Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

FOO > METABOLIC SYNDROME; EXAMPLE; OBESITY > Flashcards

METABOLIC SYNDROME; EXAMPLE; OBESITY Flashcards

1
Q

WHAT’S METABOLIC SYNDROME USED TO BE CALLED?

A

SYNDROME X

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

WHO INITIALLY NAMED METABOLIC SYNDROME THE SYNDROME X?

A

GERALD REAVEN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

WHAT EXACTLY IS METABOLIC SYNDROME?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

THE METABOLIC SYNDROME INCREASES A PERSON’S RISK OF:

A
  • T2D
  • CVD
  • CANCER
  • NEURODEGENERATIVE DISEASE
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

THE PARAMETERS OF THE METABOLIC SYNDROME?

A
  • INSULIN RESISTANCE OR DIABETES
  • HIGH BP
  • HIGH FAT IN BLOOD (TRIGLYCERIDES)
  • LOW HDL, HIGH LDL
  • OBESITY
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

% OF CHILDREN 4-5 Y.O. THAT ARE OVERWEIGHT?

A

10%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

% OF CHILDREN 10-11 Y.O. THAT ARE OVERWEIGHT?

A

20-25%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

RATES OF OBESITY IN IMMIGRANTS IN COUNTRIES LIKE THE US USUALLY INCREASE RAPIDLY WITHIN HOW MANY YRS?

A

5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

‘THRIFTY PHENOTYPE THEORY’?

A
  • 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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

EXAMPLE OF A GROUP THAT DRASTICALLY INCREASED OBESITY AND T2D RATES UPON ACCULTURATION?

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

THE MOST COMMON TRAIT TRANSMITTED TO A CHILD BY ITS PARENTS IS?

A

HEIGHT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

WHAT IS A REGRESSION COEFFICIENT AND HOW IS IT USED IN ESTIMATING HERITABILITY?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

REGRESSION COEFFICIENT FOR OBESITY?

A

0.6-0.7 (HIGH HERITABILITY)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

% OF VARIATION IN BODY WEIGHT ASSOCIATED WITH GENETIC FACTORS?

A

70%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

WHEN WAS LEPTIN IDENTIFIED?

A

1994

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

LEPTIN HAS TONIC EFFECTS. EXPLAIN?

A

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

17
Q

WHERE IS LEPTIN RELEASED FROM?

A

ADIPOSE TISSUE, SO THE LEVELS DIRECTLY RELATE TO LEVELS OF ADIPOSITY

18
Q

GENETIC MUTATIONS RELATED TO LEPTIN DEFFICIENCIES? EFFECTS? TREATMENT?

A
  • 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
19
Q

APART FROM INSULIN RESISTANCE, WHICH OTHER HORMONE CAN OBESE INDIVIDUALS DEVELOP RESISTANCE TO WHICH WILL LEAD TO INCREASED FOOD INTAKE?

A

RESISTANCE TO LEPTIN

20
Q

LEPTIN LEVELS IN THE BRAINS OF OBESE PEOPLE ARE LOWER THAN IN LEAN PEOPLE, POSSIBLE REASONS?

A
  • IMPAIRED LEPTIN TRANSPORT ACROSS THE BLOOD BRAIN BARRIER
  • IMPAIRED LEPTIN RECEPTORS
  • A ROLE OF INFLAMMATION, STRESS AND INEFFECTIVE AUTOPHAGY
21
Q

LEPTIN RELATED MUTATIONS ARE MONOGENIC OR POLYGENIC?

A

MONOGENIC

22
Q

(GWAS) GENOME WIDE ASSOCIATION STUDY IDENTIFIED HOW MANY LOCI IN THE GENOME ASSOCIATED WITH BMI?

A

97

23
Q

WHAT HAPPENS IN BRAINS OF OBESE AND LEPTIN RESISTANT INDIVIDUALS WHEN THEY ARE SHOWN PICTURES OF FOOD COMPARED TO LEAN PEOPLE?

A
  • INCREASED ACTIVITY IN THE FOOD CONTROL AREA OF THE HYPOTHALAMUS
  • INCREASED ACTIVITY IN BRAIN REWARD CENTRES
24
Q

OBESITY RELATED COMORBIDITIES/ LONG TERM COMPLICATIONS?

