Regulation of Digestion and Feeding

Regulation of Digestion and Feeding

Nervous System Regulation

• 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.

Enteric Nervous System

• 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.

Hormonal Regulation of Digestion

Gastrin

• 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.

Secretin and Cholecystokinin (CCK)

• 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).

Phases of Digestion

Cephalic Phase

• 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.

Gastric Phase

• 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).

Intestinal Phase

• 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.

Regulation of Feeding

• 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.

Neural Centers in the Hypothalamus

• 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.

Leptin

• 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.

Ghrelin

• 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.

Satiety

• 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).

Cholecystokinin (CCK)

• Stimulates the pancreas, liver, and gallbladder during the intestinal phase.
• CCK also affects feeding centers.
• Injection of CCK during eating leads to immediate cessation of feeding.
• CCK contributes to the feeling of satisfaction.