Merged from 2 sources — review for redundancy.
GLP-1 (Glucagon-Like Peptide-1) is an incretin hormone secreted by enteroendocrine L-cells in the distal ileum and colon in response to nutrient detection, particularly glucose and fats. It potentiates glucose-dependent insulin secretion from pancreatic beta cells, suppresses glucagon release from alpha cells, delays gastric emptying via vagal pathways, and promotes satiety through hypothalamic signaling. GLP-1 has a half-life of 2-3 minutes due to rapid degradation by dipeptidyl peptidase-4 (DPP IV), making it a tightly regulated metabolic messenger.
Think of GLP-1 as the kitchen manager who anticipates dinner guests before they arrive. The moment the doorbell rings (cephalic phase — sight, smell, taste of food), the manager starts preparing the dining room, even before guests sit down. When the first course arrives in the stomach, the manager sends a scout down to the far end of the house (the distal ileum) to check what's coming. When nutrients finally reach that distant checkpoint, the scout (L-cells) radios the pancreas: "Get ready to serve insulin — glucose is on its way!" The manager also tells the kitchen door (pyloric sphincter) to slow down, keeping food in the stomach longer so the pancreas isn't overwhelmed. Meanwhile, the manager announces to the brain's appetite center: "We're serving plenty — you can relax." But this manager has a security team (DPP IV) that fires them after just 2-3 minutes on the job, ensuring the response is proportional to the actual meal size. If you block that security team (with DPP-IV inhibitors or GLP-1 agonists), the manager stays on duty much longer, keeping insulin flowing and appetite suppressed.
¶ GLP-1 Secretion and Signaling Cascade
Phase 1: Cephalic Priming (Pre-Nutrient)
- Cephalic phase activation (sight, smell, taste) → vagal efferents → preemptive GLP-1 secretion from L-cells
- This accounts for ~10-15% of total incretin response before nutrients arrive
Phase 2: Nutrient-Triggered Secretion
- Nutrients (especially Glucose, fats, Amino Acids) contact L-cells in distal ileum and colon
- Glucose enters L-cells via SGLT1 (sodium-glucose cotransporter) and GLUT2
- Intracellular glucose metabolism → ↑ ATP → closure of K-ATP channels → membrane depolarization → Ca²⁺ influx → GLP-1 vesicle exocytosis
- Short-chain fatty acids (Butyrate, propionate) bind GPR41 and GPR43 on L-cells → additional GLP-1 secretion
- Bile acids activate TGR5 receptors on L-cells → enhanced GLP-1 release
Phase 3: Beta Cell Insulin Potentiation
- GLP-1 binds GLP-1 receptor (GPCR) on pancreatic beta cells
- Receptor coupling → activation of adenylyl cyclase → ↑ CAMP
- CAMP → activation of PKA (protein kinase A) and Epac2 (exchange protein activated by cAMP)
- PKA → phosphorylation of voltage-gated Ca²⁺ channels → sustained Ca²⁺ influx
- Epac2 → direct potentiation of insulin granule exocytosis machinery
- PKA → phosphorylation of CREB → transcription of insulin gene → long-term beta cell function
- Critical: GLP-1 only enhances insulin secretion when glucose >5.5 mmol/L — this is glucose-dependent potentiation, preventing hypoglycemia
Phase 4: Alpha Cell Glucagon Suppression
- GLP-1 binds GLP-1 receptors on pancreatic alpha cells
- Activation → ↑ CAMP → inhibition of glucagon exocytosis
- Paracrine insulin from beta cells (amplified by GLP-1) also suppresses alpha cells
