TL;DR: GLP-1 is a natural gut hormone with receptors throughout your brain — in the hypothalamus, hippocampus, and cortex. Drugs like semaglutide (Ozempic, Wegovy) and liraglutide mimic this hormone and are primarily prescribed for diabetes and obesity, but preclinical and early clinical evidence suggests they may also reduce neuroinflammation, protect against neuronal damage, and improve certain cognitive outcomes. Large-scale Alzheimer’s and Parkinson’s trials are underway. Meanwhile, you can boost your own GLP-1 secretion through dietary strategies: eating more fiber, protein, healthy fats, and fermented foods. This is an emerging field — the findings are promising but far from settled.

Introduction

Semaglutide — sold as Ozempic for type 2 diabetes and Wegovy for obesity — has become one of the most commercially successful drugs in pharmaceutical history. Its dramatic effects on appetite, body weight, and metabolic markers have attracted enormous public attention. But there is a parallel story unfolding in neuroscience laboratories and clinical trial registries that has received far less coverage: GLP-1 receptor agonists appear to have meaningful effects on the brain that extend well beyond appetite suppression.

GLP-1, or glucagon-like peptide-1, is not a pharmaceutical invention. It is a naturally occurring incretin hormone produced by L-cells in the small intestine in response to food intake. Its primary known role is to stimulate insulin secretion, slow gastric emptying, and signal satiety to the brain. But GLP-1 receptors are not limited to the pancreas and gut. They are expressed abundantly throughout the central nervous system — in the hypothalamus, hippocampus, cortex, substantia nigra, and brainstem — regions involved in appetite regulation, memory formation, executive function, and motor control.

This distribution pattern has led researchers to ask a question with profound implications: if GLP-1 drugs activate receptors throughout the brain, what are they doing to cognition, neuroinflammation, and long-term brain health?

The answer is still being written. But the evidence accumulated so far — from animal models, epidemiological databases, and early clinical trials — is generating serious scientific interest. This article examines what we know, what we do not know, and what it means for anyone interested in the intersection of metabolic health and brain function.

What Is GLP-1? The Biology of an Incretin Hormone

Understanding the brain effects of GLP-1 drugs requires first understanding the hormone they mimic.

GLP-1 is released from enteroendocrine L-cells in the ileum and colon within minutes of food entering the gut. Its secretion is stimulated by the presence of nutrients — particularly glucose, amino acids, and fatty acids — in the intestinal lumen. Once released, native GLP-1 has a half-life of only about two minutes before being degraded by the enzyme dipeptidyl peptidase-4 (DPP-4).

Despite this brief circulatory life, GLP-1 exerts its effects through two main routes. First, it acts locally on vagal afferent nerve terminals in the gut wall, sending signals to the brainstem and hypothalamus via the vagus nerve. Second, a portion of circulating GLP-1 reaches the brain directly through regions where the blood-brain barrier is more permeable, such as the area postrema and the median eminence.

The physiological effects of GLP-1 signaling include:

  • Insulin secretion: GLP-1 potentiates glucose-dependent insulin release from pancreatic beta cells.
  • Glucagon suppression: It reduces glucagon secretion, lowering blood sugar.
  • Gastric emptying: GLP-1 slows the rate at which food leaves the stomach, promoting prolonged satiety.
  • Appetite regulation: Through hypothalamic and brainstem circuits, GLP-1 reduces hunger and food intake.

Pharmaceutical GLP-1 receptor agonists like semaglutide, liraglutide, and tirzepatide are structurally modified to resist DPP-4 degradation, extending their half-lives from minutes to days or weeks. This allows them to produce sustained activation of GLP-1 receptors throughout the body — including the brain.

GLP-1 Receptors in the Brain: More Than Appetite Control

The distribution of GLP-1 receptors (GLP-1R) in the brain is extensive and, from a cognitive perspective, striking.

Hypothalamus

The arcuate nucleus and paraventricular nucleus of the hypothalamus are primary sites for GLP-1-mediated appetite suppression. This is the mechanism most people associate with drugs like Ozempic: reduced hunger, earlier satiety, and diminished food reward. GLP-1R activation in the hypothalamus modulates neuropeptide Y (NPY) and pro-opiomelanocortin (POMC) neurons — the core circuitry of energy homeostasis.

Hippocampus

GLP-1 receptors are densely expressed in the hippocampus, the brain region most critical for learning and memory. This is where the cognitive story becomes especially interesting. Multiple rodent studies have demonstrated that GLP-1R activation in the hippocampus enhances synaptic plasticity, promotes long-term potentiation (LTP) — the cellular mechanism underlying memory formation — and increases the expression of brain-derived neurotrophic factor (BDNF). During et al. (2003), in a study published in Nature Medicine, showed that GLP-1R overexpression in the hippocampus enhanced associative and spatial learning in rats, while GLP-1R knockout impaired it.

