ENERGY BALANCE

1
ENERGY BALANCE
Page 469-488
2

• Dynamic relationship between energy acquisition
  and expenditure
• Energy stored in adipose tissue

3
Energy Utilization and Storage

• Postprandial Phase metabolic fuels (sugars,
  fatty acids, and amino acids) enter bloodstream
• Postabsorptive Phase lowers level of metabolic
  fuels in blood --gt stores excess energy

4
Insulin Promotes Energy Storage

• pancreatic ? cells release
• glucose --gt glycogen (liver)
• glucose transport into muscle and fat cells
• necessary for glucose oxidation and lipogenesis
  (store fat)
• prevents both glycogen breakdown and mobilization
  of fat
• only energy storage hormone in vertebrates

5
Insulin Release

• Cephalic Phase due to sensory stimuli during
  food intake
• may increase hunger
• Gastrointestinal Phase due to absorption of
  nutrients from the gut

6
Diabetes Mellitus

• insufficient insulin secretion
• surplus energy not stored into fat (5 vs normal
  30-40)
• ? glucose in blood (high blood sugar, sweet
  urine)
• Brain function normal
• Other tissues starving --gt results in enormous
  food intake (hyperphagic)
• High-fat diet stops hyperphagia

7
Hyperinsulinemia

• excess insulin secretion
• Low blood sugar --gt mental confusion, dizziness,
  weakness, and hunger
• Obesity - constantly feel hungry and eat

8
Energy Mobilization

• Glucagon from pancreatic ?-cells induces
• Lipolysis - breakdown of adipose tissues
• Glycogenolysis - breakdown of stored glycogen
  (liver)
• Sympathetic Nervous System
• innervates fat cells --gt lipolysis
• innervates liver --gt glycogenolysis
• Gluconeogenesis amino acids in liver produced
  into glucose and ketone bodies

9
Long-term Food Deprivation

• Glycogenolysis
• Lipolysis
• Gluconeogenesis
• Other methods?
• Growth hormone --gt lipolysis
• Exercise--gt corticosterone or cortisol--gt
  gluconeogenesis
• Stress--gt epinephrine--gt glycogenolysis

10
Dual-Center Model

• Lateral hypothalamus - Hunger Center
• Lesions --gt loss of appetite and lack of eating
  behavior
• VMH - Satiety Center
• Lesions --gt enormous food intake and rapid weight
  gain

11
Data Dual-center model

• LH lesions interfere with all motivated behavior
• Lesion anywhere along the DA tracts that pass
  through the LH
• --gt similar behavioral deficits as LH
  lesion
• VMH may just be a part of regulatory feeding
  circuit via the autonomic (sympathetic and
  parasympathetic) nervous system

12
Current Model Metabolic Hypothesis

• Metabolic fuels (glucose, fatty acids, ketone
  bodies) make usable energy for cellular processes
• Feeding is responsive to changes in metabolic
  signals
• Animals with isolated hypothalamus display
  feeding behavior when oxidation of metabolic
  fuels is blocked

13
Blowfly Negative Feedback Loop for Satiety

• Neural signals from stomach distention
• Rate of gastric emptying

14
Insulin and Feeding Behavior

• Release associated with meal termination
• Destruction of the ? cells induces long-term
  hyperphagia
• Not a direct effect on satiety, rather may
• Facilitates the use, storage, and mobilization of
  carbohydrates
• Feedback with other hormones or the autonomic
  nervous system
• Signals CNS about peripheral levels of metabolic
  fuels via cerebrospinal fluid

15
The Liver in Insulin-Induced Feeding

• Inject insulin--gt ? blood glucose--gt ? feeding
• Add ketone bodies (used by brain)
• No difference
• Add fructose (used by liver)
• ? feeding
• Suggests the liver is important in mediating
  insulin-induced feeding

16
Cholecystokinin (CCK)

• Aids digestion during feeding
• ? food intake
• Binds to peripheral receptors that signal the
  brain, via vagus nerve, to stop eating
• Transection of the vagus blocks CCK effects on
  eating
• CCK levels during meal in blood -- slightly
  reduced with digestion around vagus -- varies
  during course of meal
• Suggests local release of CCK mediates satiety
  via the vagus nerve

17
Controversial Effects of CCK on Feeding

• CCK antagonist
• Aversive or toxic effects?
• Learned-aversion paradigm (conditioning) CCK
  paired with saccharin

18
Leptin

• Secreted by adipose
• Indicator of body fat content?

19
Leptin

• ob/ob mice do not produce leptin
• Leptin injections ? food intake and body weight
• db/db mice produce normal amount of leptin but no
  leptin receptors
• Leptin injections have no effect
• Humans??

20
Ovarian Hormones Rats

• OVX increases food intake and body mass (20-25)
• ? fat deposition
• ? locomotor activity
• Species specific
• Inject E --gt mild, transient hypophagia, ?
  activity, and ? body weight
• P has no effect without E
• Inject E P --gt still fat
• Intact females injected with P --gt weight gain

P blocks the effects of E on food intake,
adiposity, locomotor activity, and body mass
21
Eating and Body Weight During the Estrus Cycle

• Rats
• ? immediately after proestrus (high E)
• ? during diestrus (low E)
• ? during both pregnancy and pseudopregnancy (high
  P)
• Golden hamsters
• ? body mass when days are short (low E) -
  non-breeding season

22
Ovarian Hormones Primates

• Non-human primates -- ? food intake during luteal
  phase (high P)
• OVX rhesus monkeys -- mimic hormonal cycle by
  injecting with E P --gt cyclic changes in food
  intake
• Women -- ? food intake during 10 days prior to
  menstruation than during 10 days after the onset
  of menstrual bleeding

23
Ovarian Hormones Possible Methods of Action
1. May affect brain sites that control food
intake and activity -- E implants into VMH of
ovx rats 2. May affect body mass independent
from food intake and behavior -- OVX vs intact
24
Androgens

• Males --gt larger and eat more
• Androgens -- ? body mass energy consumption
• Rats
• Castration --gt ? food intake weight gain
• T replacement reverses
• Actions both centrally (CNS-induced) and
  peripherally (muscle mass)