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1.
Evid. actual. práct. ambul ; 24(4): e002166, 2021.
Article in Spanish | LILACS, UNISALUD, BINACIS | ID: biblio-1359440

ABSTRACT

En este artículo, la autora jerarquiza la relevancia de la eficacia documentada de los agonistas del péptido similar alglucagón-1 y los inhibidores del cotransportador sodio-glucosa tipo 2, que ha conducido a recientes modificaciones en el paradigma del cuidado en los pacientes con diabetes tipo 2. (AU)


In this article, the author highlights the relevance of the documented efficacy of glucagon-like peptide-1 agonists and type 2 sodium-glucose cotransporter inhibitors, which has led to recent changes in the paradigm of care in patients with type 2diabetes. (AU)


Subject(s)
Humans , Diabetes Mellitus, Type 2/drug therapy , Glucagon-Like Peptide 1/therapeutic use , Glucagon-Like Peptide 1/agonists , Sodium-Glucose Transporter 2 Inhibitors/therapeutic use , Hypoglycemic Agents/therapeutic use
2.
Rev. chil. endocrinol. diabetes ; 12(2): 124-132, abr. 2019. tab, ilus
Article in Spanish | LILACS | ID: biblio-995453

ABSTRACT

La diabetes mellitus tipo 1 (DM1), es una enfermedad crónica caracterizada por la deficiencia de insulina debido a la pérdida de células ß pancreáticas, las alteraciones hormonales en la DM 1 no se limitan a la deficiencia de insulina; existiendo también secreción inadecuadada de glucagón en el período postprandial. Aunque el control glucémico con terapias intensivas con insulina ha reducido la incidencia de complicaciones microvascular y macrovasculares. La mayoría de las personas con DM1 tienen un control glucémico subóptimo; Por lo tanto, el uso de farmacoterapia adyuvante para mejorar el control ha sido de interés clínico. El uso de estos nuevos medicamentos brindaría la oportunidad de imitar más de cerca la fisiología pancreática normal, y contrarrestar otros mecanismos fisiopatológicos diferentes a Insulinopenia; contribuyendo a lograr un mejor control metabólico y expectativa de vida.


Type 1 diabetes mellitus (T1DM), is a chronic disease characterized by insulin deficiency due to the loss of pancreatic ß cells, the hormonal alterations in T1DM are not limited to insulin deficiency; there is also a deregulated glucagon secretion in the postprandial period. Although glycemic control with intensive therapies with insulin has reduced the incidence of microvascular and macrovascular complications, most people with T1DM1 glycemic control; therefore, the use of adjuvant pharmacotherapy to improve control has been of clinical interest. The use of these new drugs would offer the opportunity to imitate more closely the normal pancreatic physiology, and to counteract other physiopathological mechanisms different from insulinopenia; contributing to achieve better metabolic control and life expectancy.


Subject(s)
Humans , Diabetes Mellitus, Type 1/drug therapy , Hypoglycemic Agents/therapeutic use , Insulin/therapeutic use , Chemotherapy, Adjuvant , Glucagon-Like Peptide 1/therapeutic use , Sodium-Glucose Transporter 2/antagonists & inhibitors , Dipeptidyl-Peptidase IV Inhibitors/therapeutic use , Metformin/therapeutic use
4.
Prensa méd. argent ; 95(8): 505-511, oct. 2008. graf
Article in Spanish | LILACS | ID: lil-521977

ABSTRACT

Type II diabetes is a disease characterized by insuline resistance and abnormalities of the B-cells, and it is associated with hyperglucosanemia, the increase of the production of hepatic glucose and with obesity. This article refers to a new therapeutic tool for the treatment of type II diabetes: the incretin system. The efficacy and safety of incretin therapy for diabetes mellitus type II, is referred in the article. Furher studies are required to achieve a definitive evaluative conclusion about these therapeutic agents.


Subject(s)
Humans , Bariatric Surgery , /diagnosis , /therapy , Incretins/therapeutic use , Glucagon-Like Peptide 1/therapeutic use
5.
Arq. bras. endocrinol. metab ; 52(2): 279-287, mar. 2008.
Article in Portuguese | LILACS | ID: lil-480997