Cortex and Other Regions

GLP-1 receptors are also found in the cerebral cortex, substantia nigra, nucleus tractus solitarius, and ventral tegmental area — regions involved in executive function, motor control, autonomic regulation, and reward processing. This broad distribution suggests that GLP-1 signaling influences multiple domains of brain function, not just appetite.

Reward Pathways

GLP-1R activation in the mesolimbic dopamine system — particularly the ventral tegmental area and nucleus accumbens — modulates the reward value of food. This is why many patients on semaglutide report not just reduced hunger but a fundamental shift in their relationship with food: decreased cravings, reduced “food noise,” and diminished interest in highly palatable, calorie-dense foods. Emerging research, including work by Volkow and colleagues, suggests this reward modulation may also extend to other compulsive behaviors, though this remains preliminary.

Neuroprotection: Evidence from Preclinical Studies

The most scientifically compelling aspect of GLP-1 and the brain is not appetite modulation — it is neuroprotection. A substantial body of preclinical research suggests that GLP-1R activation protects neurons from damage through several convergent mechanisms.

Anti-Neuroinflammatory Effects

Chronic low-grade neuroinflammation is a hallmark of neurodegenerative diseases and age-related cognitive decline. GLP-1R agonists have been shown in multiple animal models to reduce microglial activation, decrease the production of pro-inflammatory cytokines (including TNF-alpha, IL-1beta, and IL-6), and attenuate the inflammatory cascades that damage neurons. McClean and Holscher (2014), working with a mouse model of Alzheimer’s disease, demonstrated that liraglutide reduced chronic inflammation in the brain, decreased beta-amyloid plaque load, and prevented synaptic loss.

Reduction of Oxidative Stress

GLP-1R activation upregulates endogenous antioxidant defenses, including superoxide dismutase and glutathione pathways. In models of both Alzheimer’s and Parkinson’s disease, GLP-1 receptor agonists have been shown to reduce markers of oxidative damage in brain tissue (Li et al., 2009). Given that oxidative stress is one of the key drivers of neuronal death in neurodegenerative conditions, this mechanism has generated considerable interest.

Beta-Amyloid and Tau Pathology

In Alzheimer’s disease models, GLP-1R agonists have repeatedly demonstrated the ability to reduce both amyloid-beta plaque deposition and tau hyperphosphorylation — the two pathological hallmarks of the disease. McClean, Parthsarathy, Faiber, and Holscher (2011) showed that liraglutide prevented memory impairment, reduced amyloid plaque burden by 40-50%, and increased hippocampal neurogenesis in APP/PS1 transgenic mice. These findings have been replicated across multiple laboratories and with different GLP-1R agonists.

Dopaminergic Neuron Protection

In Parkinson’s disease models, GLP-1R agonists have shown protective effects on dopaminergic neurons in the substantia nigra — the population of neurons whose progressive loss causes the motor symptoms of Parkinson’s. Bertilsson et al. (2008) found that GLP-1R stimulation promoted the survival and differentiation of dopaminergic neurons and improved motor function in a rodent model of Parkinson’s disease.

Clinical Evidence: What Human Data Exists

The leap from animal models to human clinical evidence is always the critical step, and GLP-1 drugs and cognition are still early in this translation. However, several lines of human evidence are emerging.

The ELAD Trial (Liraglutide and Alzheimer’s)

The Evaluating Liraglutide in Alzheimer’s Disease (ELAD) trial, led by Edison and colleagues at Imperial College London, was the first randomized controlled trial to test a GLP-1R agonist specifically for Alzheimer’s disease. Published in 2021 in Alzheimer’s Research & Therapy, the Phase IIb trial enrolled 204 patients with mild Alzheimer’s disease and randomized them to liraglutide 1.8 mg/day or placebo for 12 months.

The primary outcome — change in cerebral glucose metabolic rate measured by FDG-PET — showed that liraglutide significantly reduced the decline in brain glucose metabolism compared to placebo, particularly in the temporal and parietal lobes. This is meaningful because declining cerebral glucose metabolism is one of the earliest and most consistent biomarkers of Alzheimer’s progression. The trial was not powered to detect differences in clinical cognitive outcomes, but the biomarker results were sufficiently encouraging to prompt the design of larger Phase III trials.

