Pick a stage
Add a GLP-1
Runs the same test with the medication on, drawn over the top.
Blood sugar
mg/dL
Insulin
relative units
What each part of the body is doing at this stage
Tap any part to read what it does. A filled dot means it is contributing to the problem at this stage.
The test here is the 75 g oral glucose tolerance test, which is what the two hour thresholds are defined against. An ordinary meal contains fat and protein and behaves differently. The curves show the direction and shape measured in research, not a prediction of your own numbers, and the insulin axis compares insulin with itself across the stages rather than with the blood sugar chart beside it. A lower curve with the medication on shows the direction of the effect measured in trials. It does not mean a diagnosis changes, which is decided on repeat testing and on A1C over months.
What the numbers actually mean
These are the current American Diabetes Association thresholds. Any one of the three tests can make the diagnosis on its own, which is why two people with the same condition can be found by completely different tests. A result outside the normal range is normally confirmed with a second test before anything is diagnosed.
| Fasting glucose | 2 hours after 75 g glucose | A1C | |
|---|---|---|---|
| Normal | Below 100 mg/dL | Below 140 mg/dL | Below 5.7% |
| Prediabetes | 100 to 125 mg/dL | 140 to 199 mg/dL | 5.7% to 6.4% |
| Diabetes | 126 mg/dL or above | 200 mg/dL or above | 6.5% or above |
Blood sugar is the last thing to change
Move the stage control from healthy to insulin resistance and watch the insulin chart rather than the blood sugar one. Insulin nearly doubles while blood sugar barely moves. That is the pancreas covering for cells that have stopped responding properly, and it works, for a while. A standard fasting glucose test taken during those years comes back normal, because it is measuring the result rather than the effort.
Blood sugar only rises once the pancreas can no longer cover the gap. Among people in the upper third of the impaired glucose tolerance range, measured on the two hour test, research using detailed insulin testing has found that more than 80 percent of beta cell function is already gone and insulin resistance is close to its maximum. At the point of a type 2 diagnosis, the UK Prospective Diabetes Study measured beta cell function at about half of normal, falling to 28 percent after six more years.
This is the reason a type 2 diagnosis so often arrives as a shock after years of normal results. The condition was developing the whole time. Nothing anyone did that year caused it, and the test that came back fine was not designed to find it.
Why the medications come from the gut
Researchers noticed something odd decades ago. If you swallow glucose, your pancreas releases far more insulin than it does when the identical amount of glucose is put straight into a vein, even though the blood sugar level reached is the same. The difference is the gut. Food passing through the intestine releases GLP-1 and GIP, and those two hormones tell the pancreas to get ready. This is called the incretin effect.
In people with normal glucose tolerance, a 75 g oral glucose load produces about 1.7 times the insulin that the same glucose produces by vein. In people with type 2 diabetes, the figure is about 1.1 times. The gut signal is close to absent. That is not a side issue of type 2 diabetes, it is one of its defining features.
GIP
When GIP was given to people with type 2 diabetes, its maximum effect on insulin was 54 percent lower than in people without diabetes. The hormone is still there, and the pancreas has largely stopped answering it.
GLP-1
GLP-1 given to the same kind of patients still produced 71 percent of the insulin response seen in people without diabetes, a difference that was not statistically significant. The pancreas still answers this one.
That 1993 result is the reason the whole class of medication exists. Of the two hormones the gut releases, one had stopped working in type 2 diabetes and the other had not. Give enough of the one that still works, and you get the insulin response back.
What a GLP-1 does about it
01
Insulin, but only when glucose is high
A GLP-1 does not force the pancreas to make insulin. It amplifies the response to glucose that is already there, and does almost nothing when blood sugar is normal. You can see this on the healthy stage above, where switching the medication on barely moves either curve. It is also why these medications rarely cause low blood sugar by themselves.
02
Less glucagon, so the liver stops adding sugar
GLP-1 suppresses glucagon from the alpha cells, which means the liver releases less glucose of its own. This is most of the reason fasting numbers improve, since fasting glucose is largely a liver measurement. The suppression is also glucose dependent, so the emergency response to an actual low blood sugar is left working.
03
The stomach empties more slowly
Food leaves the stomach at a slower rate, so glucose arrives in the blood as a gentler rise rather than a spike. This is the action behind the lower peaks on the chart, and it is also the source of the nausea and fullness that people notice in the first weeks.
04
Appetite falls, and weight follows
The medication acts on GLP-1 receptors in the brain areas it can reach, and appetite falls, which produces weight loss, and weight loss reduces insulin resistance. This is a slower path than the first three and it is a real part of the blood sugar result. Some of the benefit is the medication acting directly, and some of it is the weight change acting on the underlying resistance.
Four things the charts do not show
The stomach effect fades
With the long acting medications, semaglutide and liraglutide among them, the slowing of stomach emptying weakens over months of continuous use. The shorter acting ones keep it. The blood sugar benefit of a weekly medication is therefore thought to rest more on the insulin and glucagon effects and on weight loss than on the slowed stomach, even though the slowed stomach is what people feel first.