A

JOINT ISSUES, SLEEP APNEA, ACID REFLUX, INSULIN RESISTANCE, T2D, FATTY LIVER DISEASE, CVD, INFERTILITY

25
Q

2 GROUPS/TYPES OF OBESE INDIVIDUALS?

A

MHO - METABOLICALLY HEALTHY OBESE

MUHO - METABOLICALLY UNHEALTHY OBESE

26
Q

DIFFERENCE BETWEEN MHO AND MUHO:

A 
- ONLY SLIGHT DIFFERENCES IN ADIPOKINES
 MAIN DIFFERENCES:
- INSULIN SENSITIVITY
- INFLAMMATION STATE
- PRESENCE OR ABSENCE OF VISCERAL FAT AND FAT THAT IS ACCUMULATED IN ORGANS
27
Q

ORGAN WHERE THERE IS ESPECIALLY HIGH INAPPROPRIATE ACCUMULATION OF FAT IN OBESITY?

A

THE LIVER

28
Q

INFLAMMATION PROCESS IN OBESITY, DESCRIBE:

A
  • EXCESSIVE ADIPOSE TISSUE ACCUMULATES
  • HYPERTROPHIC ADIPOCYTES ARE UNDER STRESS AND START ATTRACTING IMMUNE CELLS
  • THERE IS AN INFILTRATION (AT LEAST IN MUHO) OF IMMUNE CELLS WITHIN ADIPOSE TISSUE
  • T CELLS AND MACROPHAGES
  • INFLAMMATORY MOLECULES IMPAIR INSULIN SIGNALLING
  • INFLAMMATORY SIGNALS INDUCE APOPTOSIS AND NECROSIS IN THE ADIPOSE TISSUE ITSELF
  • REDUCE IN FAT CELLS
  • INCREASE OF COLLAGEN IN THE ADIPOSE TISSUE, LEADING TO FIBROSIS; REDUCED ABILITY OF ADIPOSE TISSUE TO EXPAND SO THE FAT STARTS ACCUMULATING ESLEWHERE
29
Q

% OF CELLS IN ADIPOSE TISSUE IN MORBIDLY MUHO THAT ARE IMMUNE CELLS?

A

UP TO 60%

30
Q

2 TYPES OF MACROPHAGES PRESENT IN ADIPOSE TISSUE IN OBESITY + WHICH ONE IS MORE PREVALENT?

A

M1 AND M2

M1 - BAD TYPE, MUCH MORE PRESENT, INCREASES THE INFLAMMATION FURTHER

31
Q

ACCUMULATION OF WHAT IN ADIPOSE TISSUE LEADS TO FIBROSIS, INABILITY OF THE TISSUE TO FURTHER EXPAND AND ACCUMULATION OF FAT IN ANATOMICALLY INCORRECT PLACES?

A

COLLAGEN

32
Q

MHO OCCURS MORE OFTEN IN WHICH SEX AND WHY?

A

IN WOMEN, BECAUSE OF THEIR NATURAL BODY SHAPE (MORE PEAR)

33
Q

WHICH TYPE OF FAT IS MORE PROTECTIVE AGAINST THE EFFECTS OF OBESITY?

A

SUBCUTANEOUS

34
Q

WHY IS SUBCUTANEOUS FAT MORE PROTECTIVE AGAINST THE EFFECTS OF OBESITY (THAN THE VISCERAL)?

A
    • CAN EXPAND MORE THAN VISCERAL AND THUS PROTECT OTHER ORGANS
    • LESS PRONE TO INFLAMMATION BECAUSE IT’S LESS VASULARISED SO IT’S HARDER TO RECRUIT IMMUNE CELLS
  • NOT DRAINED BY THE HEPATIC PORTAL VEIN SO THE LIVER IS MORE PROTECTED
35
Q

WHICH TYPE OF FAT IS DRAINED BY THE HEPATIC PORTAL VEIN?

A

VISCERAL

36
Q

LACK OF SUBCUTANEOUS FAT INCREASES RISK OF WHAT?

A

CVD

37
Q

WHY DO SOME DEBATE WHETHER SUBCUTANEOUS AND VISCERAL FAT ARE THE SAME TYPE OF ADIPOSE TISSUE?

A

BECAUSE THEY COME FROM DIFFERENT PRECURSORS

38
Q

IN WHICH POPULATION ESPECIALLY ARE THE OBESITY RATES INCREASING?

A

CHILDREN

FOO (57 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions