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INGESTIVE BEHAVIORS

 

TABLE OF CONTENTS

Updated: April 1, 2008

LECTURE INFORMATION

KEY CONCEPTS IN THIS LECTURE

1. Under conditions of stabile body weight, there is a balance between food intake (energy in) and metabolism (energy out). Change in weight occurs when a shift from this balance occurs. For an individual there is a optimum weight as determined by a set point called the "lipostat." Because of this "lipostat" excessive eating or food deprivation often cause only temporary changes in weight. In some species, such as seasonal hibernators, there is an annual weight cycle that is determined by a change in the "lipostat." The early idea that body weight is regulated by a hypothalamic "center" involving a fasting center (Ventro-medial nucleus) and an opposing feeding center (Lateral hypothalamus) is now thought to be too simplistic.

2. Since most large animals feed intermittently, the processing of nutrients swings from feast (during meals) to famine (between meals). Short term regulation of food ingestion buffers these swings in nutrient availability. For example, following a meal blood glucose is high at which time the pancreatic hormone, insulin, is secreted to lower blood glucose by producing liver glycogen. Between meals, blood glucose falls causing secretion of another pancreatic hormone, glucagon, which coverts glycogen back to glucose. The liver monitors glucose and fatty acid titers to elicit feeding behavior via the vagus nerve. You feel sated after a meal due to distention of the stomach and release of hormones (CCK) into the blood. Both inhibit the satiety center in the medulla.

3. Long term regulation of food ingestion involves neuropeptides which stimulate feeding (e.g., Orexin, Melanin-concentrating hormone, and Neuropeptide Y) or inhibit feeding (CART and alpha-MSH). These neuropeptides reside in the Arcuate Nucleus and other hypothalamic nuclei. Leptin is a peptide hormone that is secreted when adequate white fat stores are present. Leptin inhibits feeding behavior to regulate body weight, and it is critical for reproductive competence.

4. Both body fluid volume and solute concentration are closely regulated. Body fluid volume is regulated primarily by the renin-angiotensin-aldosterone system, and body fluid solute concentration is regulated by vasopressin (=antidiuretic hormone) released from the posterior hypothalamus. Both systems act at the median preoptic area in the brain to stimulate drinking behavior.

LECTURE OBJECTIVES

1. Eating behavior plays to basic energetic demands of the body.
2. Explain the regulation of short term energy balance and long term energy balance.
3. Discuss how short-term and long-term energy balance are regulated by the endocrine and nervous systems.
4. Establish how ingestive behaviors is regulated by multiple loops involving the interaction of a number neuropeptides.
5. Explain how body fluids are regulated by adjusting fluid volume and solute concentration.

LECTURE OUTLINE

I. ENERGY BALANCE

  A. "She/He lives to eat" should be "She/He eats to live"
     1. All animal are heterotrophs
     2. Food provides the energy needed for cellular metabolism
         and growth.
     3. Principles of energy balance
              Energy in = Energy out  Stabile Weight
              Energy in > Energy out  Weight Gain
              Energy in < Energy out  Weight Loss

  B. Body Weight is determined by a set point (="Lipostat")
     1. Experimental evidence for the lipostat
          a. Animals defend against temporary weight gains & losses
          b. Lipectomy effects are temporary
          c. Lesioning the Lateral Hypothalamus lowers the set point
               1) Animals defend against temporary gain and loss
                   at the new lower level

  C.  Early ideas on weight control were inaccurate
     1. Mutual inhibition between Ventromedial nucleus (VMH)
         and LH

  D. The basic nutrients (carbohydrates, protein, and fats)
     1. Carbohydrates (=glucose) and fats (=fatty acids) are important 
         fuels for energy
     2. Brain consumes only glucose; Other cells consume 
         mainly fatty acids

II. SHORT-TERM REGULATION OF FOOD INTAKE

  A. Most large animals eat intermittently
     1.  Glycogen is an important buffer between meals

  B. Insulin and Glucagon
     1. Insulin lowers glucose levels follow a meal by:
          a. promotes glucose uptake by non-neural cells
          b. converts glucose to glycogen
          c. promotes glucose conversion to fatty acids
     2. Glucagon elevates glucose when blood titer is low

  C. Why do we get hungry?
     1. Liver monitors blood glucose and fatty acid titer 
          a. Metabolic inhibitors (2-DG, MP) injected into portal vein 
              increase feeding.
          b. Vagal afferents from liver to brain are also critical
          c. Ghrelin increases between meals

