Regulation of Digestion and Feeding

The autonomic nervous system controls the viscera.
Input from the digestive tract wall goes to the central nervous system (hypothalamus and medulla).
Output goes back to the gastrointestinal wall cells.
- Sympathetic motor neurons: Decrease secretions and motility.
- Parasympathetic motor neurons: Increase secretions and motility.

Independent nerve network within the gastrointestinal tract wall.
Neurons in the muscularis (myenteric plexus) and submucosa (submucosal plexus).
Receives information from:
- Chemoreceptors (composition of lumen contents).
- Mechanoreceptors (distension).
Functions as a reflex circuit independent of the central nervous system.
Potentially involved in digestive issues when dysfunctional.

Secreted by G cells in the gastric glands (deep regions of gastric pits).
Targets: Stomach cells (mucosal and muscle), lower esophageal sphincter, pyloric sphincter.
Effects:
- Promotes activity of mucosa and muscularis (secretion and contraction).
- Closes sphincters to trap food in the stomach.

Intestinal hormones.
Target cells: Pancreas (acinar cells), hepatocytes (liver), gallbladder, gastric mucosa cells.
Effects:
- Increase activity of pancreas and liver.
- Decrease activity of the stomach.
Enteroendocrine cells are located in the infolds between villi (intestinal glands).

Occurs before food enters the digestive tract.
Triggers: Sight, smell, taste, thought of food.
Sensory input goes to the higher brain (hypothalamus and medulla).
Output: Parasympathetic.
- Salivation.
- Increased secretion of gastric juices from gastric glands.
- Increased motility of muscularis via the vagus nerve.
Parietal cells secrete hydrogen ions (protons) for hydrochloric acid (HCl).
Chief cells secrete pepsinogen, which becomes pepsin in the acidic environment.

Begins when food enters the stomach.
Triggers:
- Stomach distension.
- Nutrient molecules (glucose, amino acids).
- Increased pH (neutralization of acidity).
Continued output from the hypothalamus and medulla via the vagal nerve.
- Increased secretion and motility in gastric glands and muscularis.
Enteric pathways also promote increased stomach activity.
Gastrin release from G cells enhances stomach activity and closes sphincters.
Food remains in the stomach for about four to five hours (depending on the meal).

Begins when food enters the duodenum.
Triggers:
- Distension.
- Nutrient molecules (glucose, amino acids).
- Decreased pH (acidic food from the stomach).
Switch in parasympathetic impulses:
- Decreased motor commands to the stomach.
- Increased motor commands to the small intestine.
Decreased gastrin release.
Increased secretion from intestinal glands.
Increased segmentation in intestinal muscularis.
Release of intestinal hormones (cholecystokinin and secretin).
- Targets: Pancreas, hepatocytes, gallbladder.
- Decreased stomach activity.
Sequential activity: Stomach works first, then the small intestine.
Movement of food through the GI tract is regulated by distension, nutrient molecules, and pH changes.

Energy balance and body weight are affected by nutrient absorption, ATP production, and storage in the liver or adipose tissue.
Feeding behavior (initiation and duration) is complex.
Factors involved:
- Hormonal effects.
- Chemicals from muscle, adipose tissue, GI tract, liver, vasculature, brain.
- Neural and hormonal inputs.
- Genetic factors.

Hypothalamic nuclei are involved in energy utilization and food intake.
Input from:
- Higher brain (emotional brain).
- Risk assessment region.
- Hormonal input from the periphery.
- Sensory input from the GI tract and associated organs.
Output: Neural or hormonal.
Local mediators and various hormones.
Pituitary gland releases ACTH and TSH.

Released by adipocytes based on triglyceride storage.
High triglyceride (positive energy balance): More leptin released.
- Binds in the hypothalamus.
- Decreased food intake.
- Increased energy expenditure (increased activity).
Low triglyceride: Less leptin released.
- Increased food intake.
- Decreased energy expenditure.
Leptin-deficient animals (knockout gene): Low activity, always hungry, insulin resistance.

Associated with the initiation of feeding.
Released by cells in the gastric gland region of the stomach.
Ghrelin levels:
- Drop following a meal.
- Rise as the digestive tract empties.
- Trigger feeding when reaching a certain level.
Decreased distension and stimulation of chemoreceptors trigger ghrelin release.

The state of feeling satisfied and stopping eating.
Neural and hormonal mechanisms control how long you eat.
Feeding centers (nuclei in the hypothalamus) receive information from:
- Stomach stretch.
- Nutrient molecules (glucose, proteins, fats).
- Chemoreceptors (more sensitive to proteins than glucose, and least sensitive to fats).
Not hardwired: Develop based on experience (satisfaction set point).