Insulin therapy in diabetes mellitus
Insulin therapy replaces or supplements endogenous insulin to control hyperglycemia, and is lifelong and mandatory in type 1 diabetes because of absolute beta-cell failure, while in type 2 diabetes it is added when oral and noninjectable agents fail to reach glycemic goals. First-line therapy is a basal-bolus regimen started at 0.4-1.0 units/kg/day in type 1 diabetes, or basal insulin glargine 10 units/day (or 0.1-0.2 units/kg/day) in type 2 diabetes, titrated to a fasting glucose target.
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What this article covers
- Overview
Insulin replaces or supplements a hormone the body cannot adequately produce or use: the only glucose-lowering therapy mandatory in type 1 diabetes, and one of several options added when other therapies fail to control type 2 diabetes.
- Epidemiology
Universal and lifelong in type 1 diabetes: because beta-cell destruction is essentially complete, every person with type 1 diabetes requires insulin from diagnosis onward.
- Risk factors
Tight glycemic targets without adequate monitoring: intensifying therapy toward a low hemoglobin A1c target raises hypoglycemia risk if not paired with structured glucose monitoring.
- Pathophysiology
Type 1 diabetes reflects near-total beta-cell destruction: autoimmune (or, less commonly, idiopathic) destruction eliminates endogenous insulin, making exogenous insulin an absolute requirement.
- Clinical features
In type 1 diabetes, insulin dependence is present from diagnosis: basal and prandial coverage is required from the outset, with rapid progression to diabetic ketoacidosis if insulin is withheld.
- Differential diagnosis
Non-insulin-requiring type 2 diabetes: adequately controlled on lifestyle measures and oral or noninsulin injectable agents, unlike a patient who has failed those measures or presents with severe hyperglycemia.
- Diagnosis
The need for insulin therapy is established by the type of diabetes and the adequacy of glycemic control on current therapy, with hemoglobin A1c and glucose monitoring data providing the objective basis for the decision.
- Management
First, in type 1 diabetes, start an intensive basal-bolus regimen at diagnosis: total daily insulin 0.4-1.0 units/kg/day, with basal insulin glargine or degludec providing about 50% of the total dose…
- Complications
Hypoglycemia: the most common significant complication; severity ranges from mild adrenergic symptoms to neuroglycopenia, seizure, and, if severe and uncorrected, death.
- Prognosis
Excellent glycemic outcomes with a well-designed regimen: basal-bolus therapy, by injection or CSII, allows most patients to reach individualized targets with manageable hypoglycemia risk.
- Prevention
Prevent hypoglycemia by avoiding insulin stacking: space sequential rapid-acting doses at least 3-4 hours apart.
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Related articles
- Diabetic ketoacidosis
Diabetic ketoacidosis is a life-threatening hyperglycemic crisis of near-absolute insulin deficiency, most common in type 1 diabetes, producing an anion-gap ketoacidosis from unrestrained lipolysis and osmotic diuresis from severe hyperglycemia. It is diagnosed by hyperglycemia, ketonemia, and an anion-gap metabolic acidosis, and treated with intravenous isotonic saline, an intravenous regular insulin bolus and infusion, and aggressive potassium repletion guided by frequent electrolyte monitoring.
- Hyperosmolar hyperglycemic state
Hyperosmolar hyperglycemic state is a life-threatening hyperglycemic crisis of older patients with type 2 diabetes, marked by extreme hyperglycemia and profound dehydration without significant ketoacidosis, because residual insulin secretion suppresses lipolysis even as it fails to control glucose. It is diagnosed by marked hyperglycemia (often >600 mg/dL) with plasma hyperosmolality above 320 mOsm/kg and minimal ketosis, and treated with aggressive isotonic fluid resuscitation, intravenous regular insulin, and careful potassium repletion.
- Hypoglycemia in adults
Hypoglycemia is a plasma glucose below 70 mg/dL, most often a complication of insulin or sulfonylurea therapy for diabetes, and in a person without diabetes it requires a Whipple triad-based evaluation for insulinoma or another endogenous cause. An alert patient is treated with 15 to 20 g of fast-acting oral carbohydrate, while a patient unable to swallow safely receives intramuscular glucagon 1 mg or intravenous dextrose 50% 25 g.
- Latent autoimmune diabetes in adults
Latent autoimmune diabetes in adults (LADA) is a slowly progressive autoimmune beta-cell destruction that presents in adulthood without an initial insulin requirement, so it is frequently misclassified as type 2 diabetes until positive islet autoantibodies are identified. First-line management follows a standard stepwise diabetes approach, but basal insulin should be started proactively as beta-cell failure progresses, since earlier insulin reduces stress on the remaining beta cells.