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Related Concept Videos

Oral Hypoglycemic Agents: α-Glucosidase Inhibitors01:19

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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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Oral Hypoglycemic Agents: Glinides01:06

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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...
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Oral Hypoglycemic Agents: Biguanides and Glitazones01:26

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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...
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Oral Hypoglycemic Agents: Sulfonylureas01:17

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Sulfonylureas are oral hypoglycemic agents utilized in treating type 2 diabetes. They are characterized by their unique sulfonylurea chemical structure. The family of sulfonylureas is divided into generations. First-generation sulfonylureas, including tolbutamide (Orinase), chlorpropamide (Diabinese), and tolazamide (Tolinase), trigger insulin release from pancreatic β cells and enhance peripheral tissues' insulin sensitivity. The second-generation members, such as glipizide...
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Diabetes: Symptoms, Diagnosis, and Complications01:15

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For most patients, experiencing several weeks of polyuria, polydipsia, fatigue, and significant weight loss may indicate the presence of diabetes. Furthermore, adults displaying the phenotypic appearance of type 2 diabetes (particularly those who are obese and not initially insulin-requiring), may have islet cell autoantibodies, suggesting autoimmune-mediated β cell destruction and a diagnosis of latent autoimmune diabetes of adults (LADA). The categorization of glucose homeostasis is...
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Glucagon-like Receptor Agonists01:24

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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...
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Developing a definition for Oral Antidiabetic Drug (OAD) Failure.

Sushil Jindal1, Sanjay Kalra2

  • 1Department of Medicine, People's College of Medical Sciences, Bhopal, India.

JPMA. the Journal of the Pakistan Medical Association
|March 25, 2020
PubMed
Summary
This summary is machine-generated.

Oral antidiabetic drug failure occurs when HbA1c remains high despite optimal therapy. This study proposes a clear definition for oral antidiabetic drug failure in clinical practice.

Keywords:
Clinical inertia, diabetes, HbA1c, insulin, insulin initiation, metformin, sulfonylurea Approach

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Area of Science:

  • Endocrinology
  • Metabolic Diseases
  • Pharmacology

Background:

  • Oral antidiabetic drug failure is frequently discussed but lacks a standardized definition.
  • Current clinical practice lacks a uniform understanding of when oral antidiabetic therapies are considered ineffective.

Purpose of the Study:

  • To develop a working definition for oral antidiabetic drug failure.
  • To establish clear criteria for identifying treatment failure in patients with type 2 diabetes on oral medications.

Main Methods:

  • Literature review and conceptual analysis of existing clinical practices.
  • Assessment of oral antidiabetic drug classes, lifestyle factors, and secondary causes of hyperglycemia.
  • Incorporation of symptomatology and glycemic control metrics (HbA1c, plasma glucose).

Main Results:

  • Proposed definition: HbA1c above goal despite optimal doses of three different oral glucose-lowering drugs (including metformin and preferably a sulfonylurea), with adequate lifestyle and no secondary causes of hyperglycemia.
  • Alternative definition: Patients exhibiting symptoms of insulinopenia (e.g., osmotic symptoms, weight loss) and uncontrolled glycemia (plasma glucose > 300 mg/dL) despite triple oral therapy.

Conclusions:

  • A precise definition of oral antidiabetic drug failure is crucial for effective diabetes management.
  • The proposed definition aids clinicians in identifying patients requiring intensified treatment strategies beyond current oral regimens.