- Net effect: ↓↓ Glucagon secretion → reduced hepatic glucose output
Phase 5: Gastric Emptying Delay
- GLP-1 activates GLP-1 receptors on vagal afferents in stomach wall
- Signal transmitted via Vagus nerve → nucleus tractus solitarius (Nucleus tractus solitarius) → dorsal motor nucleus of vagus (DMV)
- DMV → efferent vagal output → pyloric sphincter contraction
- Gastric emptying delayed by 30-50% → prolonged nutrient absorption → smoother glucose curve
Phase 6: Central Appetite Suppression
- GLP-1 crosses blood-brain barrier at circumventricular organs (Circumventricular organs)
- Binds GLP-1 receptors on neurons in arcuate nucleus (Nucleus Arcuatus) and paraventricular nucleus (Paraventricular nucleus)
- Activation of POMC (pro-opiomelanocortin) neurons → release of α-MSH → melanocortin receptor activation → ↓ appetite
- Inhibition of NPY/AgRP neurons (orexigenic) → reduced hunger signaling
- Direct GLP-1 receptor activation in hypothalamic satiety centers → "meal termination" signal
Phase 7: Rapid Degradation
- DPP IV enzyme (expressed on endothelial cells, immune cells) cleaves GLP-1 at N-terminus
- Intact GLP-1 → GLP-1(9-36) amide (inactive metabolite)
- Half-life of active GLP-1: 2-3 minutes in circulation
- Renal clearance of inactive metabolites
- This short half-life ensures tight temporal coupling to nutrient intake
graph TD
A[Nutrients in Distal Ileum] -->|Glucose via SGLT1/GLUT2| B[L-Cell Activation]
A2[SCFAs from Microbiome] -->|GPR41/43 binding| B
A3[Bile Acids] -->|TGR5 activation| B
B -->|"↑ ATP → K-ATP closure"| C["Ca²⁺ Influx"]
C --> D[GLP-1 Secretion]
D --> E[GLP-1 Receptor on Beta Cells]
E -->|Gs coupling| F["↑ cAMP"]
F --> G[PKA Activation]
F --> H[Epac2 Activation]
G --> I["Ca²⁺ Channel Phosphorylation"]
G --> J["CREB Phosphorylation → Insulin Gene Transcription"]
H --> K[Insulin Granule Exocytosis]
I --> K
K --> L[Insulin Release - Glucose Dependent]
D --> M[GLP-1 Receptor on Alpha Cells]
M --> N["↓ Glucagon Secretion"]
D --> O[Vagal Afferents]
O -->|"NTS → DMV"| P[Delayed Gastric Emptying]
D --> Q[Hypothalamic GLP-1 Receptors]
Q -->|Arcuate/PVN| R["↓ Appetite via POMC/↓NPY"]
D -->|DPP-IV cleavage| S[GLP-1 9-36 - Inactive]
S --> T[Renal Clearance]
GLP-1 function is a direct biomarker of Metabolic flexibility. Impaired incretin effect (reduced GLP-1 secretion or receptor response) is an early feature of Type 2 Diabetes, often preceding fasting hyperglycemia by years. In healthy individuals, the incretin effect accounts for 50-70% of postprandial insulin secretion; in T2D patients, this drops to 20-30%.
The GLP-1 system evolved to handle intermittent, fiber-rich meals with slow glucose release. Modern ultra-processed foods bypass normal GLP-1 signaling: rapid glucose absorption in the proximal intestine triggers insulin before distal L-cells can respond, creating a mismatch between insulin timing and incretin support. This is a Mismatch Disease mechanism contributing to Insulin resistance and beta cell exhaustion.
Lectins from wheat (wheat germ agglutinin, WGA) and legumes suppress both GIP and GLP-1 secretion by binding to L-cell surface glycoproteins. This creates an anti-diabetic effect in the short term (lower insulin spikes), but chronically impairs incretin function. This is why wheat consumption can appear "protective" in epidemiological studies while being metabolically disruptive long-term — it's suppressing a compensatory system.
