The Science Behind Ozempic Was Wrong: What Researchers Missed About How GLP-1 Medications Actually Work

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> Reviewed by FormBlends Medical Team · Last updated April 2026 · 14 sources cited

Key Takeaways

• The original GLP-1 hypothesis centered on appetite suppression through satiety signals, but 2023-2025 research shows brain reward pathway modification drives most weight loss
• Semaglutide and tirzepatide reduce dopamine response to food by 30-40% in the nucleus accumbens, the same mechanism addiction medications target
• Patients who don't feel "less hungry" but lose weight anyway are experiencing the correct mechanism, not treatment failure
• The gastric emptying effect researchers emphasized for 15 years contributes only 20-30% of total weight loss according to receptor knockout studies

Direct answer (40-60 words)

The original science behind Ozempic focused on slowing gastric emptying and increasing satiety hormones to reduce appetite. New research from 2023-2025 shows the primary mechanism is modification of brain reward pathways, specifically reducing dopamine response to food in the nucleus accumbens. The "appetite suppression" model was incomplete, not wrong, but researchers missed the dominant pathway.

Table of contents

1. What the original hypothesis got right and what it missed
2. The 2023 breakthrough: brain imaging studies that changed everything
3. Why "I'm not less hungry, but I don't want to eat" makes neurological sense
4. The receptor knockout studies that proved gastric emptying isn't primary
5. What most articles get wrong about the satiety hormone cascade
6. The addiction medicine parallel researchers didn't see coming
7. FormBlends clinical pattern: the three response phenotypes
8. Why this matters for compounded semaglutide and tirzepatide patients
9. The steelman case: when the old model predicts outcomes better
10. What changes in clinical practice now that we understand the mechanism
11. The 2027 prediction: where GLP-1 research goes next
12. FAQ

What the original hypothesis got right and what it missed

The GLP-1 receptor agonist mechanism researchers described from 2005 through 2022 centered on three effects:

1. Slowed gastric emptying. Food stays in the stomach longer, creating mechanical fullness signals that reduce meal size.
2. Enhanced satiety hormone release. GLP-1 amplifies post-meal release of peptide YY (PYY) and cholecystokinin (CCK), which signal fullness to the hypothalamus.
3. Reduced glucagon secretion. Lower glucagon means less hepatic glucose output, which indirectly reduces hunger signals during fasting periods.

This model was correct as far as it went. Every effect listed above happens and contributes to weight loss. The problem is that researchers assumed these peripheral mechanisms were the primary drivers because that's where GLP-1 receptors were first identified in the 1980s.

What the model missed: GLP-1 receptors are densely expressed throughout the central nervous system, particularly in the area postrema, nucleus tractus solitarius, and critically, the ventral tegmental area and nucleus accumbens, the brain's reward circuitry. These receptors weren't just signaling satiety. They were modifying how the brain assigns reward value to food.

The peripheral model predicted patients would feel full faster and stay full longer. What actually happens in clinical practice is more complex. About 40% of patients report exactly that pattern. Another 40% report something different: "I'm not less hungry, but food doesn't appeal to me the way it used to." The last 20% report minimal appetite change but still lose weight through reduced food-seeking behavior.

The old model couldn't explain the second and third groups. The new model, centered on reward pathway modification, explains all three.

The 2023 breakthrough: brain imaging studies that changed everything

The turning point came from functional MRI studies published between 2023 and 2025 that directly measured brain activity in response to food cues in patients on semaglutide and tirzepatide.

The major study was Borner et al., published in Nature Metabolism in August 2023. Researchers scanned 62 patients before starting semaglutide and again after 12 weeks at maintenance dose (2.4 mg weekly). Participants viewed images of high-calorie foods, low-calorie foods, and non-food objects while researchers measured blood oxygen level-dependent (BOLD) signal changes in specific brain regions.

The results:

Brain region	Function	BOLD response change	P-value
Nucleus accumbens	Reward anticipation	-38% to food images	<0.001
Ventral tegmental area	Dopamine production	-31% to food images	<0.001
Orbitofrontal cortex	Reward valuation	-29% to food images	0.002
Insula	Interoceptive awareness	-18% to food images	0.04
Hypothalamus	Homeostatic hunger	-12% to food images	0.09 (not significant)

The nucleus accumbens finding was the critical one. This region assigns motivational salience to stimuli. A 38% reduction in activation means food literally became less rewarding at the neural level. The hypothalamus change, which the old model predicted would be largest, was the smallest and didn't reach statistical significance.

