le Compte, U. Jamaludin, C. E. Hann, N. N. Razak, J. G. Chase, C. G. Pretty, and G. M. Shaw. "Modeled Insulin Sensitivity and Interstitial Insulin Action from a Pilot Study of Dynamic Insulin Sensitivity Tests." In UKACC International Conference on CONTROL 2010. Institution of Engineering and Technology, 2010. http://dx.doi.org/10.1049/ic.2010.0358.

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Jayaraj, Nivethitha, C. Mathew Cherian, and S. Ganesh Vaidyanathan. "Intelligent Insulin Infuser." In 2009 Third UKSim European Symposium on Computer Modeling and Simulation. IEEE, 2009. http://dx.doi.org/10.1109/ems.2009.64.

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Vereshchetin, Paul, Marc Breton, and Stephen D. Patek. "Mealtime correction insulin advisor for CGM-informed insulin pen therapy." In 2013 American Control Conference (ACC). IEEE, 2013. http://dx.doi.org/10.1109/acc.2013.6580277.

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Cesar, Palerm,. "Physiologic Insulin Delivery with Insulin Feedback: A Control Systems Perspective." In Modeling and Control in Biomedical Systems, edited by Rees, Stephen, Chair Andreassen, Steen and Andreassen, Steen. Elsevier, 2009. http://dx.doi.org/10.3182/20090812-3-dk-2006.00006.

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Baura, Gail D., David M. Foster, and Michael W. Schwartz. "Insulin receptors facilitate insulin transport into the central nervous system." In 1992 14th Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 1992. http://dx.doi.org/10.1109/iembs.1992.5761454.

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Baura, Foster, and Schwartz. "Insulin Receptors Facilitate Insulin Transport Into The Central Nervous System." In Proceedings of the Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 1992. http://dx.doi.org/10.1109/iembs.1992.592647.

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Nowak-Göttl, U., W. D. Kreuz, M. John, B. Krackhardt, H.-P. Grüttner, H. K. Breddin, and F. kollmann. "HAEMOSTASEOLOGICAL CHANGES IN DIABETIC CHILDREN (HUMAN INSULIN VERSUS PORCINE INSULIN." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643099.

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Changes of haemostaseological parameters are involved in pathogenesis of diabetic angiopathy. However it is not yet clear whether they are cause or consequence of the endothelial damage. We investigated coagulation parameters in 84 children with type I diabetes mellitus without clinical signs of vascular disease.Compared to the control group no significant changes could be seen in fibrinogen, plasminogen, protein C, α 1 antichymotrypsin, β-thrombo-globulin and ristocetin - induced aggregation.Additionally we could observe significant differences in patients treated with human insulin to those treated with porcine insulin. Spontaneous platelet aggregation (PAT III) and factor VIII C correlated to the duration of diabetes. Also to the mean metabolic equilibrium (HBA1) correlations could be found. Spontaneous platelet aggregation seems to be a useful parameter to assess the onset of atherosclerotic diseases in diabetic children. High values of von Willebrand factor may indicate reversible and/or irreversible damage of vascular endothelium.
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Klenner, Jacob B., Benjamin A. Van Noorden, Jennifer L. Knopp, Lui R. Holder Pearson, Anna R. Hardy, Sarah L. Vergeer, Geoffrey M. Shaw, and J. Chase. "Determining the effects of insulin Detemir on endogenous secretion of insulin." In 2019 41st Annual International Conference of the IEEE Engineering in Medicine & Biology Society (EMBC). IEEE, 2019. http://dx.doi.org/10.1109/embc.2019.8857643.

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Park, Eun-Joo, Jeff Dodds, Nadine Barrie Smith, Kullervo Hynynen, and Jacques Souquet. "Dose comparison of ultrasonic transdermal insulin delivery to subcutaneous insulin injection." In 9TH INTERNATIONAL SYMPOSIUM ON THERAPEUTIC ULTRASOUND: ISTU—2009. AIP, 2010. http://dx.doi.org/10.1063/1.3367167.

