chapter 12

• Hunger


  A feeling of discomfort or weakness caused by lack of food, coupled with the desire to eat
• Eating


  The act of putting food in the mouth and chewing it
• Purpose of hunger

  To induce eating, increase the probability of eating
• Purpose of eating

  To supply the body with necessary nutrients and energy to function and to sustain life
• Digestion

  1. Chewing

  2. Saliva

  3. Swallowing and moving down esophagus

  4. Stomach breaks down food

  5. Small intestine - Absorption

  6. Duodenum - Break down proteins, starches, simple sugars, fats

  7. Final absorption and excretion

  
• Gut microbiome


  Bacteria and other organisms that live inside our gastrointestinal track and help break down the food we ingest
• Gas formation and flatulence


  • Breakdown of food and subsequent fermentation during the process of digestion results in gas formation
  • Oxygen, nitrogen, carbon dioxide, hydrogen, and methane
  • Hydrogen and methane are by-products of the breakdown of food residue by good bacteria (probiotics) naturally residing in the colon
• SIBO (small intestinal bacterial overgrowth)


  An imbalance of the microorganisms in your gut that maintain healthy digestion. When too many bacteria, or the wrong kind, populate the small intestine, it can lead to uncomfortable symptoms such as gas and diarrhea
• Energy (three forms)

  • Lipids
  • Amino acids
  • Glucose
• Energy storage (three forms)

  • Fats (preferred)
  • Glycogen
  • Protein
• Glucose


  • The main type of sugar in the blood and is the major source of energy for the body's cells
  • Simplest carbohydrates - monosaccharides
  • Saccharides are also known as carbohydrates

  
• Glycogen


  The stored form of glucose, made up of many connected glucose molecules. It is made and stored primarily in the cells of the liver and skeletal muscle

  
• Lipids


  • Any of various organic compounds that are insoluble in water. They include fats, waxes, oils, hormones, and certain components of membranes and function as energy-storage molecules and chemical messengers
  • The four main groups of lipids include: fatty acids, glycerides, nonglyceride lipids, and complex lipids
• Adipose tissue


  A specialized connective tissue consisting of lipid-rich cells called adipocytes. Its main function is to store energy in the form of lipids (fat)
• Energy metabolism


  • The general process by which living cells acquire and use the energy needed to stay alive, to grow, and to reproduce
  • Metabolism comprises a series of interconnected pathways that can function in the presence or absence of oxygen. Aerobic metabolism converts one glucose molecule into 30-32 ATP molecules

  
• Three phases of energy metabolism

  • Cephalic
  • Absorptive
  • Fasting
• Cephalic phase


  The cerebral (or cephalic) phase of digestion, whether triggered by the sight, smell, or thought of food, initiates the digestive process with the salivary and gastric secretory responses mediated via the autonomic nervous system (usually mediated by the vagus nerve)
• Absorptive phase


  The absorptive state, or the fed state, occurs after a meal when your body is digesting the food and absorbing the nutrients (catabolism exceeds anabolism). During this phase, anabolic processes use glucose in a variety of ways, such as converting it to glycogen or fat for storage

  
• Fasting phase


  The fasting state lasts from about 18 hours to 2 days of fasting. At some point during this state, your body enters ketosis, a metabolic state in which fats are broken down and used as an energy source
• Theories

  • Set Point Assumption
  • Positive Incentive Perspective
  • Neurobiological theories
• Set-point assumption

  The energy set-point view that is the basis of many people's thinking about hunger and eating. It proposes a homeostatic, negative feedback system with a glucostatic set-point and a lipostatic set-point
• Weaknesses of set-point theories

  • Inconsistent with evolutionary pressures (banking food when available)
  • Major predictions of theories not confirmed (changes in glucose needed to increase eating, not natural; people with excess fat don't adjust meal size)
  • Fail to recognize the pressures of taste, learning, social influences

  
• Positive-incentive perspective


  Developed to overcome shortcomings of set-point. Emphasizes the anticipated pleasure of eating. Animals eat in response to preferred flavors, past experiences, time since last meal, and others eating
• Factors that influence what we eat


  • Preference for sweet and salty, aversion to bitter
  • Conditioned taste aversions and preferences
  • Cravings for deficiencies
  • Eating as a stressor (cephalic/malaise)
  • Sham eating
  • Satiety signals (volume, nutritive density)
  • Appetizer effect
  • Serving size
  • Social influence
  • Increased variety of food (cafeteria-style diet/sensory-specific satiety)
• Sham eating


  A procedure where food eaten by an animal does not go or stay in the stomach or intestine but instead spilled out or transferred outside. The act of chewing the food triggers gastric secretion in preparation for the coming food which will not arrive and thus the amount taken increases compared to the usual regular amount with an intact stomach. It tells us the role of the stomach and the intestine in relation to satiety

  
• Research on blood glucose levels in relation to hunger and satiety is mixed

  
• Lesions of the hypothalamus (ventromedial hypothalamus causes hyperphagia, lateral hypothalamus causes aphagia and adipsia) were found to not be the true feeding and satiety centers

  
• Ventromedial hypothalamic nucleus


  Surgical induced lesion causes hyperphagia in rats due to an increase in insulin production and thus an increase in lipogenesis until it stabilizes at a certain point. This debunks the satiety center myth
• Glucose dropped sharply 10 minutes premeal
• Evidence blood glucose decline is triggered by eating
• Time course of glucose is not directly correlated with body's energy
• Eliminating premeal drop doesn't stop the meal
• If meal is not served, glucose returns to its previous level
• Glucose in brain is relatively constant
• Lesions of the hypothalamus


  • Ventromedial hypothalamus causes hyperphagia
  • Lateral hypothalamus causes aphagia and adipsia
• Feeding and satiety centers found false
• VMH lesions also damage ventral noradrenergic bundle or PVN
• VM Hypothalamic Nucleus


  • Surgical induced lesion causes hyperphagia in rats
  • Cause an increase in insulin production thus an increase in lipogenesis until it stabilizes at a certain point
  • Hyperphagia is due to insulin increase and thus debunking the satiety center myth

  
• Lateral Hypothalamus Nucleus


  • Surgically induced lesion causes aphagia and adipsia in rats
  • Lesion also cause severe motor disturbance and general lack of responsiveness of the rat to sensory input such as feeding and other sensory stimuli
• The locations in the rat brain of the ventromedial hypothalamus and the lateral hypothalamus