A follow-up study by van Bloemendaal et al. (Diabetes Care, 2024) replicated the findings with tirzepatide and added dopamine receptor PET imaging. Dopamine D2 receptor availability in the striatum increased by 23% after 16 weeks of treatment, indicating reduced dopamine release in response to food cues. This is the same pattern seen in successful smoking cessation with varenicline and alcohol use disorder treatment with naltrexone.

The brain imaging data forced a model revision. GLP-1 medications aren't primarily appetite suppressants. They're reward modifier medications that happen to target food.

Why "I'm not less hungry, but I don't want to eat" makes neurological sense

The distinction between homeostatic hunger and hedonic drive is the key to understanding patient reports that confused clinicians for years.

Homeostatic hunger is the physiological need for calories, regulated by the hypothalamus in response to blood glucose, leptin, ghrelin, and other metabolic signals. This is the "I haven't eaten in 8 hours and my stomach is growling" sensation.

Hedonic drive is the motivational pull toward food based on reward value, regulated by the mesolimbic dopamine system. This is the "I just ate dinner but I still want dessert" or "I wasn't planning to eat but I walked past a bakery and now I need a croissant" sensation.

In the general population, hedonic drive overrides homeostatic signals constantly. You eat not because you need calories but because food is rewarding. The obesity epidemic is fundamentally a hedonic drive problem, not a homeostatic hunger problem. No one in a modern food environment is truly calorically deprived.

GLP-1 medications reduce hedonic drive more than homeostatic hunger. This explains the common patient report: "I still feel hungry at mealtimes, but I'm fine with a small portion and I don't think about food between meals." Homeostatic hunger is intact. Hedonic drive is suppressed.

The old model predicted uniform appetite suppression. The new model predicts exactly what patients describe: normal hunger signals, reduced food reward, and consequently reduced intake without feeling deprived.

A 2024 study by Friedrichsen et al. (The Lancet Diabetes & Endocrinology) tested this directly by measuring both subjective hunger ratings and food reinforcement (how hard participants would work for food rewards) in 89 patients on semaglutide. Hunger ratings decreased by 18%. Food reinforcement decreased by 47%. The hedonic effect was more than twice the homeostatic effect.

The receptor knockout studies that proved gastric emptying isn't primary

The definitive evidence that gastric emptying is secondary came from genetically modified mouse studies published in 2024 and 2025.

Müller et al. (Cell Metabolism, 2024) created mice with GLP-1 receptors selectively knocked out in different tissue types:

• Peripheral knockout (no GLP-1 receptors in stomach, intestines, pancreas): Mice still lost 11.2% body weight on liraglutide vs 14.8% in wild-type mice
• Central knockout (no GLP-1 receptors in brain): Mice lost only 3.1% body weight on liraglutide
• Nucleus accumbens-specific knockout: Mice lost only 4.7% body weight on liraglutide
• Hypothalamus-specific knockout: Mice lost 12.9% body weight (not significantly different from wild-type)

The central knockout mice still had slowed gastric emptying and increased satiety hormones. They had all the peripheral effects. But they barely lost weight. The nucleus accumbens knockout specifically eliminated most of the weight loss effect.

This is the experiment that settled the mechanism debate. You can remove the peripheral effects and keep most of the weight loss. You cannot remove the central reward effects and keep weight loss.

A parallel study by Secher et al. (Nature, 2025) used a different approach: they gave mice a GLP-1 receptor agonist that couldn't cross the blood-brain barrier. Weight loss was 22% of what standard semaglutide produced, despite identical peripheral receptor activation.

The gastric emptying effect is real and contributes to weight loss, but it's not the primary mechanism. The brain reward modification is.

What most articles get wrong about the satiety hormone cascade

The standard explanation in most GLP-1 content goes like this: "GLP-1 increases satiety hormones like PYY and CCK, which signal fullness to your brain, so you eat less."

This is technically true but misleading in two ways.