Low blood sugar becomes possible in combination
On its own a GLP-1 carries a low risk of hypoglycemia. Added to insulin or to a sulfonylurea such as glipizide or glimepiride, that changes, because those medications raise insulin whether or not glucose is high. Most of the hypoglycemia reported on GLP-1 medications occurred in people also taking a sulfonylurea. Doses of the other medication are often reduced when a GLP-1 is started, which is a conversation for your prescriber rather than something to adjust yourself.
How much A1C actually moves
In the SUSTAIN 2 trial, people starting at an average A1C of 8.1 percent finished 56 weeks 1.6 percentage points lower on semaglutide 1.0 mg, 1.3 points lower on 0.5 mg, and 0.5 points lower on sitagliptin, the comparison medication. That is a meaningful change and it is not a cure. A1C is a three month average, so it moves over months rather than over one meal.
Remission is a separate question
Type 2 diabetes can go into remission. In the DiRECT trial, 46 percent of the people put on a weight management program reached remission at 12 months, and more than 80 percent of those who lost over 15 kg were in remission. That trial used a diet led approach rather than a medication, so it is evidence about weight loss rather than evidence about GLP-1s specifically. What it establishes is that type 2 diabetes is not always permanent, which is a different picture from the one most people are given at diagnosis.
This is education, not medical advice
This page explains published research. It does not diagnose anything, it does not measure your own blood sugar, and the curves are illustrative shapes rather than a prediction for any individual. Type 2 diabetes is diagnosed and treated by a clinician, and decisions about starting, changing or stopping any medication belong with your prescriber. If you take insulin or a sulfonylurea, do not change a dose based on anything here.
Sources
- American Diabetes Association Professional Practice Committee. 2. Diagnosis and classification of diabetes: Standards of Care in Diabetes 2026. Diabetes Care. 2026;49(Supplement 1):S27. diabetesjournals.org. Source of every threshold in the table: fasting glucose, the two hour value after a 75 g oral glucose load, and the A1C bands for prediabetes and diabetes.
- DeFronzo RA. Banting Lecture. From the triumvirate to the ominous octet: a new paradigm for the treatment of type 2 diabetes mellitus. Diabetes. 2009;58(4):773–795. PMID 19336687. Source for the eight organ systems involved, for muscle and liver insulin resistance plus beta cell failure being the core defects, and for people in the upper third of the impaired glucose tolerance range, defined on the two hour glucose test, having lost over 80 percent of beta cell function while being close to maximally insulin resistant.
- Mari A, Bagger JI, Ferrannini E, Holst JJ, Knop FK, Vilsbøll T. Mechanisms of the incretin effect in subjects with normal glucose tolerance and patients with type 2 diabetes. PLoS ONE. 2013;8(9):e73154. doi:10.1371/journal.pone.0073154. Source of the 1.7 times figure for normal glucose tolerance and the 1.1 times figure for type 2 diabetes at a 75 g glucose load.
- Nauck MA, Heimesaat MM, Ørskov C, Holst JJ, Ebert R, Creutzfeldt W. Preserved incretin activity of glucagon-like peptide 1 (7-36 amide) but not of synthetic human gastric inhibitory polypeptide in patients with type-2 diabetes mellitus. Journal of Clinical Investigation. 1993;91(1):301–307. doi:10.1172/JCI116186. Source of the 54 percent lower maximum effect for GIP and the preserved 71 percent response to GLP-1. The result the medication class was built on.
- UK Prospective Diabetes Study Group. UK Prospective Diabetes Study 16: overview of 6 years' therapy of type II diabetes, a progressive disease. Diabetes. 1995;44(11):1249–1258. PMID 7589820. Source for beta cell function measuring about 50 percent of normal at the point of diagnosis and 28 percent six years later.
- Jalleh RJ, Rayner CK, Hausken T, Jones KL, Camilleri M, Horowitz M. Clinical consequences of delayed gastric emptying with GLP-1 receptor agonists and tirzepatide. Journal of Clinical Endocrinology & Metabolism. 2025;110(1):1–15. academic.oup.com. Source for the slowing of gastric emptying declining over time with the long acting medications while it is sustained with the short acting ones.
- Ahrén B, Masmiquel L, Kumar H, et al. Efficacy and safety of once-weekly semaglutide versus once-daily sitagliptin as an add-on to metformin, thiazolidinediones, or both, in patients with type 2 diabetes (SUSTAIN 2): a 56-week, double-blind, phase 3a, randomised trial. The Lancet Diabetes & Endocrinology. 2017;5(5):341–354. PMID 28385659. Source of the A1C figures: a baseline of 8.1 percent falling by 1.3 points on semaglutide 0.5 mg, 1.6 points on 1.0 mg, and 0.5 points on sitagliptin at 56 weeks.
- Lean MEJ, Leslie WS, Barnes AC, et al. Primary care-led weight management for remission of type 2 diabetes (DiRECT): an open-label, cluster-randomised trial. The Lancet. 2018;391(10120):541–551. PMID 29221645. Source of the 46 percent remission figure at 12 months, and of more than 80 percent remission among those who lost over 15 kg.
- Campbell JE, Drucker DJ. Pharmacology, physiology, and mechanisms of incretin hormone action. Cell Metabolism. 2013;17(6):819–837. doi:10.1016/j.cmet.2013.04.008. Source for glucose-dependent insulin secretion and glucagon suppression, and for the low hypoglycemia risk that follows from it when a GLP-1 is used on its own.