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Reports on the topic "Insulin"

1

Anthony Di Franco, Anthony Di Franco. Open Insulin. Experiment, July 2015. http://dx.doi.org/10.18258/5755.

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Muti, Paola. Insulin and Breast Cancer Risk. Fort Belvoir, VA: Defense Technical Information Center, June 2001. http://dx.doi.org/10.21236/ada395852.

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Muti, Paola. Insulin and Breast Cancer Risk. Fort Belvoir, VA: Defense Technical Information Center, June 2000. http://dx.doi.org/10.21236/ada383382.

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Silva, Rodrigo Ribeiro e., Mateus de Miranda Gauza, Julia Opolski Nunes da Silva Opolski, and Maria Eduarda Schramm Guisso. Once-Weekly Insulin Icodec vs Once-Daily Insulin Glargine U100 for Type 2 Diabetes: A Meta-analysis of Phase 2 Randomized Controlled Trials. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, May 2022. http://dx.doi.org/10.37766/inplasy2022.5.0102.

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Review question / Objective: To compare Once-Weekly Insulin Icodec and Once-Daily Insulin Glargine U100 in patients with Type 2 Diabetes Mellitus using oral hypoglycemic drugs in need of insulin therapy. Condition being studied: Patients with Diabetes Mellitus Type 2 using oral hypoglycemic drugs in need for basal insulin. Eligibility criteria: Inclusion in this meta-analysis was restricted to studies that met all the following criteria: (1) randomized trials; (2) comparing the use once weekly insulin icodec to once daily insulin glargine; (3) enrolling patients with type 1 or type 2 diabetes mellitus; (4) evaluating any of the desired outcomes; (4) articles in written on english language. We excluded studies with (1) no control group; (2) overlapping studies population; clinical trial register entry only; (3) non-human studies and (4) studies reported only as abstracts.
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Long, Cong, XUke Han, Yunjiao Yang, Tongyi Li, Qian Zhou, and Qiu Chen. Efficacy of Intranasal Insulin in Improving Cognition in Mild Cognitive Impairment or Dementia: A Systematic Review and Meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, August 2022. http://dx.doi.org/10.37766/inplasy2022.8.0054.

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Review question / Objective: How does the efficacy of Intranasal Insulin in improving Cognition in Mild Cognitive Impairment or Dementia. Condition being studied: Insulin regulates many aspects of brain function related to mild cognitive impairment (MCI) or dementia, which can be delivered to the brain center via intranasal (IN) devices. Some small, single-site studies indicated that intranasal insulin can enhance memory in patients with MCI or dementia. The pathophysiology of Alzheimer disease (AD) and diabetes mellitus (DM) overlap, making insulin an attractive therapy for people suffering from MCI or dementia. The goal of the study is to evaluate the effectiveness of IN insulin on cognition in patients with MCI or dementia.
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ZHU, Dongshan. The lifestyle changes after initiating basal insulin in insulin naive patients with type 2 diabetes: Results from the ORBIT study. Science Repository, June 2019. http://dx.doi.org/10.31487/j.jicoa.2019.02.04.

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Shi, Jinping, Feng L, Liting X, Jing L, and Xing L. Meta analysis of efficacy and safety of insulin aspart and biosynthetic human insulin in the treatment of gestational diabetes mellitus. Xi'an International Medical Center Hospital, July 2021. http://dx.doi.org/10.37766/inplasy2021.7.0047.

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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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Cleveland, Rebecca J., Marilie D. Gammon, and Ralph S. Baric. Insulin-Like Growth Factor I Polymorphisms in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, September 2002. http://dx.doi.org/10.21236/ada412654.

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Smith, Nadine, Michael Pishko, Robert Gabbay, and Jacob Werner. Closed-Loop Noninvasive Ultrasound Glucose Sensing and Insulin Delivery. Fort Belvoir, VA: Defense Technical Information Center, September 2006. http://dx.doi.org/10.21236/ada458974.

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