Temperature control, eating, and drinking

1
Temperature control, eating, and drinking

• What is the motivation?
• How is consumption regulated?
• What goes wrong?

2
Homeostasis maintains internal states within a
critical range.

• Homeostatic mechanisms are redundant
• Feedback
• Set point
• Set zone
• Set points/zones can change

3
Temperature regulation is critical

• Endotherms (Isothermic,warm-blooded)
• Ectotherms (poikilothermic, cold-blooded)
• Behavioral mechanisms
• Location choice
• Physiological mechanisms
• Control metabolism
• Brown adipose tissue thermogenesis
• BAT surrounds vital organs and C1-T12 of spinal
  cord

4
Juvenile mammals

• Link to penguin shuffle
• Huddling of rat pups
• Move to periphery of huddle when hot, to center
  when cold

5
Neural centers control temperature

• Location POA and lateral hypothalamus
• Lateral hypothalamus controls behavioral
  thermoregulation
• POA controls physiological thermoregulation
• Homeostatic redundancy
• Receptors are in the skin, body core, and
  hypothalamus
• Spinal or body centers control temperature in a
  broad range (2 -3 degrees C) hypothalamus
  controls temperature in a narrow range, and
  appears to affect the activity of the other
  systems.

6
Thirst and drinking

• Water transporting channels aquaporins
• Cellular dehydration or osmometric thirst Salt
  makes ECF hypertonic, drawing water from cells
  and dehydrating them.
• Hypovolemic or volumetric thirst loss of blood
  volume, detected by atrial baroreceptors and
  kidney blood-flow detectors

7
Reactions to thirst

• Osmometric thirst triggers receptors in
• AV3V
• supraoptic nucleus
• organum vasculosum of the lamina terminalis
  (OVLT), and possibly the lateral POA

8
What happens when osmosensory neurons are
stimulated?

• These cells stretch and contract in response to
  osmolality, thus opening and closing ion
  channels mechanically gated channels.
• Receptor activity neurally activates the
  experience of thirst, and cause the posterior
  pituitary to release ADH
• Drinking behavior is also triggered, and stops
  when enough water has entered the gi tract.

9
How do we respond to hypovolemic thirst?

• Hypovolemic thirst baroreceptors trigger ADH
  (vasopressin) release from posterior pituitary
• Absence of ADH production ? diabetes insipidus
• Blood flow receptors affect kidney action
  directly
• We experience thirst and salt hunger
• SNS activity constricts blood vessels

10
Kidney action is organizational

• Similar effects of hypovolemis thirst come from
  the renin-angiotensin system
• Renin converts angiotensis I ? angiotensis II
• Angiotensis II constricts blood vessels
• Increases secretion of ADH/vasopressin and
  aldosterone
• Acts on hypothalamus to trigger drinking behavior
• Acts on cirumventricular organs
• Sense level of angiotensis II through leaky BBB
• Subfornical organ increases activity in response
  to angiotensis II
• Note the redundant systems

11
Kidney to brain

• ADH gt Renin gt Angiotensin II gt constriction of
  peripheral blood vessels and release of
  aldosterone gt sodium retention
• Angiotensin II also acts on the subfornical organ
  (SFO), which is outside the BBB, to trigger
  drinking.
• Angiotensin II is also manufactured in the brain,
  and can trigger thirst without SFO activity.

12
Why drink if you are not thirsty?

• Positive incentive theory
• Taste Bad tasting water decreases drinking,
  sweet taste increases drinking
• Eating increases drinking Dry and protein-rich
  foods induce hypovolemic thirst, but drinking
  increases with any food. Insulin may be a
  trigger.
• Anticipation or learned drinking

13
Satiety for drink

• Sham drinking studies show that drinking is
  proportional to the length of time since the last
  drink, suggesting oral factors in satiety.
• Injected water reduces deprivation-induced
  drinking only moderately.
• Sensory-specific satiety Rats drink more
  saccharin flavored water, especially after being
  deprived of it for awhile. They drink even more
  if the flavor changes frequently.

14
Review the processes of digestion

• Digestion Energy and nutrients
• Forms of energy delivery
• Lipids, amino acids, and glucose
• Forms of energy storage
• Fats, glycogen, and proteins
• Phases of energy metabolism
• Cephalic, absorptive, and fasting
• Brain has first dibs on glucose, but will use
  ketones if fasting is prolonged.

15
Pancreatic hormones

• Insulin
• Helps us use glucose energy first (cephalic)
• Helps store energy by conversion of unused
  glucose to glycogen and fat, and amino acids to
  proteins (absorptive and cephalic)
• Helps store converted energy in appropriate
  places (absorptive and cephalic)
• Glucagon in fasting phase helps convert stored
  fat energy to free fatty acids and ketones

16
What controls eating behavior?

• Set-point theories
• Homeostatic mechanisms and negative feedback
  loops
• Glucostatic and lipostatic theories Short- and
  long-term homeostasis
• But why does weight increase long-term?
• Set-point theories ignore other influences
• Positive incentive theory

17
Items in positive incentive theory

• Species-specific preferences and aversions
• Learned preferences and aversions
• Conditioning and cultural exposure Fufu
• Deficiency selection Sodium salt preference
• Deficiency selection Aversion to low-nutrient
  tastes overcome in humans by food preparation
  and by variety of choices of foods Confusion.
• Timing factors Social influence, anticipatory
  insulin release, conditioning

18
More incentives...

• Satiety, learned knowledge of the effects of a
  familiar food decreased with novel foods in
  sham-eating studies
• Lower nutritive density, to a point
• Appetizer effect Anticipation raises hunger
• Social influence Group eating suppresses satiety
• Cafeteria effect Variety of good-tasting foods
  increases consumption and compensates for
  sensory-specific satiety

19
Regulation of food consumption

• Blood glucose levels
• Hypothalamic mechanisms
• Ventromedial hypothalamus (VMH) and satiety
• Lateral hypothalamus (LH) and eating
• Paraventricular nuclei
• Gastrointestinal sensations
• GI peptides cholecystokinin, bombesin, glucagon,
  somatostatin CSF insulin levels

20
Regulating body weight

• Set point theory
• Thermogenesis
• Settling point theory Six factors in the leaky
  barrel model.
• Amount of available food
• Incentive value of available food
• Amount of consumed energy
• Level of body fat
• Amount of energy expended
• Strength of the satiety signal

21
Disorders

• Obesity
• Anorexia nervosa
• Social influence
• Dieting trigger
• Increased cephalic phase insulin response, even
  when protesting no feelings of hunger.
• Binging and purging may cancel the incentive
  value of food, by associating food with vomit.
• Bulimia nervosa