¶ Clinical Thresholds and Biomarkers
- Normal postprandial GLP-1 peak: 15-50 pmol/L (2-3x basal levels)
- Impaired incretin response: GLP-1 response <50% of expected based on glucose load
- DPP-IV activity: elevated in obesity, metabolic syndrome, chronic inflammation
- Fasting GLP-1: 5-10 pmol/L (low diagnostic value; postprandial testing more informative)
Nutritional Enhancement:
- High-fiber diets → ↑ Butyrate production by Gut microbiome → ↑ GLP-1 secretion from L-cells
- Omega-3 fatty acids (EPA, DHA) enhance L-cell sensitivity and GLP-1 receptor expression
- Protein-rich meals stimulate GLP-1 more than carbohydrate-only meals
- Bile acids recycling through enterohepatic circulation → repeated TGR5 stimulation
Microbiome Support:
Pharmacological:
- DPP-IV inhibitors (sitagliptin, vildagliptin) extend GLP-1 half-life to 2-4 hours
- GLP-1 agonists (semaglutide, liraglutide, dulaglutide) are DPP-IV-resistant analogs
- GLP-1 agonist therapy → average weight loss 10-15% in obesity trials
- GLP-1 agonists → ↓ cardiovascular events in T2D by ~14-26% (LEADER, SUSTAIN-6 trials)
Problematic Patterns:
- Artificial sweeteners paradoxically activate L-cells through taste receptors → GLP-1 release without glucose → uncoupling of incretin-insulin axis
- Chronic NSAID use may impair L-cell function via COX-2 inhibition
- Chronic stress → ↑ cortisol → ↓ GLP-1 receptor expression on beta cells
- Metamodel 1 (Evolutionary Context): GLP-1 system designed for hunter-gatherer meal patterns, not modern grazing
- Metamodel 3 (Chronic Inflammation): IL-6, TNF-α downregulate GLP-1 receptors on beta cells → incretin resistance
- Metamodel 5 (Selfish Systems): GLP-1 represents a cooperative signal between gut and pancreas; disruption favors selfish immune/adipose expansion
- Half-life: 2-3 minutes (active GLP-1) due to DPP IV degradation; extended to >12 hours with DPP-IV-resistant agonists
- Incretin effect contribution: 50-70% of total postprandial insulin secretion in healthy individuals
- L-cell distribution: Highest density in distal ileum and colon (terminal gut sensing)
- Glucose dependency: GLP-1 only potentiates insulin when blood glucose >5.5 mmol/L — critical safety feature preventing hypoglycemia
- Gastric emptying: Delays by 30-50%, prolonging nutrient absorption and flattening glucose curves
- Weight loss with agonists: Average 10-15% body weight reduction over 68 weeks (semaglutide 2.4 mg)
- Cardiovascular benefit: GLP-1 agonists reduce major adverse cardiovascular events by 14-26% in T2D patients
- Cephalic phase: Accounts for 10-15% of GLP-1 response before nutrients reach intestine
- SCFA enhancement: Butyrate at 10 mM increases GLP-1 secretion by 60-80% in vitro
- T2D impairment: Incretin effect reduced to 20-30% of normal, contributing to postprandial hyperglycemia
- Receptor expression: GLP-1 receptors found on beta cells, alpha cells, vagal afferents, hypothalamic neurons, heart, kidneys
- DPP-IV ubiquity: Expressed on endothelial cells throughout vasculature, ensuring rapid GLP-1 inactivation
- GIP — co-incretin hormone from K-cells in proximal intestine; GLP-1 and GIP together account for full incretin effect
- Insulin — GLP-1 potentiates glucose-dependent secretion via cAMP/PKA pathway in beta cells
- Glucagon — GLP-1 suppresses secretion from alpha cells, reducing hepatic glucose output
- Cephalic phase — early sensory input primes GLP-1 secretion before nutrients arrive, anticipatory metabolic preparation
- DPP IV — enzyme that cleaves and inactivates GLP-1 within 2-3 minutes; target of gliptin drugs
- Type 2 Diabetes — characterized by impaired incretin effect (reduced GLP-1 response and receptor sensitivity)
- Metabolic flexibility — GLP-1 function reflects ability to switch between fuel sources and manage nutrient flux
- Lectins — wheat germ agglutinin and other lectins suppress GLP-1 (and GIP) release, creating paradoxical anti-diabetic effect
- Butyrate — SCFA produced by gut microbiome that stimulates GLP-1 secretion via GPR41/43 on L-cells
