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Videos de Conceptos Relacionados

Glucose Homeostasis: Pancreatic Islets and Insulin Secretion01:27

Glucose Homeostasis: Pancreatic Islets and Insulin Secretion

The pancreatic islets comprising only 1%-2% of the volume are highly vascularized and innervated mini-organs. They contain five endocrine cell types, including β cells that secrete insulin, which is synthesized as a single polypeptide chain, preproinsulin, processed to proinsulin, and finally to insulin and C-peptide. This process is complex and regulated, involving the Golgi complex, the endoplasmic reticulum, and the secretory granules of the β cell.
Insulin and C-peptide are co-secreted in...
Oral Hypoglycemic Agents: Biguanides and Glitazones01:26

Oral Hypoglycemic Agents: Biguanides and Glitazones

Biguanides, particularly metformin (Glucophage), are insulin sensitizers that enhance glucose uptake, thereby reducing insulin resistance. Unlike sulfonylureas, metformin doesn't prompt insulin secretion, which helps to curb hypoglycemia risk. Metformin is beneficial in treating conditions like polycystic ovary syndrome due to its insulin-resistance reduction capability. The drug's primary action involves curtailing hepatic gluconeogenesis, a significant contributor to high blood glucose levels...
Oral Hypoglycemic Agents: Glinides01:06

Oral Hypoglycemic Agents: Glinides

Repaglinide (Prandin) and Nateglinide (Starlix), known as glinides, are oral insulin secretagogues that stimulate insulin release from pancreatic β cells by closing the ATP-sensitive potassium channels (KATP channel). Repaglinide controls insulin release from pancreatic β cells by managing potassium efflux. It shares two binding sites with sulfonylureas and also has a unique site, indicating overlapping mechanisms of action. With a rapid onset and a 4-7 hour duration, it effectively manages...
Oral Hypoglycemic Agents: α-Glucosidase Inhibitors01:19

Oral Hypoglycemic Agents: α-Glucosidase Inhibitors

α-glucosidase inhibitors, including acarbose (Precose), miglitol (Glyset), and voglibose (Voglib) (primarily available in Asia), are drugs that control blood sugar levels by delaying the digestion of starch and disaccharides. They achieve this by inhibiting α-glucosidase enzymes in the intestine, which slow the absorption of carbohydrates in the intestine, which in turn leads to a prolonged release of the glucoregulatory hormone GLP-1 from intestinal L-cells.
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Glucagon-like Receptor Agonists01:24

Glucagon-like Receptor Agonists

Incretins include glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), which stimulate insulin secretion post-meals. In type 2 diabetes, GIP's efficacy is reduced, making GLP-1 a viable drug target. GIP originates from preproGIP.
GLP-1, when administered in high doses intravenously, triggers insulin secretion, inhibits glucagon release, slows gastric emptying, reduces food intake, and restores normal insulin secretion. However, its rapid inactivation by the...
Dipeptidyl Peptidase 4 Inhibitors01:23

Dipeptidyl Peptidase 4 Inhibitors

Dipeptidyl peptidase 4 (DPP-4) is a serine protease widely distributed in the body. It's involved in the inactivation of GLP-1 and GIP hormones, which are crucial for insulin regulation. DPP-4 inhibitors, such as sitagliptin (Januvia), saxagliptin (Onglyza), linagliptin (Tradjenta), alogliptin (Nesina), and vildagliptin (Galvus), help increase the proportion of active GLP-1, enhancing insulin secretion. These inhibitors work by competitively binding to DPP-4. This binding causes a significant...

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Updated: Jul 16, 2026

Mixed Primary Cultures of Murine Small Intestine Intended for the Study of Gut Hormone Secretion and Live Cell Imaging of Enteroendocrine Cells
09:16

Mixed Primary Cultures of Murine Small Intestine Intended for the Study of Gut Hormone Secretion and Live Cell Imaging of Enteroendocrine Cells

Published on: April 20, 2017

Los análogos del meglitinuro insulinotrópico son análogos del meglitinuro.

A Dornhorst1

  • 1Department of Metabolic Medicine, Faculty of Medicine, Imperial College, Hammersmith Hospital Campus, Du Cane Road, W12 0NN, London, UK. a.dornhorst@ic.ac.uk

Lancet (London, England)
|December 1, 2001
PubMed
Resumen

La pérdida de la secreción temprana de insulina es clave en la diabetes tipo 2. Los nuevos fármacos de meglitinida pueden restaurar esto, retrasando potencialmente la necesidad de terapia con insulina.

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Área de la Ciencia:

  • Endocrinología Endocrinología.
  • Farmacología Farmacología.
  • Enfermedades Metabólicas Las enfermedades metabólicas.

Sus antecedentes:

  • La secreción de insulina en fase temprana es crucial para el manejo del metabolismo postprandial.
  • La diabetes tipo 2 se caracteriza por la pérdida de esta liberación temprana de insulina.
  • Los agentes hipoglucémicos orales convencionales no controlan adecuadamente los niveles de glucosa postprandial.

Objetivo del estudio:

  • Explorar la lógica para el desarrollo de agentes dirigidos a la liberación de insulina en fase temprana.
  • Introducir análogos de meglitinida como una nueva clase terapéutica para la diabetes tipo 2.
  • Para discutir el potencial de estos agentes en terapias de combinación.

Principales métodos:

  • Revisión de la literatura existente sobre la fisiopatología y el tratamiento de la diabetes tipo 2.
  • Análisis del mecanismo de acción de los análogos de la meglitinida.
  • Evaluación de posibles terapias combinadas con metformina y tiazolidinedionas.

Principales resultados:

  • Los análogos de la meglitinida (repaglinida, nateglinida, mitiglinida) pueden restaurar la liberación de insulina en su fase inicial.
  • Estos agentes son adecuados para la combinación con metformina.
  • Eficacia potencial en combinación con tiazolidinedionas, que abordan la resistencia a la insulina.

Conclusiones:

  • Los agentes orales más nuevos, específicamente los meglitinidos, ofrecen un enfoque dirigido para restaurar la secreción temprana de insulina.
  • Las terapias combinadas que involucran meglitinidas pueden mejorar el control glucémico y potencialmente extender la función de las células beta.
  • El objetivo es retrasar la eventual necesidad de insulina exógena en el manejo de la diabetes tipo 2.