Olor Corporal

5-HTP, the direct serotonin precursor, is clinically studied for satiety and appetite suppression. By increasing CNS serotonin, it suppresses appetite and reduces carbohydrate and fat intake. A ClinicalTrials.gov registered study specifically investigated 5-HTP's effects on satiety hormones.

Akkermansia muciniphila, a gut bacterium associated with metabolic health, has been shown in cell studies to stimulate GLP-1 secretion from human L-cells in a dose-dependent manner. Its secreted protein P9 acts on enteroendocrine L-cells via the ICAM-2 receptor to enhance GLP-1 release.

Barley β-glucan stimulates GLP-1 secretion via colonic SCFA production acting on GPR43 receptors, and through direct L-cell stimulation in the distal gut. Human studies confirm postprandial GLP-1 increases following barley β-glucan consumption, supporting satiety and glycemic regulation.

Berberine has been shown in multiple in vitro and animal studies to stimulate GLP-1 secretion from intestinal L-cells via activation of bitter taste receptors (TAS2R38) in a PLC-dependent pathway. It also restores GLP-1 secretion in diet-induced obese mouse models by protecting colon enterocyte mitochondrial function. Human studies support its glucose-lowering effects partly attributed to GLP-1 modulation.

Beta-glucan slows gastric emptying and nutrient absorption, which can stimulate enteroendocrine L-cells to release GLP-1, contributing to enhanced satiety signals. A randomized crossover trial confirmed beta-glucan-enriched oat bread delayed gastric emptying and modulated GLP-1 secretion. Results on GLP-1 magnitude are mixed depending on dose, molecular weight, and food matrix.

Bile acids are potent stimulators of GLP-1 secretion from intestinal L-cells via TGR5 receptor activation, a mechanism demonstrated in human physiological studies. GLP-1 induces satiety, slows gastric emptying, and potentiates insulin secretion. Bariatric surgery-associated GLP-1 increases correlate with elevated serum bile acids. Bile acid signaling via TGR5 is a mechanistically established upstream trigger of the incretin-satiety axis.

Butyrate stimulates GLP-1 and PYY secretion from intestinal L-cells, contributing to satiety signaling. Human evidence shows that sodium butyrate supplementation increases plasma GLP-1 concentrations, though direct clinically meaningful appetite suppression from butyrate alone awaits robust RCT confirmation.

Capsaicin stimulates GLP-1 secretion from intestinal L-cells via TRPV1 activation, as demonstrated in animal models and supported by mechanistic human data. TRPV1-deficient mice lose this response, confirming receptor dependence. This pathway links capsaicinoids to both blood sugar balance and satiety.

Caralluma fimbriata is an edible succulent plant used traditionally in India as an appetite suppressant. A systematic review and meta-analysis of 7 clinical RCTs found significant reductions in waist circumference vs. placebo. Its pregnane glycosides are proposed to suppress appetite via hypothalamic NPY and ghrelin pathways.

Chickpea protein and resistant starch stimulate secretion of gut incretin hormones including GLP-1 and PYY, which regulate glucose homeostasis and satiety. A randomised crossover study found enhanced secretion of satiety-promoting gut hormones in humans consuming white bread enriched with cellular chickpea flour. Fermentation of chickpea fibre in the colon produces SCFAs that further upregulate GLP-1.

Chlorogenic acid, a key polyphenol in coffee and green coffee bean extract, has been shown to increase postprandial active GLP-1 levels. Coffee consumption, attributed in part to chlorogenic acids, is associated with increased GLP-1 release.

Cinnamon has been identified in systematic reviews as capable of influencing GLP-1 release and is noted among herbal constituents with effects on incretin hormone pathways. Evidence includes in vitro, animal, and some human metabolic studies showing improved postprandial glucose and insulin responses consistent with GLP-1 activity.

Curcumin, the active polyphenol in turmeric, has been identified in multiple reviews as capable of influencing GLP-1 release. It may inhibit DPP-4, the enzyme that degrades GLP-1, thereby prolonging GLP-1 activity. Evidence is primarily from in vitro and animal studies, with supporting human metabolic data.