- Vagus nerve — mediates GLP-1 effects on gastric emptying and transmits satiety signals to brainstem
- Nucleus Arcuatus — hypothalamic region where GLP-1 activates POMC neurons to suppress appetite
- Obesity — associated with incretin resistance and reduced GLP-1 efficacy; GLP-1 agonists are primary weight-loss therapy
- Gut microbiome — SCFA-producing bacteria enhance GLP-1 secretion; dysbiosis impairs incretin function
- Akkermansia-muciniphila — mucin-degrading bacterium that enhances GLP-1 secretion and metabolic health
- Metformin — first-line T2D drug that increases GLP-1 levels through microbiome modulation
- GLUT4 — insulin-dependent glucose transporter upregulated by GLP-1-mediated insulin secretion
- SGLT1 — glucose transporter on L-cells that senses luminal glucose to trigger GLP-1 release
- Bile acids — activate TGR5 receptor on L-cells to stimulate GLP-1 secretion; recycled via enterohepatic circulation
- IL-6 — inflammatory cytokine that downregulates GLP-1 receptors on beta cells, contributing to incretin resistance
- TNF-α — pro-inflammatory cytokine that impairs GLP-1 signaling and beta cell function in chronic inflammation
- Cortisol — chronic elevation reduces GLP-1 receptor expression, linking stress to metabolic dysfunction
- CAMP — second messenger activated by GLP-1 receptor, mediating both insulin potentiation and appetite suppression
- PKA — protein kinase A activated by cAMP, phosphorylates calcium channels and CREB to enhance insulin secretion
- Chronic stress — impairs GLP-1 receptor function via cortisol-mediated downregulation
- NSAID — chronic use may impair L-cell function through COX-2 inhibition and gut inflammation
- Omega-3 fatty acids — enhance L-cell sensitivity and GLP-1 receptor expression; anti-inflammatory support for incretin system
- Module 2 — Evolutionary context of glucose metabolism and incretin system design
- Module 5 — GLP-1 in metabolic regulation, insulin-glucose dynamics, and microbiome interactions
- Module 7 — Appetite regulation, satiety signaling, and clinical application of GLP-1 agonists
Glucagon-Like Peptides (GLP-1 and GLP-2) are incretin hormones secreted by enteroendocrine L-cells in the distal ileum and colon in response to nutrient ingestion. GLP-1 (7-36 amide and 7-37) regulates glucose metabolism, enhances Insulin secretion, suppresses appetite, and slows gastric emptying, while GLP-2 (33 amino acids) promotes gut barrier integrity and enterocyte proliferation. Both are rapidly inactivated by DPP IV (dipeptidyl peptidase-4), with GLP-1 having a plasma half-life of approximately 2 minutes.
Think of GLP-1 as a sophisticated restaurant manager who coordinates the entire digestive experience. The moment you smell food or take the first bite, the manager (cephalic phase) sends advance notice to the kitchen (Insulin-secreting beta cells) to prepare for incoming orders. When nutrients actually arrive in the lower intestine, L-cells release GLP-1 like radio dispatches: "Big glucose load coming, get the insulin pumps ready!" But here's the clever part—this manager only calls for insulin production when Glucose levels are actually elevated, preventing dangerous hypoglycemia (like a smart thermostat that only turns on heating when it's actually cold). GLP-1 also tells the stomach to slow down its emptying (like a bouncer controlling the flow into a club), giving the body time to process each wave of nutrients. Meanwhile, it sends satiety signals to the brain's control tower, saying "We're good, stop eating." But there's a security guard called DPP IV that deactivates these messages within 2 minutes—like messages written in disappearing ink. GLP-2, the maintenance crew, works simultaneously to repair and strengthen the gut barrier, patching up tight junctions and promoting new enterocyte growth, ensuring the infrastructure stays intact for tomorrow's meals.
GLP-1 Secretion and Action:
- L-cells in distal ileum and colon detect nutrients via:
- GLUT1 and GLUT4 transporters (glucose sensing)
- GPR40/120 (fatty acid sensing)
- Peptide transporters (protein sensing)
