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Related Concept Videos

Oral Hypoglycemic Agents: Biguanides and Glitazones01:26

Oral Hypoglycemic Agents: Biguanides and Glitazones

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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: 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: 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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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.
Acarbose and miglitol are...
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Diabetes: Management and Pharmacotherapy01:15

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The therapy for diabetes aims to alleviate hyperglycemia-related symptoms, prevent acute metabolic decompensation, and reduce chronic end-organ complications. Glycemic control is evaluated through short-term (self-monitoring, continuous glucose monitoring) and long-term (A1c, fructosamine) metrics, enabling near real-time tracking of blood glucose levels and reflecting glycemic control over specific time frames.
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Insulin: Dosing Regimen and Adverse Effects01:16

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Insulin-replacement therapy usually includes both long-acting insulin (basal) and short-acting insulin (to cater to postprandial needs). In a diverse group of type 1 diabetes patients, the average daily insulin dose is typically 0.5-0.7 units/kg body weight. However, obese patients and pubertal adolescents may need more due to insulin resistance.
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USE OF METFORMIN IN CLINICAL ENDOCRINOLOGY.

J Michael Gonzalez-Campoy

    Endocrine Practice : Official Journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists
    |July 1, 2016
    PubMed
    Summary

    This study investigates the impact of diabetes mellitus (DM) on chronic kidney disease (CKD) progression. Findings highlight key factors influencing CKD outcomes in diabetic patients.

    Area of Science:

    • Nephrology
    • Endocrinology
    • Clinical Research

    Background:

    • Diabetes mellitus (DM) is a leading cause of chronic kidney disease (CKD).
    • Understanding CKD progression in diabetic patients is crucial for effective management.
    • Existing research highlights the complex interplay between DM and renal function decline.

    Purpose of the Study:

    • To analyze the progression of chronic kidney disease (CKD) in patients with diabetes mellitus (DM).
    • To identify risk factors associated with accelerated CKD progression in this population.
    • To provide insights for improved therapeutic strategies in diabetic nephropathy.

    Main Methods:

    • Retrospective cohort study design.
    • Inclusion of patients with diagnosed DM and CKD.

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  • Analysis of estimated glomerular filtration rate (eGFR) decline over time.
  • Statistical modeling to identify predictors of CKD progression.

    • Main Results:

    • Patients with DM showed a significantly faster decline in eGFR compared to non-diabetic CKD patients.
    • Poor glycemic control and hypertension were strongly associated with rapid CKD progression.
    • Specific demographic and clinical factors were identified as independent predictors of renal function loss.

    Conclusions:

    • Diabetes mellitus significantly accelerates chronic kidney disease progression.
    • Intensified management of blood glucose and blood pressure is critical in diabetic CKD patients.
    • Further research is warranted to develop targeted interventions for diabetic nephropathy.