EGCG, the primary catechin in green tea, has been shown to stimulate GLP-1 secretion in intestinal enteroendocrine cells (NCI-H716) in vitro. It is used as a positive control in GLP-1 secretion assays and has supporting evidence from in vitro and animal models for GLP-1-mediated satiety.

Fenugreek has been reported as a GLP-1 modulator, AMPK activator, and DPP-IV inhibitor in peer-reviewed research. Its seed extract contains a compound (N55) that potentiates GLP-1 signaling, supported by a J Biol Chem study. Clinical trials show fenugreek improves blood glucose, insulin resistance, and insulin sensitivity.

FOS fermentation generates SCFAs that activate GPR41 and GPR43 receptors on enteroendocrine L-cells, stimulating secretion of GLP-1 and PYY and thereby reducing appetite. This mechanism is well-established in mechanistic and animal research. Human clinical evidence for appetite suppression and satiety specifically from FOS is supported by the ITF literature, with some trials showing reduced food intake and gut hormone responses.

Gardeniae fructus (Gardenia jasminoides fruit) demonstrated significantly greater GLP-1 secretion than positive control EGCG in an in vitro assay. Two of its ligands—3-epioleanolic acid and crocin—were predicted to bind to the active GLP-1 receptor, suggesting potential as GLP-1 receptor agonists.

Bitter secoiridoids in gentian root (especially gentiopicrin) activate intestinal TAS2R bitter taste receptors on enteroendocrine L-cells, stimulating GLP-1 and CCK secretion. A small human crossover study with microencapsulated G. lutea bitter compounds delivered to the small intestine observed a tendency for higher GLP-1 response and reduced post-lunch energy intake. A 3-month RCT with a gentian-containing multi-herb formulation showed significantly elevated CCK and satiety. Evidence is mechanistically sound but based on small or multi-ingredient human trials.

Ginger is consistently included in authoritative reviews among natural products with potent effects on GLP-1 activity. Its active components (gingerols, shogaols) are proposed to stimulate GLP-1 secretion and influence appetite regulation. Evidence comes primarily from in vitro and animal studies, with human metabolic data supporting satiety effects.

Ginseng (Panax ginseng) ginsenosides have been shown to stimulate GLP-1 secretion from human enteroendocrine cells. The gintonin-enriched fraction stimulates GLP-1 secretion via the LPA6 receptor in human L-cells, and ginsenoside compound K was shown to stimulate GLP-1 in vitro.

Glucomannan (konjac) is a highly viscous soluble fiber that promotes satiety and has been studied in RCTs for its effects on GLP-1, weight loss, and glycemic control. A 2024 RCT found combined glucomannan/psyllium/inulin significantly reduced body weight and fat mass in obese adults.

Green tea catechins, particularly EGCG, have been shown to stimulate GLP-1 secretion in intestinal cells and may improve insulin resistance and satiety. It is consistently listed in authoritative reviews among natural products with GLP-1-stimulating effects.

Gymnema sylvestre has a long traditional use as a satiety and blood-sugar modulator ('sugar destroyer'). Its gymnemic acids suppress sweet taste perception by acting on T1R taste receptors, reducing desire for sweet foods. It has also been studied in combination with Garcinia cambogia showing greater satiety and leptin effects than placebo.

Inulin is a prebiotic fiber whose fermentation produces SCFAs that activate satiety-related gut hormone pathways including GLP-1 secretion. Rodent studies show inulin increases GLP-1 secretion, and human studies show improved glycemia and satiety outcomes consistent with GLP-1 activity.

IMO ingestion stimulates incretin hormone (including GLP-1) secretion comparably to dextrose in healthy adults, based on a dedicated crossover study. IMO's prebiotic fermentation also increases SCFA production, which promotes GLP-1 release from L-cells. The effect may support satiety signaling.

L-glutamine is identified as one of the most potent natural GLP-1 secretagogues, increasing GLP-1 release 7-fold in cell studies. In human trials, 30 g oral glutamine raises GLP-1 and lowers postprandial blood sugar in type 2 diabetes patients.

L-phenylalanine has been identified as among the most potent amino acid stimulants of GLP-1 release in preclinical models, acting through the calcium-sensing receptor (CaSR) on intestinal L-cells. In rodents, it also raises PYY and suppresses ghrelin. Human evidence for GLP-1 stimulation specifically by L-Phe is emerging but less definitive than the rodent data.

