SLEEP AND METABOLISM Flashcards
DURATION OF SLEEP HAS BEEN INCREASING/DECREASING?
DECREASING (ACROSS ALL ETHNIC GROUPS, BUT MOST IN THE BLACK ETHNIC GROUP)
US:
1910 - 9 HRS/NIGHT
2010 - 6.6 HRS/NIGHT
EFFECTS OF SLEEP DEPRIVATION, EXAMPLES?
- IRRITABILITY
- COGNITIVE IMPAIRMENT
- MEMORY LAPSES OR LOSS
- IMPAIRED MORAL JUDGEMENT
- IMPAIRED IMMUNE SYSTE,
- INCREASED HEART RATE VARIABILITY
- TREMORS
- ACHES
- HIGHER RISK OF OBESITY…
WHICH SLEEPING PROBLEMS IS OBESITY ASSOCIATED WITH?
- SLEEP DISORDERED BREATHING
- OBSTRUCTIVE SLEEP APNOEA SYNDROME
U SHAPED RELATIONSHIP BETWEN OBESITY AND SLEEP?
THERE MIGHT BE BMI INCREASE IN BOTH PEOPLE SLEEPING MORE THAN AVERAGE/RECOMMENDED (BETWEEN 7 AND 8 HRS PER NIGHT) AND PEOPLE SLEEPING LESS THAN AVERAGE/RECOMMENDED
SHORT SLEEPERS COMPARED TO CONTROL, RISK OF OBESITY? (CHILDREN)
58% INCREASED RISK
STUDY ON HOW EXTENDING DURATION OF SLEEP COULD PLAY A ROLE IN OBESITY MANAGEMENT?
- RCT OF 80 OVERWEIGHT ADULTS WHO HABITUALLY SLEPT LESS THAN 6.5 HRS PER NIGHT
- INTERVENTION GROUP ALLOCATED TO 2-WEEK SLEEP EXTENSION
- THE GROUP REDUCED CALORIE INTAKE BY APPROX 270 kcal
ASSOCIATION BETWEEN SLEEP/WAKE AND FASTING/FEEDING CYCLES?
- FOOD AVAILABILITY AND PREDATION ARE LINKED TO THE LIGHT/DARK CYCLE (NO HUNTING DURING THE NIGHT UNLESS FOOD WAS SCARCE)
- THERE IS CO REGULATION OF SLEEP/WAKE AND FASTING/FEEDING CYCLES IN THE CNS AND PERIPHERAL TISSUES AT A MOLECULAR AND GENETIC LEVEL
- BODY EXPECTS EATING DURING THE LIGHT PHASE
CIRCADIAN RHYTHMS/CIRCADIAN CLOCK?
THE PHYSICAL, MENTAL AND BEHAVIOURAL CHANGES THAT FOLLOW A ROUGHLY 24-HOUR CYCLE, RESPONDING PRIMARILY TO LIGHT AND DARKNESS IN AN ORGANISM’S ENVIRONMENT
BIOLOGICAL CLOCK?
Biological clocks are organisms’ natural timing devices, regulating the cycle of circadian rhythms. They’re composed of specific molecules (proteins) that interact with cells throughout the body. Nearly every tissue and organ contains biological clocks.
MASTER CLOCK?
- AKA ‘PACEMAKER’
- IN THE SUPRACHIASMATIC NUCLEUS (SCN)
- CONSISTS OF CCA 20 000 NERVE CELLS, LOCATED IN THE HYPOTHALAMUS
- CONTROLS MELATONIN PRODUCTION (SLEEP HORMONE)
- COORDINATES ALL THE BODY CLOCKS
- CLOCK GENES ARE EXPRESSED IN OTHER BRAIN AREAS AND PERIPHERAL TISSUES
HOW ARE PERIPHERAL BODILY CLOCKS REGULATED?
THEY ARE SYNCHRONISED THROUGH HUMORAL, NUTRIENT AND AUTONOMIC WIRING
WHAT IS THE PREDOMINANT CUE FOR THE SCN CLOCK?
LIGHT
- GLUTAMATE AND PACAP (PITUITARY ADENYLATE CYCLASE-ACTIVATING PEPTIDE) ARE CO RELEASED IN THE SCN UPON PHOTIC STIMULATION
WHICH NON-PHOTIC (NOT LIGHT) STIMULI IS THE SCN CLOCK SENSITIVE TO?