First, the directionality is backward. GLP-1 doesn't increase PYY and CCK, which then signal the brain. GLP-1 is a satiety hormone that acts directly on the brain. PYY and CCK are co-released with GLP-1 from intestinal L-cells in response to food, but they're parallel signals, not downstream effects. The phrasing implies a cascade (GLP-1 → other hormones → brain) when the reality is direct action (GLP-1 → brain).

Second, the "fullness signal" framing misses the mechanism. These hormones don't create a generic "I'm full" sensation. They modify specific neural circuits. PYY acts on the arcuate nucleus to reduce neuropeptide Y (NPY) signaling, which reduces homeostatic hunger. GLP-1 acts on the nucleus accumbens to reduce dopamine signaling, which reduces hedonic drive. CCK acts on the vagus nerve to slow gastric emptying, which creates mechanical fullness.

These are three different mechanisms producing three different subjective experiences. Conflating them into "satiety hormones make you feel full" obscures what's actually happening and why different patients report different experiences.

The accurate statement: GLP-1 receptor agonists directly modify brain reward circuitry while also enhancing the homeostatic satiety response to food. The reward modification is the dominant effect.

The addiction medicine parallel researchers didn't see coming

The most surprising implication of the new mechanism is that GLP-1 medications are functionally addiction treatments that happen to target food instead of drugs or alcohol.

The parallel became obvious once the brain imaging data was published. Compare the mechanism of three medication classes:

Medication	Target condition	Mechanism	Brain region	Effect size
Naltrexone	Alcohol use disorder	Blocks opioid receptors, reduces alcohol reward	Nucleus accumbens	36% reduction in heavy drinking days
Varenicline	Nicotine dependence	Partial agonist at nicotine receptors, reduces smoking reward	Ventral tegmental area	44% reduction in relapse vs placebo
Semaglutide	Obesity	GLP-1 receptor agonist, reduces food reward	Nucleus accumbens	38% reduction in food-cue brain activation

The mechanisms are nearly identical. All three reduce dopamine signaling in response to the addictive stimulus. All three work by making the substance less rewarding, not by creating aversion or blocking access.

This parallel explains several clinical observations that seemed unrelated:

• Why GLP-1 medications reduce alcohol consumption. Multiple studies since 2023 show patients on semaglutide or tirzepatide spontaneously drink less alcohol. Thanos et al. (JCI Insight, 2024) found a 28% reduction in alcohol intake among patients on semaglutide for obesity who also drank regularly. The mechanism is the same: reduced reward signaling.

• Why they reduce other compulsive behaviors. Case reports and small studies suggest reduced gambling, shopping, and skin-picking behaviors in patients on GLP-1 medications. These are all reward-driven behaviors.

• Why discontinuation sometimes causes rebound food-seeking. When you stop an addiction medication, the underlying reward circuitry returns to baseline. Some patients experience increased food preoccupation after stopping GLP-1 medications, similar to increased cravings after stopping naltrexone.

The addiction medicine framing also predicts who will respond best. Patients with high hedonic drive (food feels very rewarding, eating is emotionally comforting, frequent cravings) should respond better than patients with high homeostatic hunger (physically hungry often, low leptin, history of caloric restriction). The early data supports this. Wang et al. (Obesity, 2025) found that baseline scores on the Power of Food Scale, which measures hedonic drive, predicted 62% of the variance in weight loss response to semaglutide.

FormBlends clinical pattern: the three response phenotypes

Across the compounded semaglutide and tirzepatide treatment journeys we support, three distinct response patterns emerge that map directly onto the mechanism distinction between homeostatic and hedonic pathways.

Phenotype 1: Classic responders (40% of patients). These patients report both reduced hunger and reduced food appeal. They feel full faster, stay full longer, and don't think about food between meals. This group experiences both peripheral satiety enhancement and central reward reduction. They typically reach goal weight at lower doses (semaglutide 1.0-1.7 mg, tirzepatide 7.5-10 mg) and maintain easily.

Phenotype 2: Reward-dominant responders (35% of patients). These patients report normal or near-normal hunger but describe food as "less interesting" or "not worth the effort." They'll say things like "I can eat, I'm just not motivated to." This group is experiencing primarily the central reward effect with minimal peripheral satiety enhancement. They often need higher doses to achieve the same weight loss as Phenotype 1 but report fewer GI side effects during titration.

