METABOLIC SYNDROME; EXAMPLE; OBESITY Flashcards
WHAT’S METABOLIC SYNDROME USED TO BE CALLED?
SYNDROME X
WHO INITIALLY NAMED METABOLIC SYNDROME THE SYNDROME X?
GERALD REAVEN
WHAT EXACTLY IS METABOLIC SYNDROME?
A GROUP OF DYSFUNCTIONS THAT INCREASE THE RISK OF DEVELOPING A DISEASE.
A PERSON HAS TO HAVE AT LEAST 3 OF THE FOLLOWING PARAMETERS FOR THE DIAGNOSIS OF METABOLIC SYNDROME:
- INSULIN RESISTANCE OR DIABETES
- HIGH BP
- HIGH FAT IN BLOOD
- LOW HDL, HIGH LDL
- OBESITY
THE METABOLIC SYNDROME INCREASES A PERSON’S RISK OF:
- T2D
- CVD
- CANCER
- NEURODEGENERATIVE DISEASE
THE PARAMETERS OF THE METABOLIC SYNDROME?
- INSULIN RESISTANCE OR DIABETES
- HIGH BP
- HIGH FAT IN BLOOD (TRIGLYCERIDES)
- LOW HDL, HIGH LDL
- OBESITY
% OF CHILDREN 4-5 Y.O. THAT ARE OVERWEIGHT?
10%
% OF CHILDREN 10-11 Y.O. THAT ARE OVERWEIGHT?
20-25%
RATES OF OBESITY IN IMMIGRANTS IN COUNTRIES LIKE THE US USUALLY INCREASE RAPIDLY WITHIN HOW MANY YRS?
5
‘THRIFTY PHENOTYPE THEORY’?
- AIMS TO EXPLAIN WHY PEOPLE, WHEN PUT IN SITUATION WHERE FOOD IS MORE AVAILABLE AND ACTIVITY CHANGES SUDDENLY ACCUMULATE LOTS OF FAT
- PROPOSED THAT PEOPLE WERE ALWAYS PRONE TO BE FATTER IN ORDER TO BE ABLE TO ACCUMULATE RESERVES OF ENERGY IN TIMES OF PLENTY AND BE ABLE TO USE RESERVES WHEN THE TIMES ARE HARDER (KIND OF EVOLUTIONARY ABILITY)
EXAMPLE OF A GROUP THAT DRASTICALLY INCREASED OBESITY AND T2D RATES UPON ACCULTURATION?
THE PIMA PEOPLE, NATIVE AMERICAN TRIBE (USED TO BE FAR FROM OVERWEIGHT, NOW HAVE ONE OF THE HIGHEST OBESITY AND T2D RATES IN THE COUNTRY)
THE MOST COMMON TRAIT TRANSMITTED TO A CHILD BY ITS PARENTS IS?
HEIGHT
WHAT IS A REGRESSION COEFFICIENT AND HOW IS IT USED IN ESTIMATING HERITABILITY?
THE COEFFICIENT ESTIMATES RELATIONSHIP BETWEEN A PREDICTOR VARIABLE AND THE RESPONSE, RANGE 0-1, THE CLOSER IT IS TO 1 THE MORE TRANSMITTABLE/HERITABLE THE TRAIT IS
REGRESSION COEFFICIENT FOR OBESITY?
0.6-0.7 (HIGH HERITABILITY)
% OF VARIATION IN BODY WEIGHT ASSOCIATED WITH GENETIC FACTORS?
70%
WHEN WAS LEPTIN IDENTIFIED?
1994
LEPTIN HAS TONIC EFFECTS. EXPLAIN?
LEVELS OF LEPTIN DO NOT VARY IN SHORT TERM IN RESPONSE TO FOOD BUT RATHER IS A SIGNAL ON THE LEVEL OF OUR ENERGY STORES
WHERE IS LEPTIN RELEASED FROM?
ADIPOSE TISSUE, SO THE LEVELS DIRECTLY RELATE TO LEVELS OF ADIPOSITY
GENETIC MUTATIONS RELATED TO LEPTIN DEFFICIENCIES? EFFECTS? TREATMENT?
- THERE ARE MUTATIONS IN THE LEPTIN GENE THAT CAN INHIBIT ITS PRODUCTION AND LEAD TO OBESITY BECAUSE FOOD INTAKE IS NOT APPROPRIATELY DECREASED WHEN NEEDED
- THERE CAN ALSO BE MUTATIONS IN LEPTIN RECEPTORS ON AgRP AND POMC NEURONS
- LEPTIN CAN BE INJECTED
APART FROM INSULIN RESISTANCE, WHICH OTHER HORMONE CAN OBESE INDIVIDUALS DEVELOP RESISTANCE TO WHICH WILL LEAD TO INCREASED FOOD INTAKE?
RESISTANCE TO LEPTIN
LEPTIN LEVELS IN THE BRAINS OF OBESE PEOPLE ARE LOWER THAN IN LEAN PEOPLE, POSSIBLE REASONS?
- IMPAIRED LEPTIN TRANSPORT ACROSS THE BLOOD BRAIN BARRIER
- IMPAIRED LEPTIN RECEPTORS
- A ROLE OF INFLAMMATION, STRESS AND INEFFECTIVE AUTOPHAGY
LEPTIN RELATED MUTATIONS ARE MONOGENIC OR POLYGENIC?
MONOGENIC
(GWAS) GENOME WIDE ASSOCIATION STUDY IDENTIFIED HOW MANY LOCI IN THE GENOME ASSOCIATED WITH BMI?
97
WHAT HAPPENS IN BRAINS OF OBESE AND LEPTIN RESISTANT INDIVIDUALS WHEN THEY ARE SHOWN PICTURES OF FOOD COMPARED TO LEAN PEOPLE?
- INCREASED ACTIVITY IN THE FOOD CONTROL AREA OF THE HYPOTHALAMUS
- INCREASED ACTIVITY IN BRAIN REWARD CENTRES
OBESITY RELATED COMORBIDITIES/ LONG TERM COMPLICATIONS?
JOINT ISSUES, SLEEP APNEA, ACID REFLUX, INSULIN RESISTANCE, T2D, FATTY LIVER DISEASE, CVD, INFERTILITY
