CONTROL OF THE FOOD INTAKE Flashcards
WHAT IS FEEDING BEHAVIOUR CONTROLLED BY?
- PHYSIOLOGICAL COMPONENTS (HUNGER)
- ENVIRONMENT
- OUR REWARD PROCESSES
- GENETICS
MAIN CONTROL OF FOOD INTAKE OCCURS IN WHICH PART OF THE BRAIN?
HYPOTHALMUS
WHICH PART OF THE BRAIN APART FROM THE HYPOTHALAMUS ALSO PLAYS A ROLE IN FOOD INTAKE BY RELAYING THE NERVOUS SIGNALS FROM PNS TO CNS?
THE BRAINSTEM
WHICH NUCLEI OF THE HYPOTHALAMUS IS INVOLVED IN REGULATING FOOD INTAKE?
ARCUATE NUCLEUS
WHAT ARE THE 2 TYPES OF NEURONS IN ARCUATE NUCLEUS OF THE HYPOTHALAMUS AND WHAT ARE THEIR ROLES + NAMES?
POMC (PRO-OPIOMELANOCORTIN) AND CART (COCAINE- AND AMPHETAMINE REGULATED TRANSCRIPT) NEURONS; INHIBITORS OF FOOD INTAKE; ANOREXIGENIC
NPY (NEUROPEPTIDE Y) AND AgRP (AGOUTI RELATED PEPTIDE) NEURONS; STIMULATE FOOD INTAKE; OREXIGENIC
ARCUATE NUCLEUS IS CONNECTED TO WHICH 2 OTHER TYPES OF NUCLEI?
VENTROMEDIAL AND LATERAL
WHICH NUCLEUS IS KNOWN AS THE ‘SATIETY CENTRE’ BECAUSE IT IS INVOLVED IN SUPPRESSING FOOD INTAKE?
VENTROMEDIAL NUCLEUS
WHICH NUCLEUS IS KNOWN AS THE ‘HUNGER CENTRE’ BECAUSE IT ACTIVATES FOOD INTAKE?
LATERAL NUCLEUS
MECHANISM OF STOPPING FOOD INTAKE?
- POMC NEURONS PRODUCE aMSH (a-MELANOCYTE STIMULATING HORMONE) AND THIS WILL ACTIVATE NEURONS IN VENTROMEDIAL NUCLEUS TO DECREASE INTAKE
- CART DOESN’T ACT DIRECTLY ON VENTROMEDIAL NUCLEUS BUT RATHER SUPPRESSES NEURONS OF THE LATERAL HYPOTHALAMUS SO THEY CAN’T ACTIVATE FOOD INTAKE
MECHANISM OF INCREASING FOOD INTAKE?
- AgRP PRODUCED AND SUPPRESSES VENTROMEDIAL NUCLEUS SO IT CAN’T DECREASE INTAKE
- NPY ACTIVATES NEURONS IN THE LATERAL HYPOTHALAMUS
WHAT IS EPISODIC REGULATION OF FOOD INTAKE/EPISODIC SIGNALS?
- SHORT TERM REGULATION
- VARIES WITH FEEDING PATTERNS
- GENERATED BY FOOD INTAKE
- MAINLY INHIBITORY TOWARDS FURTHER INTAKE
- INVOLVES GUT HORMONES LIKE CCK, GLP-1,PYY
OTHER NAME FOR EPISODIC SIGNALS/EPISODIC FOOD INTAKE REGULATION?
TRANSIENT SIGNALS
WHAT IS TONIC REGULATION OF FOOD INTAKE/ TONIC SIGNALS?
- LONG TERM REGULATION
- GENERATED BY TISSUE STORES (HOW FULL THE ADIPOSE TISSUE IS)
- CONSTANT REGULATION OF FOOD INTAKE BASED ON ENERGY LEVELS
- INVOLVES MOLECULES SECRETED BY THE ADIPOSE TISSUE (E.G. LEPTIN, ADIPSIN, RESISTIN, ADIPONECTIN..)
WHAT IS COMMON NAME FOR ALL MOLECULES SECRETED BY THE ADIPOSE TISSUE?
ADIPOKINES
WHAT IS CHOLECYSTOKININ AND WHAT IS ITS FUNCTION?
CCK IS A NEUROPEPTIDE AND A GUT HORMONE
IT REGULATES PANCREATIC ENZYME SECRETION, GI MOTILITY AND ACTS AS A SATIETY SIGNAL
WHERE IN THE GI TRACT IS CCK SYNTHESISED?
SMALL INTESTINE
IS CCK RELEASED BEFORE OR AFTER A MEAL AND FROM WHERE?
AFTER A MEAL, SIMULTANEOUSLY FROM INTESTINAL CELLS AND NEURONS
WHAT IS GLUCAGON-LIKE PEPTIDE 1 AND WHEN AND WHERE IS IT SECRETED?
GLP-1 IS AN INCRETIN SECRETED IN THE COLON FOLLOWING A MEAL, ESP HIGH IN CARBOHYDRATES
WHAT EFFECTS DOES GLP-1 HAVE ON FOOD INTAKE AND IN WHICH CONDITION CAN THIS PROPERTY BE USED?
IT STRONGLY REDUCES IT, SO IT CAN BE USED IN OBESITY
WHAT DOES ‘POSTPRANDIAL’ MEAN?
AFTER A MEAL
WHAT ARE INCRETINS?