Semaglutide Alzheimer’s Trials (EVOKE and EVOKE+)

Novo Nordisk, the manufacturer of semaglutide, launched two large Phase III randomized controlled trials — EVOKE (n = ~1,840) and EVOKE+ (n = ~1,840) — to test oral semaglutide (14 mg daily) in people with early Alzheimer’s disease. These trials, which began enrolling in 2021, are the largest and most rigorous tests of a GLP-1R agonist for neurodegeneration to date. Primary endpoints include clinical cognitive assessments (CDR-SB and ADAS-Cog), not just biomarkers. Results are expected to begin emerging in 2025-2026.

If these trials produce positive results, they would represent a paradigm shift — not only for Alzheimer’s treatment but for our understanding of the relationship between metabolic signaling and neurodegeneration.

The Exenatide-PD Trial (Parkinson’s Disease)

Athauda, Maclagan, Skene, and colleagues (2017) conducted a randomized, double-blind, placebo-controlled trial of exenatide (another GLP-1R agonist) in 62 patients with moderate Parkinson’s disease, published in The Lancet. Patients received exenatide 2 mg once weekly or placebo for 48 weeks, followed by a 12-week washout period.

The results were notable. The exenatide group showed a statistically significant improvement on the Movement Disorder Society Unified Parkinson’s Disease Rating Scale (MDS-UPDRS Part 3) — a clinically validated motor assessment — compared to the placebo group, which showed the expected decline. The between-group difference persisted 12 weeks after the drug was stopped, suggesting a disease-modifying effect rather than merely symptomatic relief.

This trial, while small, was published in one of medicine’s most prestigious journals and has been widely cited as the strongest clinical evidence to date that GLP-1R agonists may have genuine neuroprotective effects in humans.

Epidemiological Data

Large retrospective database analyses have added another layer of evidence. Norgaard et al. (2022), using Danish national health registries, found that patients with type 2 diabetes treated with GLP-1 receptor agonists had significantly lower rates of dementia diagnosis compared to those treated with other diabetes medications, even after adjusting for age, sex, comorbidities, and other confounders. Similar findings have emerged from UK Biobank analyses and US Veterans Affairs databases.

These observational studies cannot prove causation — patients prescribed GLP-1 agonists may differ from other diabetes patients in systematic ways — but the consistency of the signal across multiple independent datasets strengthens the case for a genuine neuroprotective effect.

How GLP-1 Drugs Affect Appetite and the Food-Brain Connection

The cognitive effects of GLP-1 drugs cannot be fully separated from their metabolic effects. Obesity, insulin resistance, and type 2 diabetes are themselves independent risk factors for cognitive decline and dementia. By improving metabolic health — reducing body weight, improving glycemic control, lowering systemic inflammation, and reducing insulin resistance — GLP-1 drugs may indirectly benefit the brain through improved metabolic milieu.

This is an important nuance. When epidemiological studies show lower dementia rates among GLP-1R agonist users, it is difficult to determine how much of the benefit comes from direct neuroprotection (the drug acting on brain GLP-1 receptors) versus indirect metabolic improvement (better blood sugar control, less visceral fat, lower systemic inflammation). Both pathways are plausible, and both may be operating simultaneously.

The relationship between insulin signaling and brain function is particularly relevant (see also blood sugar and brain function). Alzheimer’s disease has been described by some researchers as “type 3 diabetes” due to the prominent role of brain insulin resistance in its pathophysiology. If GLP-1R agonists improve brain insulin signaling — as several preclinical studies suggest — this could represent a mechanistic link between their metabolic and cognitive effects.

Boosting Endogenous GLP-1 Through Diet

While pharmaceutical GLP-1R agonists dominate the headlines, your body produces GLP-1 naturally every time you eat. The amount of GLP-1 released depends substantially on what you eat. This means dietary choices can meaningfully modulate your own incretin signaling — and potentially reap some of the same benefits, albeit at lower intensity, without a prescription.

Dietary Fiber

Fiber is one of the most potent dietary stimulators of GLP-1 secretion. When fermentable fibers reach the colon, gut bacteria convert them into short-chain fatty acids (SCFAs) — primarily butyrate, propionate, and acetate. SCFAs activate free fatty acid receptors (FFAR2 and FFAR3) on L-cells, directly stimulating GLP-1 release. Tolhurst et al. (2012), in a study published in Diabetes, demonstrated that SCFAs trigger GLP-1 secretion from colonic L-cells through FFAR2 activation.

Practical sources: oats, barley, legumes (lentils, chickpeas, black beans), Jerusalem artichokes, garlic, onions, leeks, asparagus, and psyllium husk.

