antiobesity

2. Nutrient Regulation Helps Prepare for Future Needs
• Aside from obtaining energy from ingested food, nutrients are
needed for growth, maintenance, and repair of the body.
• Such as 9 essential amino acids
• Some fatty acids
• Vitamins
• Minerals
• The nervous system
• Controls digestion
• Monitors nutrient levels and energy balance
• Anticipates future requirements

3. Nutrient Regulation Helps Prepare for Future Needs
Basal metabolism
• Basal metabolism is energy used for heat production, maintenance of
membrane potentials and life-sustaining processes.
• Basal metabolism consumes around 55% of food energy
– Around 12% for active behavioral processes
• Which depends on activity level of the individual
• Kleiber’s equation for the rate of basal metabolism—a rule that
relates energy expenditure to body weight:
– kcal/day = 70 × weight 0.75
– For individuals with normal caloric intake and activity levels
• Restricting calories tends to lower basal metabolism
• Restricting calories (50 -75 %) tends to increase longevity
• Drugs to increase basal metabolism through changes in
mitochondria?
Details not on the exam

4. The Relation between Body Size and Metabolism
Details not on the exam

5. Figure 13.17 Metabolic Adaptation in The Biggest Losers

6. Nutrient Regulation Helps Prepare for Future Needs
Glucose is the principal sugar used for energy.
Glycogen is a complex carbohydrate, made by the combining of
glucose molecules, stored for a short term in the liver and
muscles.
Glycogenesis is the process of converting glucose to glycogen,
regulated by the pancreatic hormone insulin, released by beta
cells in the islets of Langerhans.
Glucagon, another pancreatic hormone released by alpha cells in the
islets of Langerhans, mediates glycogenolysis –conversion of
glycogen back into glucose when blood glucose levels drop.
Lipids (or fats) for longer-term storage, are deposited in adipose
tissue.
Gluconeogenesis is the process of converting fat and proteins to
glucose and ketones, a form of fuel.

7. The Role of Insulin in Energy Utilization
Glycogenesis
glycogenolysis

8. Insulin Is Crucial for the Regulation of Body Metabolism
• Glucose transporters span the cell membrane and
interact with insulin to bring glucose into the cell.
• Three sequential mechanisms trigger insulin release:
• 1.The sensory stimulus of food evokes insulin release, in
anticipation of glucose—the cephalic phase.
• 2. Food causes gut hormone release, which stimulates the
pancreas to secrete insulin—the digestive phase.
• 3. Glucodetectors in the blood and liver detect glucose and
signal the pancreas to release insulin—the absorptive phase.
• Information from glucodetectors in the liver travels via the vagus nerve
to the nucleus of the solitary tract (NST) in the hypothalamus.
• This system informs the brain of glucose levels, and efferent fibers to
the pancreas modulate insulin release.

9. Regulation of Eating
• Satiety is the feeling of fulfillment or satisfaction.
• Hunger is the internal state of an animal seeking food.
• The brain integrates insulin and blood glucose levels with other
information to decide whether to initiate eating.
• No single brain region has control of appetite, but the
hypothalamus is important to regulation of:
– Metabolic rate
– Food intake
– Body weight
• Historically, a dual-center hypothesis proposed two appetite
centers in the hypothalamus: (now considered outdated)
– One for signaling hunger
– One for signaling satiety

10. The Hypothalamus Coordinates Multiple
Systems That Control Hunger
• Ventromedial hypothalamus (VMH) lesions cause animals to eat
to excess (hyperphagia) and become obese, suggesting the VMH is
a satiety center.
• Lateral hypothalamus (LH) lesions cause aphagia—refusal to
eat—suggesting LH is a hunger center.
• However, the dual-center hypothesis proved to be too simple.
• VMH-lesioned animals exhibit a dynamic phase of obesity with
hyperphagia (overeating) until they become obese, on a rich diet.
• Their increased weight stabilizes in a static phase of obesity; this
weight is maintained even after food manipulations.

11. Changes in Body Weight after Hypothalamic Lesions

12. The Hypothalamus Coordinates Multiple Systems
That Control Hunger
• The arcuate nucleus of the hypothalamus contains
an appetite control circuits governed by hormones,
such as insulin.
• Other peripheral peptide hormones are
• Leptin,
• Ghrelin
• PYY3–36.

