Ramadan fasting changes the entire rhythm of eating. Instead of meals spread through the day, food is consumed before dawn and after sunset, with nothing in between for as long as 16 to 18 hours. For people managing diabetes with insulin, that shift creates a real challenge: blood sugar can swing low during the fast and then spike sharply after the sunset meal, known as iftar.
A recent study published in Diabetes Research and Clinical Practice used continuous glucose monitors to map exactly when and how those swings happen. Researchers then looked at whether adding a GLP-1 receptor agonist, a class of peptide-based therapy that influences insulin release and digestion, could smooth out the pattern without raising the risk of dangerous lows.
The study included 54 adults split across three matched groups: people with type 2 diabetes on basal-bolus insulin alone, people with type 2 diabetes on basal-bolus insulin plus a GLP-1 receptor agonist (either semaglutide or tirzepatide, a dual GLP-1 and GIP agonist), and people with type 1 diabetes on basal-bolus insulin. CGM data covered four weeks before Ramadan and the full 29 days of Ramadan 2025.
The post-iftar problem
The most striking finding from the CGM data was that poor glycemic control during Ramadan was not driven by the fasting window itself. It was driven almost entirely by the hours after iftar. When researchers separated the fasting and non-fasting periods in the data, the non-fasting window after the sunset meal was where blood sugar climbed and stayed elevated.
In the group using basal-bolus insulin alone, researchers documented a marked deterioration in glycemic metrics specifically during non-fasting hours. This pattern held even when pre-Ramadan baseline numbers were accounted for. The finding suggests that the composition and timing of iftar, combined with how insulin acts over several hours, creates a window where glucose control becomes particularly difficult to maintain.
What continuous glucose monitoring revealed
Continuous glucose monitors record blood sugar readings every few minutes throughout the day and night, giving researchers a far more detailed picture than a single fasting blood draw or periodic finger-prick test. The study used a widely available sensor-based monitor across all participants.
Key metrics reported included time in range, which measures what percentage of the day glucose stays within a target band, and a glucose management indicator, which estimates average blood sugar control over the monitoring period. Researchers also calculated incremental post-iftar area under the curve, a measure of how high and for how long blood sugar remained elevated in the four hours following the sunset meal. That last metric gave the clearest view of the specific post-iftar spike the researchers were tracking.
The effect of add-on GLP-1 receptor agonist therapy
When researchers compared the two type 2 diabetes groups head to head, the difference in post-iftar glucose behavior was substantial. Participants using basal-bolus insulin alone spent roughly 37 percent of monitored time within the target glucose range. Participants on basal-bolus insulin plus a GLP-1 receptor agonist spent about 74 percent of monitored time in range. The difference was statistically significant, with a p-value of 0.007.
The glucose management indicator followed the same direction. The adjunct therapy group recorded an estimated indicator of 6.9 percent, compared with 8.3 percent in the insulin-only group, a difference the study authors noted as statistically meaningful at p equal to 0.004.
The post-iftar area under the curve, the most direct measure of that sunset meal spike, showed a reduction of approximately 61 percent in the group using add-on therapy. In absolute terms, the researchers reported values of roughly 102,000 versus 260,000 milligrams per deciliter times minutes across the four-hour post-iftar window. That is a greater than twofold difference in cumulative post-meal glucose exposure.
Hypoglycemia and tolerability
One concern with adding any glucose-modifying agent to insulin is the potential for hypoglycemia, meaning blood sugar falling below a safe threshold. During extended fasting periods, that risk is especially relevant. The study reported that add-on therapy did not increase hypoglycemia compared with the insulin-only group, and no participants discontinued treatment during Ramadan.
The tolerability finding matters because GLP-1 receptor agonists are known to slow gastric emptying and can cause nausea, particularly when first introduced. The study did not report significant tolerability problems requiring withdrawal, though the abstract does not detail the full adverse event profile.
How GLP-1 receptor agonists act on post-meal glucose
GLP-1, or glucagon-like peptide-1, is a signaling molecule the gut releases in response to food. It prompts the pancreas to release insulin in proportion to glucose levels, slows the rate at which the stomach empties food into the small intestine, and reduces the release of glucagon, a hormone that raises blood sugar. Together, those effects blunt the sharp rise in blood glucose that typically follows a large meal.
Tirzepatide, which was included alongside semaglutide in the adjunct group, adds a second receptor target. It also activates the GIP receptor, another incretin pathway, which the literature suggests may further support insulin response and fat metabolism. The study grouped both agents together as the adjunct cohort, so the data does not distinguish between their individual contributions.
The mechanism aligns with what the study observed. If post-iftar hyperglycemia is the primary driver of Ramadan dysglycemia in insulin-treated individuals, then a therapy that specifically attenuates post-meal glucose excursions would logically have the greatest impact during the non-fasting window. The CGM data appeared to confirm that pattern directly.
Study limitations and context
The study involved 54 participants after screening 140, and the two type 2 diabetes groups were matched one to one by age, baseline HbA1c, and BMI. Matching helps control for confounding variables, but the relatively small sample size means the findings should be interpreted as early evidence rather than definitive proof. The type 1 diabetes group provided a descriptive comparison but was not the focus of the adjunct therapy evaluation.
The study did not randomly assign participants to treatment arms. People were already on their respective regimens before Ramadan began, which introduces the possibility of selection differences that matching alone cannot fully resolve. Larger randomized trials would be needed to confirm the magnitude of effect the researchers observed.
Despite those caveats, the CGM-based approach is a meaningful methodological strength. Capturing glucose data continuously across both fasting and non-fasting windows allowed researchers to pinpoint exactly when glucose control deteriorates, rather than relying on summary statistics that can obscure time-of-day patterns.