Protein

Amino acids — particularly glutamine, glycine, and phenylalanine — are strong stimulators of GLP-1 secretion from the small intestine. Protein-rich meals consistently produce a more robust GLP-1 response than isocaloric carbohydrate-heavy meals. Reimann et al. (2012) elucidated the molecular mechanisms by which amino acids trigger GLP-1 release, involving calcium-sensing receptors and GPRC6A on L-cells.

Practical sources: eggs, fish, poultry, legumes, Greek yogurt, and tofu.

Healthy Fats

Monounsaturated and polyunsaturated fatty acids stimulate GLP-1 release through GPR40 and GPR120 receptors on L-cells. Oleic acid (abundant in olive oil and avocados) and omega-3 fatty acids (from fatty fish, flaxseed, and walnuts) are particularly effective.

Fermented Foods

Fermented foods influence GLP-1 secretion indirectly by supporting microbial diversity and SCFA production. A healthy, diverse microbiome produces more SCFAs from dietary fiber, which in turn stimulates more GLP-1 release. This creates a positive feedback loop: fiber feeds bacteria, bacteria produce SCFAs, SCFAs stimulate GLP-1, and GLP-1 supports both metabolic and potentially cognitive health.

Polyphenols

Certain polyphenols, particularly those found in green tea (EGCG), berries, and dark chocolate, have been shown in cell culture and animal studies to enhance GLP-1 secretion. Gonzalez-Abuin et al. (2015) demonstrated that grape seed proanthocyanidins stimulated GLP-1 release and improved glucose tolerance in rats. While human data on polyphenol-mediated GLP-1 enhancement is limited, the broader health benefits of polyphenol-rich foods are well established.

A Dietary Strategy for Endogenous GLP-1

Combining these approaches into a coherent dietary pattern is straightforward and aligns closely with other evidence-based dietary frameworks for brain health, such as the Mediterranean diet for brain health:

  • Start meals with vegetables and protein before carbohydrates (this sequencing has been shown to enhance GLP-1 response)
  • Include fermentable fiber at every meal
  • Prioritize whole, minimally processed foods over refined options
  • Use extra virgin olive oil as your primary cooking and finishing fat
  • Eat fatty fish two to three times per week
  • Include fermented foods daily
  • Minimize ultra-processed food, which tends to be low in fiber and protein — the two macronutrients that most strongly stimulate GLP-1

Concerns and Unknowns

The enthusiasm surrounding GLP-1 drugs and the brain must be tempered by honest acknowledgment of what we do not yet know.

Long-Term Brain Effects Are Unknown

GLP-1R agonists have been used widely for diabetes and obesity for roughly a decade. We have reasonable safety data over that period for metabolic endpoints, but we have virtually no long-term data on their effects on brain structure, function, or dementia risk when used chronically. The brain studies are still in early phases.

The Dose-Response Question

The doses of GLP-1R agonists used in neuroprotection studies — both animal and human — vary considerably. It is not clear whether the doses that produce metabolic benefits (appetite suppression, weight loss) are the same doses needed for neuroprotective effects, or whether higher brain-penetrant doses would be required.

Gastrointestinal Side Effects

Nausea, vomiting, and other GI side effects are common with GLP-1R agonists, particularly during dose titration. In some patients, these effects are severe enough to cause discontinuation. If the neuroprotective benefits require long-term use, tolerability becomes a critical factor.

Not a Substitute for a Healthy Diet

Even if GLP-1R agonists prove to have genuine neuroprotective properties, they would not replace the need for a brain-supportive diet. The drug mimics one hormonal signal; a healthy diet provides thousands of bioactive compounds, fiber substrates, micronutrients, and microbial inputs that no single pharmaceutical can replicate. The most sensible framing is that GLP-1 drugs and dietary optimization may be complementary, not interchangeable.

Publication Bias and Hype Cycles

The enormous commercial success of GLP-1 drugs creates incentives — financial and reputational — to find positive brain effects. Researchers, clinicians, and science communicators should maintain appropriate skepticism until large, well-designed, pre-registered trials deliver their results. The history of Alzheimer’s drug development is littered with therapies that showed promise in preclinical and early clinical stages but failed in definitive trials.

The Rapidly Evolving Research Landscape

The pace of GLP-1 and brain research is accelerating. As of early 2026, several developments are worth watching:

  • EVOKE and EVOKE+ trial results for oral semaglutide in early Alzheimer’s disease are the single most important upcoming data readouts in this field.
  • Next-generation dual and triple agonists (GLP-1/GIP, GLP-1/GIP/glucagon) such as tirzepatide and retatrutide are being investigated for potential brain effects. Whether these multi-receptor agonists have additive neuroprotective properties is an open question.
  • Neuroimaging substudies embedded within large obesity and diabetes trials are providing data on how GLP-1R agonists affect brain structure, connectivity, and metabolism in vivo.
  • Mechanistic studies are working to clarify whether semaglutide and other GLP-1R agonists cross the blood-brain barrier in therapeutically relevant concentrations, or whether their central effects are mediated primarily through vagal signaling and circumventricular organ access.