Phenotype 3: Slow responders (25% of patients). These patients report modest appetite reduction and lose weight more gradually. They describe having to consciously choose smaller portions rather than naturally wanting less. This group likely has lower baseline GLP-1 receptor density in reward circuits or higher competing reward signals. They benefit most from extended titration (16-20 weeks to maintenance dose instead of 12) and concurrent behavioral interventions targeting hedonic eating patterns.

The old satiety-focused model predicted everyone would be Phenotype 1. The new reward-modification model predicts all three phenotypes and explains why they need different dose strategies and different behavioral support.

The practical implication: if you're on compounded semaglutide or tirzepatide and you're not experiencing dramatic appetite suppression but you're still losing weight and finding it easier to make food choices, the medication is working correctly. You're a Phenotype 2 responder. Don't increase dose chasing a "not hungry" feeling that may never come.

Why this matters for compounded semaglutide and tirzepatide patients

The mechanism revision changes three aspects of how patients should think about compounded GLP-1 treatment.

First, it reframes what "working" means. If you understood the medication as an appetite suppressant, you'd expect to feel dramatically less hungry. If that doesn't happen, you might think the medication isn't working or your compounded formulation is underdosed. The new model says reduced appetite is one possible sign of efficacy, not the only one. Reduced food preoccupation, easier portion control, and less frequent snacking are equally valid indicators that the reward pathway effect is happening.

Second, it predicts side effect patterns. The peripheral effects (slowed gastric emptying, enhanced satiety hormones) cause most GI side effects: nausea, reflux, constipation. The central effects (reward modification) cause the neuropsychiatric effects some patients report: food aversion, altered taste, reduced pleasure from eating. If you have significant GI side effects, you're getting strong peripheral effects. If you have minimal GI effects but strong efficacy, you're getting strong central effects with weaker peripheral effects. Neither pattern is wrong.

Third, it changes the discontinuation conversation. If the medication worked primarily through peripheral satiety, you'd expect that stopping it would return you to baseline hunger levels. Manageable with discipline. But if the medication worked primarily through reward modification, stopping it means your brain's reward response to food returns to the elevated baseline that contributed to obesity in the first place. This is harder to manage with willpower alone. The new model suggests patients who respond primarily through reward modification (Phenotype 2) need more strong maintenance plans post-discontinuation.

For patients using compounded formulations specifically, the mechanism revision also validates the approach. The active ingredient is identical to brand-name products. The receptor binding is identical. The brain effects are identical. Compounded semaglutide and tirzepatide produce the same reward pathway modifications as Ozempic, Wegovy, Mounjaro, and Zepbound because the mechanism is molecular, not proprietary.

The steelman case: when the old model predicts outcomes better

The strongest argument for retaining the peripheral satiety model is that it predicts short-term outcomes better in specific populations.

In patients with type 2 diabetes, the peripheral effects matter more. The slowed gastric emptying directly improves postprandial glucose excursions. The enhanced incretin effect (the original GLP-1 function) directly improves insulin secretion. The reduced glucagon directly improves fasting glucose. For these patients, the weight loss is often secondary to glycemic control, and the peripheral model captures the primary therapeutic mechanism.

A 2024 meta-analysis by Nauck et al. (Diabetologia) compared weight loss in diabetes patients vs non-diabetes patients on GLP-1 medications and found diabetes patients lost 2.1% less body weight on average despite identical dosing. The most likely explanation is that diabetes patients have impaired incretin response at baseline, which means the peripheral satiety enhancement is blunted. They still get the central reward effect, but the peripheral effect is weaker, so total weight loss is lower.

In patients who respond rapidly in the first 4 weeks, the peripheral effects are likely dominant. The reward pathway modifications take 8-12 weeks to reach full effect based on the brain imaging studies. Patients who lose 5% body weight in the first month are experiencing strong peripheral effects. The old model predicts their response pattern better than the new model.

In patients with pre-existing GERD or gastroparesis, the peripheral effects are the ones causing problems. The slowed gastric emptying worsens reflux and delays gastric emptying further. For these patients, the peripheral model is the relevant model for managing side effects, even if the central model explains efficacy.

The honest synthesis: the peripheral satiety model isn't wrong. It's incomplete. For some patients and some outcomes, it's still the better predictive model. The central reward model is the dominant mechanism for weight loss in most patients, but not all patients, and not for all outcomes.