- cephalic phase activation occurs via vagal cholinergic input → muscarinic receptors on L-cells → GLP-1 release BEFORE nutrients reach intestine
- Direct nutrient contact → depolarization of L-cell membrane → Ca²⁺ influx → exocytosis of GLP-1
GLP-1 Receptor Signaling Cascade:
GLP-1 → GLP-1R (Gs-coupled GPCR on pancreatic beta cells) → adenylyl cyclase activation → ↑cAMP → protein kinase A (PKA) activation → multiple downstream effects:
-
Beta Cell Pathway:
- PKA → KATP channel closure → depolarization → voltage-gated Ca²⁺ channels open → Insulin exocytosis (ONLY when glucose >5.5 mmol/L)
- PKA → CREB phosphorylation → insulin gene transcription
- GLP-1 → ↓Glucagon secretion from alpha cells (via paracrine somatostatin release from delta cells)
-
CNS Appetite Pathway:
- GLP-1R activation in hypothalamic nucleus arcuatus → ↑POMC/CART neurons (anorexigenic) and ↓AgRP/NPY neurons (orexigenic)
- Vagal afferents from gut → nucleus tractus solitarius (NTS) → satiety signaling
-
Gastric Emptying:
- GLP-1 → vagal efferents → delayed gastric motility via ↓cholinergic tone to stomach smooth muscle
DPP-IV Degradation:
- DPP IV (CD26 enzyme on endothelial cells, brush border) cleaves N-terminal His-Ala dipeptide from GLP-1 (7-36) → inactive GLP-1 (9-36)
- T½ of active GLP-1 = 1.5-2 minutes
- Renal clearance of degraded peptides
GLP-2 Mechanism:
- GLP-2 → GLP-2R (Gs-coupled) on enterocytes, enteric neurons, and subepithelial fibroblasts
- ↑crypt cell proliferation via insulin-like growth factor-1 (IGF-1) pathway
- ↓intestinal permeability via upregulation of tight junction proteins (ZO-1, occludin)
- ↓enterocyte apoptosis
- ↑mucosal blood flow via nitric oxide (NO) release
graph TD
A[Nutrient ingestion] --> B[L-cell activation]
A --> C[Cephalic phase vagal input]
B --> D[GLP-1 secretion]
C --> D
D --> E[GLP-1R on beta cells]
D --> F[GLP-1R in hypothalamus]
D --> G[Vagal afferents]
D --> H[DPP-IV enzyme]
E --> I["cAMP ↑ → PKA"]
I --> J{Glucose > 5.5 mmol/L?}
J -->|Yes| K["Insulin secretion ↑"]
J -->|No| L[No insulin release]
F --> M["POMC/CART ↑"]
F --> N["AgRP/NPY ↓"]
M --> O[Appetite suppression]
N --> O
G --> P[NTS activation]
P --> Q[Gastric emptying delay]
P --> O
H --> R[GLP-1 degradation]
R --> S["T½ = 2 minutes"]
T[GLP-2 secretion] --> U[GLP-2R on enterocytes]
U --> V["Gut barrier integrity ↑"]
U --> W["Enterocyte proliferation ↑"]
Metabolic Integration:
GLP represents the gut's primary mechanism for translating nutrient arrival into systemic metabolic coordination. In Type 2 Diabetes, GLP-1 secretion is often blunted (30-50% reduction), contributing to postprandial hyperglycemia and impaired satiety—a classic example of gut-brain axis dysfunction. The rapid DPP IV degradation explains why food context matters: slow eating and mindful consumption prolongs the cephalic phase GLP-1 response, improving glycemic control without changing macronutrient content.
Evolutionary Mismatch:
The incretin system evolved for intermittent, fiber-rich meals that trigger sustained L-cell activation in the distal gut. Modern ultra-processed foods bypass this system—rapid proximal absorption means minimal distal nutrient exposure, reducing GLP release. This contributes to insulin resistance and overconsumption, as the satiety brake fails. The GLP-1 analog market (Ozempic, Wegovy) artificially restores this lost signal, but represents treatment of symptom rather than cause.
Therapeutic Interventions:
- DPP-IV inhibitors (sitagliptin, linagliptin): Block GLP-1 degradation, extending T½ to ~60-90 minutes. Effective in diabetes but don't address root dysfunction.
- GLP-1 receptor agonists (semaglutide, liraglutide): DPP-IV-resistant analogs with T½ of hours to days. Produce 10-15% weight loss but may suppress natural incretin production long-term.
- Dietary strategies: High-fiber, low-GI meals promote sustained L-cell activation. Resistant starch reaches colon intact, maximizing GLP secretion.
- Microbiome modulation: SCFAs (especially butyrate) enhance L-cell differentiation and GLP secretion. Dysbiosis reduces incretin response.