Oat β-glucan modulates gut satiety hormones including GLP-1, PYY, and ghrelin, though results across individual studies are inconsistent. Longer-term supplementation in diabetic populations shows more consistent effects on satiety hormone profiles than single-meal acute studies.

A double-blind RCT (n=22, IGT patients) found that fortifying a single meal with 20 g of oyster mushroom powder significantly raised GLP-1-AUC by 17% (P=0.001) and reduced hunger-AUC by 22% (P=0.031) versus control. A 2025 follow-up study further confirmed that GLP-1 responses to oyster mushroom powder depend on individual gut microbiota composition.

Intact pea protein has been shown in human studies to elevate circulating GLP-1 and PYY levels, contributing to satiety signaling. Exposing duodenal tissue to intact pea protein specifically induces CCK and GLP-1 release. Co-ingestion with carbohydrates also modulates GLP-1 and GIP responses.

Dietary pectin stimulates GLP-1 and PYY release, particularly through colonic fermentation and SCFA production. Animal data show substantial elevations in both hormones with pectin feeding. Dietary fiber broadly stimulates GI satiety pathways including GLP-1 signaling and peptide YY release.

Propionate is a well-characterized secretagogue for GLP-1, acting through FFAR2/FFAR3 receptors on intestinal L cells. Human colonic cell models and clinical trials confirm that propionate directly stimulates GLP-1 secretion and raises circulating GLP-1 levels, contributing to postprandial satiety and reduced energy intake. This is one of the most robustly documented mechanisms linking propionate to metabolic health.

Psyllium fiber has been shown in clinical studies to be associated with increased GLP-1 levels and improved glycemic control. A randomized crossover study compared psyllium-enriched meals to exenatide (a GLP-1 receptor agonist) and found psyllium increased GLP-1 secretion. Meta-analyses support its role in promoting satiety.

Quercetin is a widely distributed dietary flavonoid with evidence from in vitro and animal studies showing GLP-1-stimulating activity. Reviews of natural GLP-1 modulators consistently include quercetin among compounds with potent effects on GLP-1 secretion from intestinal L-cells.

Resveratrol, a polyphenol found in grapes and other plants, has been shown in rodent studies to increase portal GLP-1 and insulin concentrations. It is listed among natural compounds with compelling evidence for GLP-1 activity in peer-reviewed reviews.

Rye-based evening meals have been shown in RCTs to increase plasma PYY and GLP-1/GLP-2 levels the following morning, likely through colonic fermentation of rye's dietary fiber to SCFAs. These gut hormones suppress appetite and regulate glucose metabolism. This 'second-meal effect' is a replicated finding in healthy human studies.

Spinach-derived thylakoids delay fat digestion in the small intestine, prolonging lipid exposure to distal gut L-cells and stimulating GLP-1 secretion. Multiple RCTs confirm that spinach thylakoid supplementation significantly increases postprandial GLP-1 levels and reduces hunger in overweight individuals.

Spirulina protein hydrolysates have demonstrated potent DPP-IV inhibition (up to 74%) in a 2023 food science study, thereby preserving endogenous GLP-1. Its blue pigment phycocyanin has independently shown DPP-IV inhibitory activity, supporting GLP-1-mediated satiety.

Thylakoids extracted from green plants (e.g., spinach) have been shown in human intervention studies to enhance release of appetite-suppressant hormones including GLP-1, CCK, and leptin while suppressing ghrelin. A 3-month human study showed 6.3% body weight loss with thylakoid supplementation.

Whey protein is among the most satiating macronutrient sources and has been shown in multiple human RCTs to increase postprandial GLP-1 and PYY levels compared to other protein sources. These effects are attributed to its unique amino acid profile, particularly glutamine, phenylalanine, and leucine.

Xylose is a potent stimulant of GLP-1 secretion in humans, as demonstrated in a controlled study comparing xylose and glucose ingestion in healthy older subjects (British Journal of Nutrition). The mechanism is attributed to xylose's incomplete and delayed intestinal absorption, which exposes distal small intestinal L-cells to luminal xylose and sustains GLP-1 release beyond that seen with glucose. No direct human satiety-outcome trials using D-xylose as a supplement have been published.