13. Integration of Appetite Signals in the Hypothalamus
Part B Details not on the exam

14. Role of Leptin
• Fat cells produce leptin and secrete it into the
bloodstream.
• Leptin works to suppress hunger
– Leptin receptors (ObR) are located in the hypothalamus
• Leptin’s effects on the arcuate neucleus are long-lasting.
• Leptin activates POMC/CART neurons but inhibits
NPY/AgRP neurons

15. Role of Ghrelin
• Peptide hormone released from cells in the stomach
• Increases growth hormone secretion (GH-releasing)
• Increases during fasting and decreases after a meal
• Increased levels produce increased appetite
• Receptors located in the arcuate nucleus, lateral hypothalamic area,
accumbens nucleus, ventral tegmental area
• Obese individuals
– have low baseline levels
– levels do not drop after a meal so no signal for “just ate a meal”

16. Role of PYY3-36
• Pancreatic Peptide Tyrosine Tyrosine
• Small peptide from the small intestine
– from cells in the ileum and colon
– low baseline levels that increase quickly when eating
• Increased levels decrease appetite
• Receptors located in the arcuate nucleus and vagus
nerve input to the brainstem

17. The Hypothalamus Coordinates Multiple
Systems That Control Hunger
• Hypothalamic mechanisms integrate appetite signals.
• The paraventricular nucleus (PVN) and the lateral
hypothalamus (LH) are primary targets of the arcuate
nucleus.
• Orexigenic neurons of the lateral hypothalamus act to
increase appetite and food intake, whereas anorexigenic
neurons of the PVN act to decrease appetite and feeding.
• Orexin “hypocretin” is a peptide produced in the LH
• that regulates arousal, wakefulness, and appetite
• increases the craving for food and meal size by suppressing
inhibitory postingestive feedback
• some studies suggest that the stimulatory effects of orexin on
feeding may be due to general

18. Details not on the exam

19. Regulation of Energy Intake Is A Complex Process
• Integration of multiple signals from
• Internal homeostatic mechanisms
• External sensory cues
• social context
• availability of food
• learned behaviors
• cognitive factors
• habits

20. Cognitive and Emotional Influences on Eating
• Cognitive
– Sensory
• Taste & Odor
• Visual
– Memory
• Early childhood eating habits
• Food preferences generally
• Cultural influences
• Emotional
– Food sensory input can activate
• Reward system
• Disgust system
– Negative emotions
• Fear, sadness, anger can disrupt eating
• Sometimes increases and sometimes decreases eating

21. Role of Learning in Eating
• Learning can influence eating in a variety of ways
• Most mammals are born with a preference for sweet and salty
tastes and with an aversion to bitter tastes
• Learn to avoid any taste followed by illness
– conditioned taste aversion
• Learn to prefer tastes that improve their health
– conditioned taste preference
• These forms of learning are robust and adaptive

22. Positive-Incentive Models of Feeding
• Many brain circuits are activated in response to seeing food
cues,
– Prefrontal cortex
– Orbitofrontal cortex
– Inferior temporal cortex
– Insula
– Striatum
– Amygdala
– Hippocampus
– Hypothalamus
• High hedonic value food produces greater activation of the
brain circuits

23. Positive-Incentive Models of Feeding
• Major influences of taste, learning & social factors on feeding
• Additional (complimentary) theory of feeding & hunger
– based on idea that we eat because eating is pleasurable rather
than to satisfy some setpoint for glucose or fat.
– When good food is present, we will eat regardless
– Hunger determined by many factors
• Taste
• Previous experience with food
• Time of day
• Time since last meal
• Social environment

24. Sensory Signals and Positive Incentives
• The homeostasis “set point” explanation of eating regulation can
not explain eating a piece of pecan pie and whipped cream at the
end of a large meal
• In rats, a small amount of artificial sweetener saccharin added to
their diet leads to an increase in consumption and marked weight
gain
• Positive-incentive properties of food (i.e., anticipated pleasurable
effects) rather than internal deficits
• Deprivation increases food's positive incentive properties
• Positive energy balance “Over eating” reduce food’s incentive
signals especially in the Insula and Hypothalamus
– For individuals with good regulation i.e. “thin”
– But not for individual’s whom tend to be overweight

25. Sensory-Specific Satiety
• Eating one particular food (chocolate cookie) reduces
incentive value of its taste
• Cafeteria diet has variety so incentive value does not drop as
quickly
– rats increase consumption & body weight
– many choices allows switching as incentive value for a particular food
falls