ABSTRACT

Desde o Diabetes Control and Complications Trial (DCCT), a terapia insulínica intensiva tem sido direcionada para alcançar valores de glicemia e hemoglobina glicada (HbA1c) tão próximos do normal quanto a segurança permita. Entretanto, a hiperglicemia (especialmente a hiperglicemia pós-prandial) e a hipoglicemia continuam a ser um problema no manejo do diabetes tipo 1. O objetivo de associar outras drogas à terapia insulínica é diminuir a glicemia pós-prandial. A terapia adjunta pode ser dividida em três grupos, conforme seu mecanismo de ação: 1. Aumento da ação da insulina (metformina e tiazolidinedionas); 2. Alteração da liberação de nutrientes no trato gastrintestinal (acarbose e amilina); 3. Outros modos de ação [pirenzepina, fator de crescimento insulina-símile (IGF-1) e peptídeo semelhante ao glucagon 1 (GLP-1). Muitos desses agentes mostraram, em estudos de curto prazo, diminuição de 0,5 por cento a 1 por cento na HbA1c, diminuir a hiperglicemia pós-prandial e as doses diárias de insulina.


Since Diabetes Control and Complications Trial (DCCT), intensive therapy has been directed at achieving glucose and glycosylated hemoglobin (HbA1c) values as close to normal as possible regarding safety issues. However, hyperglycemia (especially postprandial hyperglycemia) and hypoglicemia continue to be problematic in the management of type 1 diabetes. The objective of associating other drugs to insulin therapy is to achieve better metabolic control lowering postprandial blood glucose levels. Adjunctive therapies can be divided in four categories based on their mechanism of action: enhancement of insulin action (e.g. the biguanides and thiazolidinediones), alteration of gastrointestinal nutrient delivery (e.g. acarbose and amylin) and other targets of action (e.g. pirenzepine, insulin-like growth factor I and glucagon-like peptide-1). Many of these agents have been found to be effective in short-term studies with decreases in HbA1c of 0.5-1 percent, lowering postprandial blood glucose levels and decreasing daily insulin doses.


Subject(s)
Humans , Blood Glucose/drug effects , Diabetes Mellitus, Type 1/drug therapy , Glycated Hemoglobin/metabolism , Hypoglycemic Agents/therapeutic use , Insulin/therapeutic use , Thiazolidinediones/therapeutic use , Acarbose/metabolism , Acarbose/therapeutic use , Amyloid/metabolism , Amyloid/therapeutic use , Drug Therapy, Combination , Diabetes Mellitus, Type 1/metabolism , Gastrointestinal Tract/drug effects , Gastrointestinal Tract/metabolism , Glucagon-Like Peptide 1/analogs & derivatives , Glucagon-Like Peptide 1/metabolism , Glucagon-Like Peptide 1/therapeutic use , Hyperglycemia/drug therapy , Hyperglycemia/metabolism , Hypoglycemia/drug therapy , Incretins/metabolism , Incretins/therapeutic use , Insulin-Like Growth Factor I/metabolism , Insulin-Like Growth Factor I/therapeutic use , Metformin/therapeutic use , Muscarinic Antagonists/metabolism , Muscarinic Antagonists/therapeutic use , Postprandial Period , Pirenzepine/metabolism , Pirenzepine/therapeutic use
6.
Cardiovasc. j. Afr. (Online) ; 19(2): 77-83, 2008.
Article in English | AIM | ID: biblio-1260373

ABSTRACT

Glucagon-like peptide-1 is an incretin hormone proposed to have insulinomimetic effects on peripheral insulin-sensitive tissue. We examined these effects on the heart by using isolated; perfused rat hearts and adult ventricular myocytes. During normoxic perfusion; no effects of escalating concentrations of GLP-1 on either heart rate or left ventricular developed pressure were found. With functional performance as readout; we found that GLP-1 directly protected the heart against damage incurred by global low-flow ischaemia. This protection was sensitive to the presence of iodo-acetate; implicating activation of glycolysis; and was abolished by wortmannin; indicative of Pi-3-kinase as mediator of protection. in addition; GLP-1 had an infarct-sparing effect when supported by the presence of the dipeptidyl peptidase-iv inhibitor valine pyrrolidide. GLP-1 could not directly activate protein kinase B (also called Akt) or the extracellular regulated kinases Erk1/2 in hearts or cardiocytes under normoxic conditions; but phosphorylation of the AMP-activated kinase (AMPK) on Thr172 was enhanced. in addition; the glycolytic enzyme phosphofructokinase-2 was activated dose dependently. During reperfusion after ischaemia; modulation of the phosphorylation of PKB/Akt as well as AMPK was evident. GLP-1 therefore directly protected the heart against low-flow ischaemia by enhancing glycolysis; probably via activation of AMP kinase and by modulating the profile of activation of the survival kinase PKB/Akt


Subject(s)
Glucagon-Like Peptide 1/therapeutic use , Heart , Ischemia/prevention & control
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