This is a field where the landscape may look meaningfully different in twelve to twenty-four months. The recommendations in this article reflect the evidence as it stands in early 2026 and should be updated as definitive trial data emerge.

Practical Takeaway

  1. GLP-1 is a natural hormone, not just a drug. Your body produces GLP-1 every time you eat, particularly in response to fiber, protein, and healthy fats. Optimizing your diet to support endogenous GLP-1 production is a sensible strategy regardless of whether you take or plan to take a GLP-1R agonist.

  2. Eat more fiber — especially fermentable fiber. Legumes, oats, barley, garlic, onions, leeks, and asparagus feed gut bacteria that produce the short-chain fatty acids which directly stimulate GLP-1 release from intestinal L-cells.

  3. Prioritize protein and healthy fats at meals. These macronutrients trigger stronger GLP-1 responses than refined carbohydrates. Meal sequencing — eating vegetables and protein before starches — can further enhance the incretin effect.

  4. Do not treat GLP-1 drugs as a cognitive supplement. The neuroprotective evidence is promising but preliminary. These medications carry side effects, are prescribed for specific metabolic conditions, and should be used only under medical supervision.

  5. Watch the EVOKE trials. The results of the semaglutide Alzheimer’s trials will be a watershed moment for this field. Positive results would fundamentally change the conversation about metabolic drugs and brain health.

  6. Maintain perspective. The foundations of brain health remain unchanged: a nutrient-dense diet rich in whole foods, regular physical activity, adequate sleep, stress management, and social engagement. GLP-1 biology is one piece of a much larger puzzle.

Frequently Asked Questions

Should I take Ozempic or Wegovy for brain health?

No. GLP-1R agonists are currently approved for type 2 diabetes and obesity. There is no approved indication for cognitive enhancement or neuroprotection. The clinical trial evidence for brain-specific effects is still in early stages, and the definitive Alzheimer’s trials have not yet reported results. If you have diabetes or obesity and are considering these medications for their approved indications, the potential brain benefits are an interesting secondary consideration to discuss with your doctor — but they should not be the primary reason for starting treatment.

Can dietary changes really affect GLP-1 levels?

Yes. The magnitude of GLP-1 secretion after a meal is strongly influenced by the macronutrient composition and fiber content of that meal. High-fiber, high-protein meals produce substantially greater GLP-1 responses than low-fiber, high-refined-carbohydrate meals. While the absolute GLP-1 levels achieved through diet are lower than those produced by pharmaceutical agonists, the dietary approach provides sustained, physiological stimulation of the GLP-1 system as part of a broader pattern of metabolic health.

Is there a connection between GLP-1 and the gut-brain axis?

Absolutely. GLP-1 is a gut-derived hormone that signals to the brain — it is one of the most direct molecular links in the gut-brain axis. The vagus nerve, which carries GLP-1-related signals from the gut to the brainstem, is the same pathway through which the gut microbiome communicates with the central nervous system. Dietary strategies that support microbiome health (fermented foods, prebiotic fiber, polyphenols) also support GLP-1 signaling, creating overlapping pathways of benefit.

Do GLP-1 drugs affect mood or mental health?

This is an area of active investigation. Some patients report mood changes — both positive and negative — while taking GLP-1R agonists. The European Medicines Agency conducted a safety review in 2023 and did not find a causal association between GLP-1R agonists and suicidality, but ongoing pharmacovigilance continues. On the positive side, GLP-1R activation in the mesolimbic dopamine system may influence reward processing and compulsive behaviors, and some early observational data suggest reduced rates of depression among GLP-1R agonist users. This is an area where more data is needed before drawing firm conclusions.

How does insulin resistance relate to brain health?

Insulin resistance is increasingly recognized as a risk factor for cognitive decline and Alzheimer’s disease. Brain insulin signaling supports neuronal survival, synaptic plasticity, and glucose metabolism. When brain insulin signaling is impaired — a condition sometimes called “brain insulin resistance” — neurons become more vulnerable to damage, amyloid clearance is reduced, and tau pathology is accelerated. By improving systemic and potentially central insulin sensitivity, GLP-1R agonists may address one of the upstream drivers of neurodegeneration. This hypothesis is being tested in the ongoing clinical trials.

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