Incretins are hormones produced in the gut that play a vital role in blood glucose regulation and metabolic health. Whilst there are no natural sources of incretins in food—as these are hormones made within the body—certain dietary patterns can stimulate your body's own incretin production. Understanding how diet influences incretin secretion may help support metabolic function, particularly for those at risk of type 2 diabetes. This article explores the science behind incretins, how different foods trigger their release, and evidence-based dietary strategies that may enhance natural incretin activity. It also clarifies the important distinction between dietary approaches and incretin-based medications prescribed for diabetes management.
Summary: There are no natural dietary sources of incretins, as GLP-1 and GIP are hormones synthesised within the body, but certain foods—particularly proteins, carbohydrates, fats, and fibre—can stimulate the body's own incretin production.
- Incretins (GLP-1 and GIP) are gut hormones that enhance insulin secretion in response to food intake and account for 50–70% of postprandial insulin release in healthy individuals.
- Dietary proteins, carbohydrates, and fats trigger incretin secretion by stimulating enteroendocrine cells in the small intestine, with protein-rich meals particularly effective at stimulating GLP-1.
- Soluble and fermentable dietary fibres may enhance incretin secretion indirectly through production of short-chain fatty acids by gut microbiota, though clinical significance requires further study.
- Incretin-based medications (GLP-1 receptor agonists and DPP-4 inhibitors) are licensed treatments for type 2 diabetes that cannot be replicated by dietary approaches alone.
- People with type 2 diabetes should consult their GP or diabetes specialist before making significant dietary changes, and should never stop or adjust prescribed diabetes medications without medical advice.
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What Are Incretins and How Do They Work in the Body?
Incretins are a group of metabolic hormones produced primarily in the gastrointestinal tract in response to food intake. The two principal incretin hormones are glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), both of which play crucial roles in glucose homeostasis and metabolic regulation. These hormones are secreted by specialised enteroendocrine cells—L-cells in the distal small intestine and colon produce GLP-1, whilst K-cells in the proximal small intestine secrete GIP.
The primary mechanism of action of incretins involves the incretin effect, which accounts for approximately 50–70% of postprandial insulin secretion in healthy individuals, though this effect is substantially reduced in people with type 2 diabetes. When nutrients, particularly carbohydrates and fats, enter the gastrointestinal tract, they stimulate the release of GLP-1 and GIP into the bloodstream. These hormones then bind to specific receptors on pancreatic beta cells, potentiating glucose-dependent insulin secretion. Importantly, this effect only occurs when blood glucose levels are elevated, which minimises the risk of hypoglycaemia.
Beyond their insulinotropic effects, incretins exert several other metabolic actions. GLP-1 suppresses glucagon secretion from pancreatic alpha cells, slows gastric emptying, and promotes satiety through central nervous system pathways. GIP also influences lipid metabolism and may have effects on bone formation, though evidence in humans remains emerging. Both hormones are rapidly degraded by the enzyme dipeptidyl peptidase-4 (DPP-4), with half-lives of only 2–5 minutes for GLP-1 and approximately 7 minutes for GIP.
In type 2 diabetes, the incretin effect is impaired—particularly due to reduced responsiveness to GIP, with variable GLP-1 secretion. Understanding the physiological role of incretins has led to significant therapeutic advances in type 2 diabetes management, including the development of GLP-1 receptor agonists and DPP-4 inhibitors. However, there is growing interest in how dietary factors and lifestyle modifications might naturally support incretin function in those at risk of metabolic conditions.
Natural Sources of Incretins in Food and Diet
It is important to clarify a common misconception: incretins themselves are not directly obtained from food. Unlike vitamins or minerals, GLP-1 and GIP are endogenous hormones synthesised within the human body by intestinal cells. Therefore, there are no dietary sources that provide pre-formed incretin hormones. However, certain foods and nutrients can stimulate the body's own production and secretion of these hormones, effectively supporting natural incretin activity.
The primary dietary triggers for incretin secretion are macronutrients—particularly carbohydrates, proteins, and fats. When these nutrients reach the small intestine, they interact with nutrient-sensing receptors on enteroendocrine cells, initiating the release of GLP-1 and GIP. Different macronutrients stimulate incretin secretion through distinct mechanisms and to varying degrees.
Carbohydrates, especially glucose, are potent stimulators of both GLP-1 and GIP secretion. Complex carbohydrates that are digested more slowly may provide a more sustained incretin response compared to rapidly absorbed simple sugars, though evidence is mixed. Dietary proteins and their constituent amino acids also effectively stimulate incretin release. Emerging evidence suggests that certain amino acids, such as glutamine and arginine, may be particularly effective, though further human studies are needed to confirm these effects.