FEEDING, SOCIAL INTERACTION, SLEEP DEPRIVATION, EXERCISE
CLOCK and BMAL1?
The mammalian circadian clock relies on the master genes CLOCK and BMAL1 to drive rhythmic gene expression and regulate biological functions under circadian control.
WHICH NUCLEUS INCLUDES APPETITE STIMULATING AND APPETITE INHIBITING NEURONAL CIRCUITS?
ARCUATE NUCLEUS IN HYPOTHALAMUS
WHERE IS LEPTIN SECRETED FROM?
ADIPOSE TISSUE (SATIETY SIGNAL)
WHERE IS GHRELIN SECRETED FROM?
THE STOMACH (APPETITE STIMULATING)
HOW DOES SHORT SLEEP DURATION INFLUENCE GHRELIN AND LEPTIN LEVELS?
- DEACREASES LEPTIN
- INCREASES GHRELIN
- INCREASES HUNGER AND APPETITE
OREXIN SYSTEM? CONNECTION TO SLEEP AND METABOLISM?
- HYPOTHALAMIC OREXIN NEURONS REGULATE AROUSAL
- OREXIN A AND OREXIN B (AKA HYPOCRETIN A AND HYPOCRETIN B) HAVE POTENT WAKE PROMOTING EFFECTS AND STIMULATE FOOD INTAKE
- OREXIN SYSTEM ACTIVATES THE APPETITE-PROMOTING NEUROPEPTIDE Y
- SLEEP DEPRIVATION RESULTS IN INCREASED OREXINERGIC ACTIVITY (ANIMAL MODELS)
HOW DOES LACK OF SLEEP AFFECT DIETARY EFFORTS?
- CAN UNDERMINE THEM
- CONTRIBUTES TO LOSS OF FAT-FREE MASS INSTEAD OF ADIPOSE TISSUE
- LEADS TO INCREASED GHRELIN AND HUNGER
- SLEEP RESTRICTION MIGHT ATTENUATE THE EFFECTS OF CALORIC RESITRICTION!!!!!!!!!
WHICH SLEEP TIMING IN CHILDREN AND ADOLESCENTS IS ASSOCIATED WITH POORER DIETARY CHOICES?
LATE SLEEPING TIME
SLEEP DEBT IS ASSOCIATED WITH? (SLEEPING 4 HRS PER NIGHT FOR 6 NIGHTS)
- LOWER GLUCOSE TOLERANCE
- INCREASED INSULIN RESISTANCE
- DECREASED LEPTIN
- INCREASED SLEEPINESS
- INCREASED SYMPATOVAGAL BALANCE; INCREASED SYMPATHETIC OUTPUT (The concept of “sympathovagal balance” reflects the autonomic state resulting from the sympathetic and parasympathetic influences.)
- INCREASED CORTISOL
- ALTERED GENE EXPRESSION!
SLEEP DEBT HAS A HARMFUL IMPACT ON CARBOHYDRATE METABOLISM AND ENDOCRINE FUNCTION + MIGHT INCREASE THE SEVERITY OF AGE RELATED CHRONIC DISORDERS
SLEEP MIGHT HAVE A POTENTIALLY LARGE EFFECT ON RESTING ENERGY EXPENDITURE, ACTING THROUGH:
UCP2 EXPRESSION (UNCOUPLING PROTEIN)
Uncoupling protein 2 (UCP2) is an inner mitochondrial membrane protein that belongs to the uncoupling protein family and plays an important role in lowering mitochondrial membrane potential and dissipating metabolic energy with prevention of oxidative stress accumulation.
- normally leptin increases uncoupling proteins, thus increasing mitochondrial membrane permeability, increase metabolism and decrease fat reserves
- lack of sleep decreases leptin and decreases this effect, ultimately leading to increased fat reserves
- lack of sleep might also directly reduce membrane permeability in mitochondria
UCP2?
Uncoupling protein 2 (UCP2) is an inner mitochondrial membrane protein that belongs to the uncoupling protein family and plays an important role in lowering mitochondrial membrane potential and dissipating metabolic energy with prevention of oxidative stress accumulation.