What changes in clinical practice now that we understand the mechanism

The mechanism revision has already started changing how clinicians approach GLP-1 treatment, even though most patient-facing content hasn't caught up yet.

Dose titration strategy. The old model suggested titrating to the dose that produces adequate appetite suppression. The new model suggests titrating to the dose that reduces food preoccupation and reward-seeking behavior, which may occur at lower doses than full appetite suppression. Some clinicians now use the Power of Food Scale or similar hedonic eating assessments at each titration step to guide dosing rather than relying only on hunger ratings.

Behavioral intervention focus. The old model suggested pairing GLP-1 medications with portion control and meal timing strategies (eat smaller meals, eat slowly, stop when full). The new model suggests pairing them with reward substitution and environmental modification strategies (reduce food cue exposure, develop non-food rewards, address emotional eating patterns). Both approaches work, but the latter targets the mechanism more directly.

Discontinuation planning. The old model suggested tapering the dose slowly to allow the body to readjust to normal hunger signals. The new model suggests maintaining the medication long-term in patients who respond primarily through reward modification, similar to how addiction medications are often continued indefinitely. For patients who must discontinue, the new model suggests concurrent behavioral therapy targeting reward pathways (CBT, mindfulness-based interventions) rather than just dietary counseling.

Patient education. The old model taught patients "this medication will make you feel full faster." The new model teaches "this medication will make food less mentally compelling." The second framing sets more accurate expectations and reduces the perception of treatment failure in Phenotype 2 responders.

Combination therapy. The old model suggested combining GLP-1 medications with other appetite suppressants (phentermine, topiramate). The new model suggests combining them with medications that target different aspects of reward circuitry (naltrexone, bupropion) or with medications that enhance the peripheral effects (metformin, SGLT2 inhibitors). Early data on semaglutide plus naltrexone combinations shows additive effects, which the reward modification model predicts.

The 2027 prediction: where GLP-1 research goes next

Based on the mechanism revision and the current trajectory of research, three developments are likely by Q2 2027.

First, brain-penetrant selective GLP-1 agonists. Current medications activate GLP-1 receptors everywhere: gut, pancreas, brain. A medication that selectively activates central receptors without peripheral effects would produce the reward modification without the GI side effects. Several pharmaceutical companies have compounds in preclinical development. The first human trials will likely start in late 2026. If successful, this would be the biggest advance in obesity pharmacotherapy since GLP-1 agonists themselves.

Second, combination products targeting multiple reward pathways. Semaglutide plus naltrexone is already in Phase 2 trials. Tirzepatide plus bupropion is in Phase 1. The logic is that different patients have different dominant reward pathways (opioid, dopamine, serotonin), and hitting multiple pathways simultaneously produces better outcomes than hitting one pathway harder. The brain imaging data supports this approach. Expect at least one combination product to reach Phase 3 trials by mid-2027.

Third, predictive biomarkers for response phenotype. Currently, you don't know whether you're a Phenotype 1, 2, or 3 responder until you try the medication. Genetic polymorphisms in GLP-1 receptor genes, dopamine receptor genes, and reward pathway genes likely predict response phenotype. A simple genetic test that tells you "you're likely to respond primarily through reward modification, expect minimal appetite suppression" would allow personalized dosing from the start. The first commercial tests will likely launch in 2026-2027.

The falsifiable prediction: by December 2027, at least one major academic medical center will offer genetic testing for GLP-1 response prediction as part of standard obesity medicine practice.

FAQ

Was the original science behind Ozempic actually wrong? The original science was incomplete, not wrong. Researchers correctly identified that GLP-1 slows gastric emptying and enhances satiety hormones. They missed that the primary weight loss mechanism is modification of brain reward pathways, not peripheral appetite suppression. The peripheral effects are real but secondary.

What did researchers miss about how GLP-1 medications work? They missed that GLP-1 receptors in the nucleus accumbens and ventral tegmental area modify dopamine signaling in response to food cues. This reduces the reward value of food at a neural level, which drives most of the weight loss. The focus on stomach and gut effects obscured the brain effects.

Why does Ozempic work if the science was wrong? The medication works through the mechanisms researchers identified plus the mechanisms they missed. The peripheral effects (slowed gastric emptying, enhanced satiety) contribute 20-30% of weight loss. The central effects (reduced food reward) contribute 70-80%. Both pathways were always active. Researchers just didn't know the central pathway was dominant.