Dietary fats trigger incretin secretion as well, though the response may be delayed compared to carbohydrates, reflecting the slower digestion and absorption of lipids. Some evidence suggests that long-chain fatty acids may be more effective than short-chain fatty acids in stimulating GLP-1 release, though this requires further confirmation in human studies. Additionally, dietary fibre, particularly soluble and fermentable fibres, can enhance incretin secretion indirectly through the production of short-chain fatty acids (SCFAs) during colonic fermentation, though the clinical significance of this mechanism remains under investigation.
Rather than seeking foods containing incretins, individuals interested in supporting their natural incretin response should focus on consuming a balanced diet rich in whole foods—including adequate protein, high-fibre carbohydrates, and healthy fats—that may help stimulate the body's own hormone production.
How Diet Influences Incretin Hormone Production
The composition, timing, and quality of dietary intake may influence the magnitude and duration of incretin hormone secretion, though individual responses vary and long-term clinical benefits from dietary incretin modulation are not yet established.
Macronutrient composition appears to be a primary determinant of incretin response. Mixed meals containing carbohydrates, proteins, and fats typically elicit a more robust and sustained incretin secretion compared to meals composed of a single macronutrient. Research suggests that protein-rich meals may be particularly effective at stimulating GLP-1 secretion, whilst both carbohydrates and fats are strong triggers for GIP release. The glycaemic index and glycaemic load of carbohydrate-containing foods may also influence incretin dynamics, though evidence is inconsistent, with some studies showing enhanced responses to lower glycaemic index foods whilst others report no significant differences.
Dietary fibre may play a multifaceted role in incretin regulation. Soluble fibres, such as beta-glucans found in oats and barley, and viscous fibres like those in legumes, can slow gastric emptying and nutrient absorption, potentially prolonging incretin secretion. Furthermore, fermentable fibres serve as substrates for gut microbiota, which produce short-chain fatty acids (SCFAs) such as butyrate, propionate, and acetate. These SCFAs may directly stimulate L-cells to secrete GLP-1, though this mechanism is supported mainly by preclinical and small human studies, and clinical significance remains uncertain.
The gut microbiome itself is increasingly recognised as a potential mediator of incretin responses, though evidence is emerging. Dietary patterns that promote a diverse microbiome—characterised by high fibre intake and limited ultra-processed foods—may support incretin secretion, though robust interventional human data are limited. Conversely, an imbalanced microbiome may impair incretin function.
Meal timing and frequency may also matter. Some preliminary evidence suggests that incretin response may vary throughout the day, with potentially greater sensitivity in the morning, though this requires further confirmation. Regular meal patterns, as opposed to erratic eating schedules, may help maintain consistent incretin function. Important safety note: People taking insulin or sulfonylureas should consult their GP or diabetes specialist before attempting time-restricted eating or intermittent fasting, as these approaches may increase the risk of hypoglycaemia.
Incretin-Based Medications vs Natural Incretin Support
Incretin-based therapies are established treatment options for type 2 diabetes, but it is essential to understand how these medications differ from natural incretin support through diet and lifestyle.
Incretin-based medications fall into two main categories: GLP-1 receptor agonists (such as semaglutide, liraglutide, and dulaglutide) and DPP-4 inhibitors (such as sitagliptin, linagliptin, and saxagliptin). GLP-1 receptor agonists are synthetic analogues that mimic natural GLP-1 but are resistant to DPP-4 degradation, resulting in much longer half-lives and sustained pharmacological effects. These medications can reduce HbA1c by approximately 11–16 mmol/mol (1.0–1.5%) and often promote significant weight loss, though effects vary by agent and dose. DPP-4 inhibitors work by preventing the breakdown of endogenous incretins, thereby prolonging their activity, typically reducing HbA1c by approximately 5–9 mmol/mol (0.5–0.8%).
These medications are licensed by the MHRA and recommended by NICE for specific indications in type 2 diabetes management. According to NICE guideline NG28, GLP-1 receptor agonists may be considered for adults with type 2 diabetes when certain criteria are met, including inadequate glycaemic control on other therapies and specific BMI thresholds (typically BMI ≥35 kg/m² in people of White European descent, or ≥32.5 kg/m² in people of South Asian or other Black, African, Afro-Caribbean, or mixed ethnicity, with adjustments for other ethnic groups). NICE recommends continuing GLP-1 receptor agonist therapy only if there is a beneficial metabolic response (typically a reduction in HbA1c of at least 11 mmol/mol [1.0%] and weight loss of at least 3% of initial body weight at 6 months).
Common adverse effects of GLP-1 receptor agonists include nausea, vomiting, and diarrhoea, particularly during dose escalation. Important UK safety warnings include risks of pancreatitis and gallbladder disease; patients should be advised to seek medical attention if they experience severe abdominal pain. DPP-4 inhibitors are generally well-tolerated, though post-marketing surveillance has identified risks including severe joint pain (arthralgia), bullous pemphigoid (a rare skin reaction), and—for saxagliptin and alogliptin—a potential increased risk of heart failure in susceptible individuals. Patients should not stop or adjust their diabetes medicines without medical advice. If you experience any side effects, including those not listed in the patient information leaflet, report them via the MHRA Yellow Card Scheme at yellowcard.mhra.gov.uk or via the Yellow Card app.
