MetS Flashcards

1
Q

Classification of human obesity based on BMI

A

Caucasion population

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2
Q

History of BMI

A
  • Started in 1830s → wanted to come up with ideal formula to decide on ideal man
  • 1970s → first used in research to measure obesity
  • More recently→ Can correlate with metabolic risks and CVDs (No perfect though does not consider individual body comp)
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3
Q

Graph interpretation

A

On the graph can see that for 1 waist circumference measurement there can be a range of BMIs associated with it. Hence BMI may not be good for assessing obesity

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4
Q

Waist circumference risk

A

↑ waist circumference ↑ risk for CVD

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5
Q

Difference between subcutaneous and visceral fat distribution with same waist circumference and BMI

A
  • subcutaneous → associated with high quality lifestyle patterns → normal TAG with increase waist girth
  • visceral → associated with low quality lifestyle patterns → elevated TAGs with hypertryglyceridemic waist → ↑ metabolic abnormalities
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6
Q

metabolic abnormalities/ clinical outcomes with hypertriglyceridemic waist

A
  • presence of atherogenic metabolic triad
  • ↑ cholesterol/HDL
  • postprandial hyperlipidemia
  • glucose intolerance
  • hyperinsulinemia
  • ↑ blood pressure
  • ↑ risk of CVD
  • ↑ risk Coronary artery disease
  • ↑ annual progression rate of aortic calcification
  • ↑ risk of T2D
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7
Q

Interpret graph

A

depending on ethnicity, more predisposed to fat distributions
* Asians are more prone to developing visceral fat, followed by caucasian, then african

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8
Q

What defines someone of MetS?

A

Must have: Central obesity (with ethnic specific values) and two of the following (If BMI > 30 kg/m2, central obesity can be assumed)
1. Increased TG level (>= 150 mg/dL)
2. Reduced HDL cholesterol (<40 mg/dL in males and <50 mg/dL in females)
3. Raised blood pressure (systolic >= 130 or diastolic >= 85 mmHg)
4. Impaired fasting glucose >= 5.6 mM (prediabetes or diabetes)

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9
Q

ethnic specific values of WC as a measure of central obesity

A
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10
Q

Prevalence of MetS (and obesity)?

A
  • 13% of all adults around the world are obese
  • 40% are overweight
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11
Q

How has obesity changed since 1960?

A

overweight has stayed relatively similar at about 40% in men and 25% women but obesity has gone up by almost 30%

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12
Q

prevalence of overweight children

A

31% of Canadian children are overweight

image is US but has risen from 5% to 20%

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13
Q

Consequences of obesity in adults

A
  • 3X increased risk of heart attack or stroke
  • 5X increased risk of T2D
  • CVD is the 2nd leading cause of death in Canada, 1st in the world
  • 80% of T2D patients will die from CVD
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14
Q

Consequences of obesity in children

A
  • Non-alcoholic fatty liver disease(NAFLD)
  • Polycystic ovarian syndrome
  • CVD risk
  • T2D
  • Unknown health problems as adults (obesity hasnt really been an issue till now)
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15
Q

Cascade for association of visceral fat with increased metabolic risk

A
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16
Q

interpret graph

A

Survival decrease significantly for participants with both MetS and T2D
* MS only decreased by 10%
* DS only decreased by 25%
* MS + DS decreased by 30%

17
Q

Interpret graph

A

Shows that there might be good fat (subcutaneous) and bad fat (visceral)
* non-obese shows normal circulating glucose and insulin
* obese low visceral shows mostly normal circulating glucose and some hyperinsulinemia/ IR
* obese high visceral shows glucose intolerance and high hyperinsulinemia/IR (about 3x greater than normal)

18
Q

Interpret

A

Visceral fat was decreased by about 45 cm2 which is about 6 cm reduction in waist but BMI remained the same
* may have accumulated muscle mass
* More water retention with muscle addition

If solely looked at BMI would be lead falsely to believe that it did not do anything. So can appreciate the reduction in visceral fat and waist circumference with this study

19
Q

The adipose tissue as an endocrine organ

A

Different fat depots in the body will behave differently
* anti-hyperglycaemic (subcutaneous): lean adipocytes act as signalling tissue to secrete good messengers and hormones for fat metabolism
* Pro-hyperglycaemic: (visceral) when adipocyte grows larger it gains more fat and then it can switch to secreting more harmful things such as cytokines

20
Q

What messengers/ hormones are released with anti-hyperglyceamic adipocytes?

A
  • leptin: exerts immediate effects by acting on the brain to regulate appetite and adjust food intake and energy expenditure accordingly
  • adiponectin: increases insulin sensitivity (more you have the more insulin sensitive)
  • visfatin & omentin: not much known
21
Q

What messengers/ hormones are released with pro-hyperglyceamic adipocytes?

A
  • resistin: may resist insulin action and impairs glucose homeostasis
  • cytokines (TNF-a, IL-6): inflammation
  • MCP-1: attracts other immune cells and cytokines
  • leptin: increases with more fat and can become leptin resistant
22
Q

Inflammation in MetS

draw cascade

A

Visceral fat accumulates around important organs which brings in macrophages as a response causing inflammatory mediator response such as cytokines and immune cell infiltration producing deliterious effects resultiing in low-grade systemic inflammation.

23
Q

Result of macrophage infiltration

A
  • promotes IR
  • pancreatic islet deterioration (bet cells enlarge to compensate, apoptosis may occur)
  • systemic inflammation
24
Q

Systemic inflammation resulting in T2D and CVD

A
  • decrease in insulin production
  • athersclerosis
25
Q

Relationships between dietary patterns or diet components and low-grade inflammation

A

potential patterns to help: Hypoenergetic, Mediterranean, Vegetarian, …
* literature argues both sides of the story however so hard to say

26
Q

association between CVD related death and omega 6:3 fatty acids

A

Can look at omega 6 and 3 and see that CVD fit with these ratios. Have lead to believe that 3 may be a way to prevent CVDs but controversial
* CVD increasing by 7x with high 6:3 of 50:1

27
Q

Metabolic fate of Omega-6 vs -3 FAs

A