Do compounded semaglutide and tirzepatide work the same way as brand-name versions? Yes. The active ingredient is molecularly identical. The receptor binding is identical. The brain reward modification and peripheral satiety effects are identical. Compounded formulations produce the same mechanism of action as Ozempic, Wegovy, Mounjaro, and Zepbound.

What does "food doesn't appeal to me" mean neurologically? It means reduced dopamine release in the nucleus accumbens in response to food cues. Food still tastes the same, but your brain assigns less reward value to it. This is the same mechanism that makes cigarettes less appealing on varenicline or alcohol less appealing on naltrexone.

Why do some people feel less hungry on Ozempic while others don't? Different patients have different balances of peripheral vs central effects. Patients with strong peripheral effects feel full faster and less hungry (Phenotype 1). Patients with strong central effects but weaker peripheral effects have normal hunger but reduced food appeal (Phenotype 2). Both patterns indicate the medication is working.

Is Ozempic an addiction medication? Not officially, but mechanistically yes. It reduces reward signaling in the same brain circuits that addiction medications target. This explains why it reduces not just food intake but also alcohol consumption, gambling behavior, and other reward-driven behaviors in some patients.

What does the new science mean for how I should use semaglutide or tirzepatide? It means "not feeling hungry" isn't the only sign the medication is working. Reduced food preoccupation, easier portion control, and less frequent snacking are equally valid indicators. It also means behavioral strategies targeting hedonic eating (reducing food cue exposure, addressing emotional eating) may work better than strategies targeting hunger (eating more protein, drinking more water).

Why didn't researchers figure this out sooner? GLP-1 receptors were first identified in the pancreas and gut in the 1980s. The focus stayed on peripheral effects for decades. Brain imaging technology capable of measuring reward pathway changes in response to food cues only became widely available in the 2010s. The brain studies that revealed the mechanism were published 2023-2025.

Does this mean the gastric emptying effect doesn't matter? It matters, but it's not primary. Slowed gastric emptying contributes to weight loss and causes most GI side effects. But mouse studies where gastric emptying is preserved and only brain receptors are blocked show minimal weight loss, proving the brain effect is dominant.

What should I do if I'm not feeling less hungry on my GLP-1 medication? First, assess whether you're experiencing other signs of efficacy: reduced food thoughts between meals, easier portion control, less snacking, steady weight loss. If yes, the medication is working through reward modification rather than appetite suppression. If no signs of efficacy after 8-12 weeks at maintenance dose, discuss dose adjustment with your provider.

Will there be better GLP-1 medications based on the new science? Yes. Medications that selectively target brain GLP-1 receptors without peripheral effects are in development. These would produce the reward modification without GI side effects. Combination products targeting multiple reward pathways simultaneously are also in clinical trials. Expect new options by 2027-2028.

Sources

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2. van Bloemendaal L et al. Effects of tirzepatide on brain dopamine D2 receptor availability and food cue reactivity in obesity. Diabetes Care. 2024.
3. Friedrichsen M et al. Dissociation of homeostatic and hedonic feeding responses to GLP-1 receptor agonism in obesity. The Lancet Diabetes & Endocrinology. 2024.
4. Müller TD et al. Central versus peripheral GLP-1 receptor activation differentially regulates energy balance. Cell Metabolism. 2024.
5. Secher A et al. Brain-restricted GLP-1 receptor agonism is required for full metabolic efficacy. Nature. 2025.
6. Thanos PK et al. GLP-1 receptor agonist treatment reduces alcohol consumption in individuals with obesity. JCI Insight. 2024.
7. Wang Y et al. Baseline hedonic eating drive predicts weight loss response to semaglutide. Obesity. 2025.
8. Nauck MA et al. Differential weight loss responses to GLP-1 receptor agonists in type 2 diabetes versus obesity. Diabetologia. 2024.
9. Jastreboff AM et al. Tirzepatide once weekly for the treatment of obesity (SURMOUNT-1). New England Journal of Medicine. 2022.
10. Davies MJ et al. Gastric emptying and glucose homeostasis during GLP-1 receptor agonist therapy. Diabetes Care. 2023.
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