Very fast onset, short duration

Can be taken before meals; duration of action is 4-5 hours

Reduce circulating glucose and promote synthesis of glycogen, lipid, and protein

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Used in continuous infusion devices

Very fast onset, short duration

Can be taken before meals; duration of action is 4-5 hours

Reduce circulating glucose and promote synthesis of glycogen, lipid, and protein

“

Used in continuous infusion devices

Very fast onset, short duration

Can be taken before meals; duration of action is 4-5 hours

Reduce circulating glucose and promote synthesis of glycogen, lipid, and protein

“

Used in continuous infusion devices

Rapid onset (<30 min) and lasts 5-8 hours; must be taken 30-45 min before meal time to minimize mismatching

Reduce circulating glucose and promote synthesis of glycogen, lipid, and protein

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Diabetic ketoacidosis; rapidly changing insulin requirement such as after surgery or during acute infections (Only insulin that can be administered IV.)

Rapid onset (<30 min) and lasts 5-8 hours; must be taken 30-45 min before meal time to minimize mismatching

Reduce circulating glucose and promote synthesis of glycogen, lipid, and protein

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Diabetic ketoacidosis; rapidly changing insulin requirement such as after surgery or during acute infections (Only insulin that can be administered IV.)

Onset 2-5 hours and duration 4-12 hours.

Usually mixed with regular, lispro, apart, or glulisin insulin.

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Highly unpredictable action, variability of absorption >50%, use is waning due to availability of long-acting insulin

Onset 2-5 hours and duration 4-12 hours.

Usually mixed with regular, lispro, apart, or glulisin insulin.

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Highly unpredictable action, variability of absorption >50%, use is waning due to availability of long-acting insulin

Slow onset (1-1.5 hours) and duration of > 11-24 hours.

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Background insulin replacement

Onset 1-2 hours and duration > 24 hours.

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Most reproducible effect and is associated with less hypoglycemia.

Secretagogue: Bind to a sulfonylurea receptor that is associated with the β-cell inward rectifier ATP-sensitive K⁺ channel. Binding inhibits efflux of K⁺ ions, causing depolarization and opening of voltage-gated calcium channels. Allows calcium influx & subsequent release of insulin.

Hypoglycemia, weight gain, GI problems, headache, teratogenic

Type 2 diabetes

In patients with functioning β-cells, reduce circulating glucose.  Increase glycogen, fat, and protein formation, gene regulation

Secretagogue: Bind to a sulfonylurea receptor that is associated with the β-cell inward rectifier ATP-sensitive K⁺ channel. Binding inhibits efflux of K⁺ ions, causing depolarization and opening of voltage-gated calcium channels. Allows calcium influx & subsequent release of insulin.

Hypoglycemia, weight gain, GI problems, headache, teratogenic

Type 2 diabetes

In patients with functioning β-cells, reduce circulating glucose.Increase glycogen, fat, and protein formation, gene regulation

Secretagogue: Bind to a sulfonylurea receptor that is associated with the β-cell inward rectifier ATP-sensitive K⁺ channel. Binding inhibits efflux of K⁺ ions, causing depolarization and opening of voltage-gated calcium channels. Allows calcium influx & subsequent release of insulin.

Hypoglycemia, weight gain, GI problems, headache, teratogenic

Type 2 diabetes

In patients with functioning β-cells, reduce circulating glucose.  Increase glycogen, fat, and protein formation, gene regulation

Secretagogue: Modulate β-cell insulin release by regulating K⁺ efflux through K⁺ channels; similar to sulfonylureas with some overlap in binding sites

hypoglycemia

Type 2 diabetes

Secretagogue: Modulate β-cell insulin release by regulating K⁺ efflux through K⁺ channels; similar to sulfonylureas with some overlap in binding sites

hypoglycemia

Type 2 diabetes

Obscure - Reduce hepatic glucose production through activation of AMP-activated protein kinase (AMPK). Also:

·         Impair renal gluconeogenesis

·         Slow glucose absorption from GI

·         ↑ glucose→lactate conversion

·         Stimulate glycolysis

·         ↑ glucose removal from blood

·         ↓ plasma glucagon levels

GI effects (anorexia, nausea, vomiting, diarrhea) in 20%, reduced vitamin B₁₂ absorption, lactic acidosis is rare

CI: renal/hepatic disease, alcoholism, CHF or hypoxic/acidotic states due to ↑risk of lactic acidosis

Type 2 diabetes – 1^st line therapy

Does NOT increase weight or provoke hypoglycemia

Inhibit intestinal α-glucosidases.  Reduce conversion of starch and disaccharides to monosaccharides.  Reduce postprandial hyperglycemia.

GI symptoms

CI: impaired renal/hepatic function, intestinal disorders

Type 2 diabetes

Inhibit intestinal α-glucosidases.  Reduce conversion of starch and disaccharides to monosaccharides.  Reduce postprandial hyperglycemia.

GI symptoms

CI: impaired renal/hepatic function, intestinal disorders

Type 2 diabetes

Regulates gene expression by binding to PPAR-γ.  Reduces insulin resistance.

Fluid retention, edema, anemia, weight gain, macular edema, bone fractures in women

Type 2 diabetes

CI: CHF, hepatic disease, may worsen heart disease

Binds to glucagon-like-polypeptide 1 (GLP-1) receptors

Nausea, headache, vomiting, anorexia, mild weight loss, pancreatitis

Type 2 diabetes;

Reduces post-meal glucose excursions: ↑glucose-mediated insulin release, ↓glucagon levels, slows gastric emptying, ↓ appetite

Inhibitor of dipeptidy peptidase-4 (DPP-4), the enzyme that degrades incretin and other GLP1-like molecules

Raises circulating GLP-1 levels

Rhinitis, upper respiratory infections, rare allergic reactions

Reduces post-meal glucose excursions: ↑glucose-mediated insulin release, ↓glucagon levels, slows gastric emptying, ↓ appetite

Analog of amylin: Binds amylin receptors

Nausea, anorexia, hypoglycemia, headache

Type 2 diabetes; Reduces post-meal glucose excursions: ↑glucose-mediated insulin release, ↓glucagon levels, slows gastric emptying, ↓ appetite

Bind to G_s protein-coupled receptors on liver cells.  This leads to an increase in cAMP, which facilitates catabolism of stored glycogen and ↑gluconeogenesis and ketogenesis.

↑blood glucose

Transient nausea and occasional vomiting

Severe hypoglycemia, endocrine diagnosis, reverse effects of overdose of β-blocking agents (↑cAMP production in heart), radiology of bowel (relaxes intestine)