  D. Why do you feel sated after a meal?
     1. Stomach distention, high glucose, and intestinal release of 
         CCK acts via the vagus
          a. This center is in the area postrema in the medulla
          b. Turns off feeding behavior
     2. PYY from gut also inhibits feeding
     3. Ghrelin decreases immediately following a meal **

III. LONG-TERM REGULATION OF FOOD INTAKE

  A. Lateral Hypothalamus (LH) and other nuclei are important in
      feeding behavior
     1.  LH secretes Orexin and Melanin-concentrating Hormone (MCH)

  B. Neuropeptide Y (NPY) and AgRP stimulate feeding
     1. NPY and AgRP present in Arcuate Nucleus (ARC)
     2. Both act at PVN and LH (stimulates release of Orexin
         and MCH)

  C. Leptin, a hormone, provided another breakthrough
     1. Long-term regulation: Obese Mice and Leptin
          a. Leptin is secreted by well-nourished fat cells
          b. Leptin acts on the neuropeptide pathways in the 
              hypothalamus inhibiting NYP
          c. Leptin also influences reproduction and insulin level **

  D. CART and MSH inhibit feeding
     1. High Leptin initiates secretion of these neuropeptides (via ARC) 
     2. AgRP/MSH competition for the MC4 receptor may regulate weight
          a. Evidence

  E. Two opposing pathways regulate feeding behavior and ultimately body weight
     1. The NPY/ArRP pathway stimulates feeding and is the default
          a. NPY strongly inhibits the "stop feeding" pathway
     2. The CART/MSH pathway inhibits feeding **

IV. REGULATION OF THIRST

  A. Why regulate body fluids?
     1. Fluid compartments in the body
          a. Intracellular (67%), interstitial (26%), and vascular (7%)
     2. Volumetric thirst verses osmometric thirst

  B. Regulation of body fluids
     1. Renin-angiotensin-aldosterone system (volumetric)
     2. Neural control via the median preoptic nucleus (osmometric)
          a. ADH (=vasopressin) from the PVN and SON conserves water in the kidney

STUDY QUESTIONS

  1. List the three general nutrients present in the food that we eat. For what purposes is each ultilized in the body? See Figure 13.2. Also, be sure to view the animation on the Carlson CD.

  2. Liposuction is tauted as one way to loose weight, but the fat removal is often only temporary since new fat depots form after several months. Why does this happen? Similarily, dieting results in weight loss, but for many that loss often is only temporary. Why?

  3. What experimental evidence suggests the existence of a set point ("lipostat") for weight?

  4. During hunger what blood signals and neural pathways activate feeding behavior?

  5. Explain why exercise is so important as part of a weight loss program?

  6. Diagram how the following hormones and neuropeptides regulate feeding: Leptin, Neuropeptide Y, Orexin, Cocaine- and amphetamine-regulated transcript (CART), and Melanin-concentrating Hormone (MCH). Which inhibit and which stimulate feeding? What is the source of each? Also, AgRP and MSH increase and decrease feeding, respectively. How is this accomplished at the level of the MC4 receptor? What is the experimental evidence that the MC4 receptor is centrally involved?

  7. Ob/Ob mice lack leptin, but there is another genetic mutant for a non-functional leptin receptor. Would these mice have a weight problem? Why? If you repeated the parabiosis experiment using a wild type mouse and a mouse lacking the leptin receptor, what result would you expect? Why would you expect this outcome?

  8. The key to understanding long-term weight regulation ultimately rests with Leptin. What determines circulating Leptin titer, and how does changing Leptin titer regulate weight?

  9. You want to determine if Leptin acts at the Arcuate Nucleus (ARC). How would you go about establishing that action? That is, what procedures/approaches might you use to demonstrate that Leptin acts at the ARC.

  10. Given your understanding of how hormones and neuropeptides regulate body weight, why does lesioning the lateral hypothalamus lower the body weight?

  11. Some women marathon runners have difficulty conceiving a child probably because of low body fat. What endocrine factor might influence this inability? Explain.

  12. What are osmometric thrist and volumetric thrist? How do neural and hormonal system regulate these two types of thrist?

ADDITIONAL INFORMATION ON THE INTERNET

Eating Disorders from the NIMH

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