Clinical Thresholds:
- Fasting GLP-1: 5-10 pmol/L (normal)
- Postprandial peak: 15-50 pmol/L (healthy response)
- DPP IV activity: >20 mU/mL (normal; elevated in metabolic syndrome)
- GLP-1 response blunted by >30% in obesity and T2D
GLP-2 Clinical Applications:
- Short bowel syndrome: Teduglutide (GLP-2 analog) promotes intestinal adaptation
- IBD: GLP-2 reduces intestinal barrier permeability and inflammation
- Biomarker of L-cell function: Low GLP-2 indicates distal gut dysfunction
Metamodel Connections:
- Selfish Brain: GLP-1 suppression represents immune/metabolic system protecting brain glucose access during perceived scarcity (chronic stress → cortisol → ↓incretin sensitivity)
- Evolutionary Scars: Loss of fiber-fermenting microbiome reduces SCFA-driven L-cell function
- Text-Context: Same meal produces different GLP responses based on eating speed, stress state, and circadian timing
- GLP-1 has plasma half-life of 1.5-2 minutes due to rapid DPP IV cleavage; GLP-1 analogs extend this to days
- Glucose-dependent action: GLP-1 enhances Insulin secretion ONLY when glucose >5.5 mmol/L, preventing hypoglycemia
- L-cells comprise ~1% of intestinal epithelium but are concentrated in distal ileum and colon
- cephalic phase releases GLP-1 within 10 minutes of food sight/smell, before nutrient absorption begins
- GLP-1 reduces appetite via dual pathway: hypothalamic POMC/CART activation + vagal NTS signaling
- DPP IV inhibitors (gliptins) increase active GLP-1 levels by 2-3 fold but don't match analog potency
- GLP-2 increases intestinal villus height by 30-40% and reduces Intestinal permeability markers (zonulin, LPS)
- 70% of incretin effect is mediated by GLP-1 (vs 30% by GIP) in healthy individuals
- Bariatric surgery (gastric bypass) increases GLP-1 levels by 3-5 fold, explaining metabolic benefits beyond weight loss
- Artificial sweeteners trigger cephalic GLP-1 release but without nutrient-driven second phase, potentially disrupting metabolic learning
- GIP — co-secreted incretin from K-cells in proximal intestine; complementary glucose-lowering effects but GIP also promotes fat storage
- DPP IV — serine protease that degrades GLP-1 within 2 minutes; therapeutic target in diabetes
- cephalic phase — vagal activation triggers anticipatory GLP-1 release before nutrients reach L-cells
- L-cells — enteroendocrine cells in distal gut that produce both GLP-1 and GLP-2
- GLUT4 — glucose transporter upregulated by GLP-1-stimulated Insulin in muscle/adipose
- GLUT1 — constitutive glucose transporter in L-cells enabling nutrient sensing
- Insulin — anabolic hormone whose secretion is potentiated by GLP-1 in glucose-dependent manner
- Glucagon — catabolic hormone suppressed by GLP-1 via paracrine somatostatin release
- intestinal barrier permeability — reduced by GLP-2 through tight junction upregulation and enterocyte proliferation
- gut barrier — structural integrity maintained by GLP-2-driven mucosal growth and repair
- SCFAs — microbial metabolites (butyrate, propionate) that stimulate L-cell GLP secretion
- butyrate — SCFA that enhances L-cell differentiation and incretin production
- Type 2 Diabetes — characterized by 30-50% reduction in meal-stimulated GLP-1 response
- appetite — suppressed by GLP-1 via hypothalamic POMC/CART neurons and vagal satiety signals
- glucose metabolism — regulated by GLP-1's dual action: enhanced insulin + suppressed glucagon
- microbiome — fiber-fermenting bacteria produce SCFAs that drive L-cell function
- gut-brain axis — GLP-1 is key signaling molecule from gut to brain for nutrient status
- vagus nerve — carries GLP-1-triggered satiety signals from gut to brainstem NTS
- insulin resistance — worsened by impaired GLP-1 secretion/signaling in metabolic syndrome
- inflammation — chronic inflammation impairs L-cell function and GLP secretion; GLP-2 has anti-inflammatory effects
- obesity — associated with blunted GLP-1 response and increased DPP IV activity
- leptin — adipokine that synergizes with GLP-1 for appetite suppression but resistance to both develops in obesity
- cortisol — chronic elevation impairs incretin sensitivity as part of stress-induced metabolic dysregulation
- POMC — pro-opiomelanocortin neurons in arcuate nucleus activated by GLP-1 to reduce appetite
- nucleus tractus solitarius — brainstem nucleus receiving vagal GLP-1 satiety signals
- tight junctions — intestinal barrier structures strengthened by GLP-2 signaling
- Module 2 — GLP as part of nutrient sensing and evolutionary context of incretin system
- Module 5 — GLP/GIP suppression as therapeutic target in diabetes; DPP-IV inhibition
- Module 7 — GLP-1 in satiety regulation and interaction with artificial sweeteners