GUT DERIVED PEPTIDE HORMONES RAPIDLY SECRETED AFTER A MEAL WHICH STIMULATE INSULIN SECRETION AND LEAD TO LOWERING OF BLOOD GLUCOSE LEVELS
WHAT IS PEPTIDE TYROSINE TYROSINE (PYY), WHERE AND WHEN IS IT SECRETED?
A PEPTIDE GUT HORMONE SECRETED AFTER A MEAL IN THE COLON
WHAT DOES PYY ACT ON AND WHAT IS THE RESULT OF ITS FUNCTIONING?
ON NPY NEURONS, DELAYS GASTRIC EMPTYING (FEELING FULL FOR LONGER)
EFFECTS AND ROLE OF GUT HORMONE GHRELIN?
RELEASED BEFORE A MEAL, ACTIVATES HUNGER AND FOOD INTAKE, INCREASES GASTRIC MOTILITY, INCREASES FAT STORAGE AND DECREASES FAT UTILIZATION
WHAT IS AMYLIN AND WHAT DOES IT DO?
PEPTIDE HORMONE SECRETED BY THE PANCREAS AFTER A MEAL TO INHIBIT GLUCAGON SECRETION. IT DECREASES FOOD INTAKE, DELAYS GASTRIC EMPTYING AND IT IS INVOLVED IN BODY WEIGHT REGULATION
WHICH HORMONE IS AMYLIN COSECRETED WITH AND FROM WHERE?
INSULIN, PANCREATIC BETA CELLS
WHAT IS THE HYPOTHALAMIC PATHWAY OF FUNCTIONING FOR GLP-1, CKK, PYY, INSULIN AND AMYLIN?
THEY INHIBIT NPY/AgRP NEURONS SO THEY STOP THEM FROM ACTING ON LATERAL AND VETROMEDIAL HYPOTHALAMUS TO INCREASE FOOD INTAKE
THEY DO NOT ACT ON POMC/CART NEURONS!!!!!!!!
WHICH NEURONS OF THE ARCUATE NUCLEUS OF THE HYPOTHALAMUS DOES GHRELIN ACTIVATE?
AgRP
HOW CAN AMYLIN INJECTION BE BENEFICIAL IN OBESE INDIVIDUALS?
IT CAN BLOCK HYPERPHAGIC MANIFESTATIONS
WHERE IS THE HORMONE LEPTIN SECRETED FROM AND WHAT DOES IT DO TO FOOD INTAKE?
SECRETED BY THE ADIPOSE TISSUE, INHIBITS FOOD INTAKE
HOW IS FOOD INTAKE INHIBITED BY LEPTIN?
- LEPTIN HAS RECEPTORS AT THE SURFACE OF BOTH POMC/CART AND NPY/AgRP NEURONS
- LEPTIN WILL ACTIVATE THE FOOD INTAKE SUPRESSING NEURONS AS WELL AS BLOCK THE FOOD INTAKE STIMULATING NEURONS
- THIS MAKES IT A VERY STRONG SUPPRESSOR
LEPTIN IS ASSOCIATED WITH EPISODIC OR TONIC SIGNALS?
TONIC
AMPK; AMP-ACTIVATED PROTEIN KINASE
- WHAT IS TI + ROLE
ONE OF THE CENTRAL ENZYMES IN METABOLISM WHICH REGULATES MITOCHONDRIA BIOGENESIS AND LEVEL OF ENERGY IN THE CELL
WHAT IS AMPK SOMETIMES CALLED BECAUSE OF ITS FUNCTION IN REGULATING CELLULAR ENERGY?
‘THE ENERGY SENSOR OF THE CELL’
WHAT ACTIVATES AMPK?
LOW ENERGY LEVELS IN THE CELL
WHAT ARE KINASES?
ENZYMES WHICH ADD A PHOSPHATE GROUP TO OTHER MOLECULES
WHAT IS THE RELATIONSHIP BETWEEN POST MEAL HORMONES AND AMPK?
THE POST MEAL HORMONES INHIBIT IT BECAUSE ATP LEVELS ARE HIGH AFTER A MEAL
WHICH GUT HORMONE ACTIVATES AMPK?
GHRELIN
HOW DOES GLUCOSE REGULATE FOOD INTAKE?
- CIRCULATING GLUCOSE TAKEN UP BY GLUT2
- ONCE INSIDE THE CELLS, UNDERGOES GLYCOLYSIS AND PRODUCES PYRUVATE
- PYRUVATE GOES TO THE MITOCHONDRIA TO PRODUCE ATP
- ATP LEVELS RISE, K+ CHANNELS CLOSE, Ca2+ CHANNELS OPEN
- A LOT OF POSITIVE CHARGE IN THE CELL, DEPOLARIZATION INDUCED
- FOLLOWED BY RELEASE OF NEUROTRANSMITTERS THAT WILL SHUT DOWN FOOD INTAKE
- AMPK INACTIVATED WHEN GLUCOSE IS PRESENT AND CAN MAKE ATP
EFFECTS OF BLEND FOODS VS TASTY, HFSS FOODS ON THE BRAIN?
BLEND FOOD GENERATES INFO IN HYPOTHALAMUS LEADING TO SATIETY SIGNALS SO EATING STOPS
FOOD THAT TASTES GOOD ACTIVATES THE REWARD SYSTEM AND DOPAMINE & ENDOGENOUS OPIATES ARE PRODUCED
WHAT CONSEQUENCES CAN ACTIVATION OF REWARD CIRCUIT HAVE ON THE FOOD INTAKE REGULATORS?
- CAN LEAD TO INCREASE OF NPY NEURONS
- CAN BLOCK EFFECTS OF CCK, GLP1 AND LEPTIN
