The GI Tract Flashcards
Criteria for a healthy gut
- effective digestion and absorption of food
- absence of GI illness
- normal and stable intestinal microbiota
- effective immune system
- status of well-being
Digestive tract
- oral cavity
- esophagus
- stomach
- small intestine
- large intestine
Accessory organs
- pancreas
- liver
- gallbladder
Saliva
water (99%), electrolytes, mucus, enzymes, antibacterial and antiviral compounds
- enzymes
- mucins
Enzymes of the oral cavity secretions
- Salivary amylase (hydrolyzes a 1-4 bonds in starch)
- Lingual lipase (hydrolyzes dietary triglycerides)
- Lysozyme (antibacterial enzyme)
Mucins
glycoproteins that lubricate food and protect the oral mucosa
Brushing teeth
- oral bacteria
- dental carries, periodontal diseases, oral cancer
- diabetes
- Cardiovascular disease -oral microbiota in atherosclerotic plaques/ bacteria linked to cholesterol levels
Stomach functions
- produces acid, enzymes and intrinsic factor and hormones
- regulates hunger and satiety
- relaxes and accommodates
- protects itself from exogenous agents
- mixes, grinds, and empties
Damaging factors of the stomach
- systemic diseases
- H. pylori
- NSAIDS, asparin, SSRI
- toxic foods
- alcohol
Structure of the stomach
-GI motility dependent on contractility pattern
Cells of the stomach
- Neck/mucous cells
- chief cells
- parietal cells
Neck/mucous cells
- secretes mucus and lubricates the ingested GI contents
- protect the gastric mucosa from mechanical and chemical damage (bicarbonate release, pH 6-7 at mucosa
Chief Cells
- Release pepsinogen
- degraded to pepsin in the presence of acid
- main proteolytic enzyme in the stomach (optimal pH ~3.5)
Parietal Cells
-secretes hydrochloric acid (HCl)
Parietal cells Important in:
- activation of the zymogen pepsinogen to pepsin
- denaturation of proteins
- killing many bacteria ingested along with food
Within parietal cell, HCl released by:
- gastrin released by G cells into the blood
- acetylcholine released from vagus nerve
- histamine released from GI mast cells
Gastroesophageal Reflux Disease
- Reflux of stomach contents back into esophagus
- relaxation of gastroesophageal sphincter
GERD can cause:
- Barrett’s esophagus
- Chronic inflammation of esophagus
- gastroesophageal reflux
- is the cause of abou 1/3 of esophageal cancers
Symptoms of Gerd
heart burn
Regulatory peptides: Gastrin
- synthesized by enteroendocrine cells called G-cells in the stomach and proximal small intestine
- Stimulates the release of HCl
- stimulates pepsinogen release
What response leads to release of Gastrin?
Released in response to vagal stimulation, ingestion of specific substances or nutrients, gastric distention, Hl in contact with gastric mucosa, local and circulation hormones
Ghrelin
- produced in stomach
- orexigenic hormone
- elevated in the fasted state
- increases appetite and food intake
- rises after diet - induced weight loss
- Annorexia & obese- dysregulaiton of ghrelin pathway
- Gastric bypass - decrease
Nutrients of Ghrelin
- CHO - suppresses
- protein - suppresses?
- Fat - no effect
Orexigenic hormone
stimulates food intake through hypothalamus, brainstrem
Gut-Brain Axis
- Communication between the gut and the brain through nutrients,hormones, and nerves
- also intestines
Meal related signals: Gut-brain axis
- direct effect of food - increase in aa, glucose, and fa act directly on hypothalamus
- visual - activats hypothalamus
- neuronal - signals from physical measures - stomach distension
- humoral- gut derived hormones
Neuronal signal
- Signals from physical measures - stomach distension
- the weight or volume of food determined by meal size
- stretch receptors signal brain through vagus nerve to brainstem
- neurons integrate sensory information from mouth GI tract, organs
- forwarded to hypothalamus and integrated with long-term regulators
Response to Nutrient Ingestion
- food intake
- gastric accommodation: intra-gastric pressure drop
- further filling: intra-gastric pressure rise
- activation of tension receptors in the proximal stomach
- triggering of TLESRs
- Meal induced satiety –> Termination of food intake
Helicobacter Pylori
- Gram neg bacteria
- primary cause of ulcers
H pylori symptoms
- pain
- weight loss
- loss of appetite
- vomiting
causes of ulcers
- smoking
- high alcohol intake
- stress
- NSAIDS
The small intestine
-Chyme moving from the stomach into the duodenum (initial pH 2)
How is the duodenum protected against the gastric acidity?
- pancreati secretion of bicarbonate with buffering capacity
- mucus containing secretions from Brunner’s glands
- viscous, alkaline (pH 8.2 - 9.3), protect the epithelial mucosa form damage
4 tissue layers of the GI tract
- Mucosa (epithelial cells that live 2-5 days)
- Submucosa- connective tissue (has blood vessels and nerves)
- Muscularis - smooth muscle, mixes food
- Serosa (connective tissue) - support and protection
Function of the Gut Interface
- Filter with selective permeability – allows for movement of needed nutrients from lumen into circulation
- Barrier with selective permeability – prevention of penetration by harmful microorganisms
Components of the Intestinal Barrier
- unstirred water layer (rate-limiting step in transport of nutrients and drugs)
- adhesive mucous gel layers (physical friction, chemical digestion, bacterial adhesion, diffusion barrier)
- Water: mucosal surface interface (phospholipids, NSAIDS)
Paracellular Uptake
- paracellular
- unmediated passive diffusion
- intestinal permeability increases following ingestion of hypertonic solution (food)
Intestinal permeability
- the facility with which the intestinal epithelium allows molecules to pass through by non-mediated passive diffusion
- paracellular
Increase Permeability
- Ethanol and oxidants –> disrupt microtubules
- TPN –> mucous gel layer is disrupted, hyperpermeability
- saturated fat
- green and black pepper extracts, MCT, chitosan
Decrease permeability
- EGCG (reduced inflammaiton)
- fermented soy milk
- probiotics and prebiotics
Microbiota
- large, functionally stable community of bacteria
- ~100 trillion microbial cells
- ~1,000 bacterial species in the GI microbiota
- unique to the individual
- nutrient metabolism, barrier funciton, immunity
- impacted by diet
Factors impacting metabolic disease
- environment
- Microbiota
- genetics
