Glucose Values Affected by Basal vs. Prandial Insulin
Basal insulin primarily controls fasting, pre-lunch, and pre-dinner glucose values, while prandial insulin primarily controls post-breakfast, post-lunch, and post-dinner glucose values. 1
Basal Insulin Effects
The principal action of basal insulin is to restrain hepatic glucose production and limit hyperglycemia overnight and between meals. 1
Specific Glucose Values Controlled by Basal Insulin:
Fasting glucose - Basal insulin directly controls overnight hepatic glucose production, making fasting glucose the primary target for basal insulin titration 1
Pre-lunch glucose - This between-meal value reflects basal insulin coverage during the morning interprandial period 1, 2
Pre-dinner glucose - This value represents basal insulin control during the afternoon interprandial period 1, 2
Titration Strategy for Basal Insulin:
Basal insulin should be titrated based on fasting plasma glucose values, with increases of 2-4 units every 3 days until fasting glucose reaches 80-130 mg/dL 1, 3
When basal insulin exceeds 0.5 units/kg/day without achieving glycemic targets, this signals "overbasalization" - adding prandial insulin becomes necessary rather than continuing to escalate basal insulin 1
Prandial Insulin Effects
Prandial insulin is designed to control postprandial glucose excursions following meals. 1
Specific Glucose Values Controlled by Prandial Insulin:
Post-breakfast glucose - Controlled by rapid-acting insulin administered before breakfast 1
Post-lunch glucose - Controlled by rapid-acting insulin administered before lunch 1
Post-dinner glucose - Controlled by rapid-acting insulin administered before dinner 1
Initiation and Titration of Prandial Insulin:
Start with 4 units of rapid-acting insulin before the largest meal, or use 10% of the current basal insulin dose 1
Prandial insulin should be titrated by 1-2 units or 10-15% every 3 days based on postprandial glucose readings 2 hours after meals 1, 3
Critical Clinical Distinction
A common pitfall is attempting to control postprandial hyperglycemia by escalating basal insulin beyond 0.5 units/kg/day. 1 This leads to overbasalization with clinical signals including:
- High bedtime-to-morning glucose differential (≥50 mg/dL) 1, 3
- Hypoglycemia between meals 1
- High glucose variability 1
When fasting glucose is controlled but A1C remains elevated after 3-6 months of optimized basal insulin, postprandial hyperglycemia is the culprit and requires prandial insulin coverage, not more basal insulin. 1
Physiologic Basis
In normal physiology, basal insulin represents approximately 40-50% of total daily insulin production and maintains glucose homeostasis during interprandial and overnight fasting periods 1, 2, 4
Prandial insulin secretion increases 3-10 times over basal rates during the 4-hour postprandial period following meals 1, 4
Loss of first-phase insulin secretion in type 2 diabetes impairs postprandial glucose control and requires exogenous prandial insulin replacement 4