Regulation of Food Intake

Neural Control Centers - Brain's Hunger Hubs

• Hypothalamus: Key regulator.
  • Lateral Hypothalamic Area (LHA): Hunger center.
    • Stimulation ↑eating; Lesion → aphagia.
    • Orexigenic: Orexin, MCH.
  • Ventromedial Nucleus (VMN): Satiety center.
    • Stimulation ↓eating; Lesion → hyperphagia.
    • Anorexigenic.

  ⭐ VMN lesions: hyperphagia, obesity. LHA lesions: aphagia, wasting.

  • Arcuate Nucleus (ARC): Integrates hormones (leptin, ghrelin, insulin).
    • NPY/AgRP neurons (orexigenic) → LHA.
    • POMC/CART neurons (anorexigenic, via α-MSH) → VMN.
  • Paraventricular Nucleus (PVN): Releases TRH, CRH (↓intake).
• Brainstem:
  • Nucleus of Solitary Tract (NTS): Receives satiety signals (CCK, vagal).
• Higher Centers:
  • Limbic, PFC: emotion, cognition.

📌 Mnemonic: LHA - Lateral Hunger. VMN - Ventromedial Moderation (Satiety).

Gut-Brain Axis Hormones - Tummy Talks & Tells

• Orexigenic (Appetite Stimulating):
  • Ghrelin ("Hunger Hormone"):
    • Source: Stomach (P/D1 cells).
    • Action: Stimulates NPY/AgRP neurons (arcuate nucleus) → ↑ appetite.
    • Levels: ↑ pre-meal, ↓ post-meal.
• Anorexigenic (Appetite Suppressing):
  • Leptin ("Satiety Hormone"):
    • Source: Adipose tissue.
    • Action: Inhibits NPY/AgRP, stimulates POMC/CART neurons → ↓ appetite, ↑ energy expenditure.
    • Note: Leptin resistance common in obesity.
  • Insulin:
    • Source: Pancreatic β-cells.
    • Action: Central anorexigenic effects; inhibits NPY/AgRP.
  • CCK (Cholecystokinin):
    • Source: I-cells (duodenum, jejunum).
    • Action: ↓ food intake, meal size; signals via vagus nerve.
  • GLP-1 (Glucagon-like peptide-1):
    • Source: L-cells (ileum, colon).
    • Action: ↓ appetite, slows gastric emptying, ↑ insulin secretion.
  • PYY (Peptide YY 3-36):
    • Source: L-cells (ileum, colon), released postprandially.
    • Action: ↓ appetite (inhibits NPY neurons).

⭐ Ghrelin is the only known peripheral orexigenic hormone; its levels rise before meals and fall sharply after eating, signaling hunger to the brain.

Long-Term Regulators - Fat's Feedback Loop

• Adiposity signals reflecting body fat stores, primarily Leptin and Insulin.
• Leptin:
  • Source: Adipose tissue.
  • Action: Proportional to fat mass; signals satiety to hypothalamus (arcuate nucleus).
  • Mechanism: Stimulates anorexigenic POMC/CART neurons; inhibits orexigenic NPY/AgRP neurons.
  • Effect: ↓ Food intake, ↑ Energy expenditure.
  • 📌 Leptin = Lose weight (feel full).
  • Leptin resistance: Impaired CNS response despite high leptin levels, common in obesity.
• Insulin:
  • Source: Pancreatic β-cells.
  • Action: Also acts as an adiposity signal in the CNS, synergizing with leptin.
  • Effect: Contributes to ↓ food intake.

⭐ In most obese individuals, leptin levels are high, indicating leptin resistance rather than deficiency.

Integrative & Other Influences - The Full Plate

• Sensory cues: Sight, smell, taste (cephalic phase stimulation).
• Psychological: Stress (variable effect), mood, learned habits, social factors.
• Environmental: Food availability, portion sizes, food advertising.
• Sleep: Deprivation (< 7 hrs) → ↑ghrelin, ↓leptin → ↑hunger.
• Physical activity: Modulates energy balance and appetite.
• Other states: Pregnancy, lactation ↑intake; illness (e.g., fever) ↓intake.

⭐ Sleep deprivation (< 7 hrs/night) alters appetite hormones (↑ghrelin, ↓leptin), promoting hunger and potential weight gain.

High‑Yield Points - ⚡ Biggest Takeaways

• Hypothalamus is key: Lateral (LH) is feeding center (↑ by ghrelin); Ventromedial (VMH) is satiety center (↑ by leptin, CCK).
• Ghrelin (stomach) is the primary orexigenic hormone, stimulating hunger.
• Leptin (adipose tissue) is anorexigenic, signaling satiety and ↑ energy expenditure.
• PYY (ileum/colon) & CCK (duodenum) promote short-term satiety.
• Insulin & GLP-1 also act centrally to reduce food intake.
• Arcuate nucleus: NPY/AgRP stimulate feeding; POMC/CART inhibit feeding.