Natural incretin support through dietary modification cannot replicate the pharmacological potency of these medications. Whilst a healthy diet may help optimise endogenous incretin secretion, incretin responsiveness is often impaired in individuals with type 2 diabetes—particularly due to reduced GIP responsiveness, with variable GLP-1 secretion. Dietary approaches may help preserve incretin function in those at risk of diabetes (non-diabetic hyperglycaemia, also known as pre-diabetes) or provide complementary benefits alongside medication, but they cannot substitute for prescribed therapy when clinically indicated.
That said, dietary strategies offer advantages including the absence of medication-related adverse effects, broader metabolic benefits, and suitability for diabetes prevention. For individuals with non-diabetic hyperglycaemia (pre-diabetes) or those seeking metabolic optimisation, focusing on natural incretin support through diet represents a safe, evidence-based approach. However, anyone with diagnosed diabetes should consult their GP or diabetes specialist before making significant dietary changes or considering medication adjustments.
Evidence for Dietary Approaches to Enhance Incretin Response
A growing body of research has examined how specific dietary interventions may influence incretin secretion and metabolic outcomes, though it is important to note that evidence quality varies, long-term clinical outcome benefits are not established, and further research is needed in many areas.
Protein-enriched diets have demonstrated particular promise. Several studies have shown that increasing dietary protein intake, particularly at breakfast, can enhance GLP-1 secretion and improve postprandial glucose control. Systematic reviews have found that protein preloads before meals consistently increased GLP-1 levels and reduced subsequent glucose excursions. Whey protein appears especially effective, possibly due to its rapid digestion and high content of branched-chain amino acids, though mechanisms require further clarification.
Dietary fibre interventions have also shown beneficial effects on incretin responses in some studies. Research indicates that diets high in soluble fibre may increase postprandial GLP-1 secretion, likely mediated through SCFA production by gut microbiota. Some trials have demonstrated that supplementation with fermentable fibres improved GLP-1 responses and insulin sensitivity in individuals with type 2 diabetes over 12 weeks, though results are not consistent across all studies.
Low glycaemic index diets may support more sustained incretin secretion by providing gradual nutrient delivery to the intestine. However, evidence is mixed, with some studies showing enhanced GLP-1 responses whilst others report no significant differences compared to higher glycaemic index diets.
Emerging research on time-restricted eating and intermittent fasting suggests these approaches might influence incretin dynamics, though mechanisms remain unclear and clinical significance is uncertain. Some studies indicate that prolonged fasting periods may enhance incretin sensitivity upon refeeding. Important safety note: People taking insulin or sulfonylureas should consult their GP or diabetes specialist before attempting these dietary patterns, as they may increase the risk of hypoglycaemia.
Limitations of current evidence include heterogeneity in study designs, small sample sizes, and short intervention durations. Most studies measure acute incretin responses rather than long-term metabolic outcomes. Additionally, there is no established link between specific dietary patterns and prevention of incretin-related metabolic dysfunction.
For practical application, individuals interested in supporting natural incretin function should consider a balanced diet emphasising whole foods, adequate protein, high fibre intake (in line with the NHS Eatwell Guide), and limited ultra-processed foods. Those with existing metabolic conditions should discuss dietary modifications with their healthcare provider to ensure approaches are appropriate and safe alongside any prescribed treatments.
Frequently Asked Questions
Can you get incretins directly from food?
No, incretins are not present in food. GLP-1 and GIP are hormones produced by your own intestinal cells in response to eating, so you cannot consume them directly, but certain foods can stimulate your body to produce them.
Which foods best stimulate natural incretin production?
Protein-rich foods, particularly whey protein, appear especially effective at stimulating GLP-1 secretion. Mixed meals containing carbohydrates, proteins, healthy fats, and high-fibre foods typically elicit robust incretin responses, though individual variation exists.
Can dietary changes replace incretin medications for type 2 diabetes?
No, dietary approaches cannot replicate the pharmacological effects of prescribed incretin-based medications. Whilst diet may support natural incretin function, people with type 2 diabetes should never stop or adjust their medications without consulting their GP or diabetes specialist.
The health-related content published on this site is based on credible scientific sources and is periodically reviewed to ensure accuracy and relevance. Although we aim to reflect the most current medical knowledge, the material is meant for general education and awareness only.
The information on this site is not a substitute for professional medical advice. For any health concerns, please speak with a qualified medical professional. By using this information, you acknowledge responsibility for any decisions made and understand we are not liable for any consequences that may result.
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