Obesity Flashcards

1
Q

What are the two mechanisms by which body fat accumulates?

A
  • Adipose Hypertrophy

- Adipose Hyperplasia

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2
Q

What is the difference between visceral and subcutaneous adipose tissue in terms of where it is located?

A

Subcutaneous fat is located under the skin, visceral fat is located around the organs

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3
Q

What is the role of fat (specifically white adipose tissue) in the body in normal quantities?

A

It is an energy storage and metabolically regulatory endocrine organ that regulates lipid handling, inflammation and immune function

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4
Q

What are the most popular methods of body composition measurement?

A
  • BMI
  • Skinfold Calipers
  • DEXA *
  • Hydrostatic Weighing *
  • Air Displacement Plethysmography
  • Electrical Bioimpedence
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5
Q

What is the gold standard body composition measure, and how does it work?

A

-Hydrostatic Weighing:

Body density is estimated by submerging the body in water, then the Siri equation is used to estimate bodyfat percentage

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6
Q

When is hypertrophy vs hyperplasia more likely to occur?

A
  • Hypertrophy is more likely over small time frames and small amounts of weight gain
  • Hyperplasia occurs when a significant amount of weight is gained.
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7
Q

What is adipose dysfunction?

A

-When you accumulate too much adipose tissue, the immune function changes to cause an accumulation of white blood cells in the tissue, and an inappropriate release of hormones such as increased leptin and decreased adiponectin.

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8
Q

What are the endocrine functions of adipose tissue?

A

Secretion of hormones for:

  • Control of nutritional intake
  • Control of insulin sensitivity and inflammatory process mediators and processes
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9
Q

What is the function of leptin? How does it differ in normal vs dysfunctional adiposity?

A

It is a mediator of long term energy balance (unlike ghrelin which is short term), suppressing hunger/food intake.
Low/normal levels in Normal Adiposity
Very high levels in dysfunctional adiposity, concomitant with leptin resistance
(Klok et al 2007)

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10
Q

What is the function of adiponectin?

A
  • Increased fatty acid oxidation and inhibition of hepatic glucose production, leading to improved insulin sensitivity and lower plasma glucose (Lihn et al 2005)
  • Anti inflammatory and anti-atherogenic effects
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11
Q

What are the hormones released by adipose tissue in relation to regulation of nutritional intake?

A
  • Leptin
  • Angiotensin (mechanism is unknown, Yoshida et al., 2012)

Both reduce food intake/hunger

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12
Q

What are the hormones released by adipose tissue in relation to regulation of insulin sensitivity and inflammation (adipokines)?

A

Adiponectin, Resistin, IL-6, Visfatin and TNF alpha, among others

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13
Q

What is adipogenesis?

A

Differentiation of pre-adipocytes into mature fat cells

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14
Q

What are the two main phenotypes of macrophage in adipose tissue?

A

M1 and M2 macrophages

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15
Q

What are M1 macrophages?

A

Macrophages that produce pro-inflammatory cytokines, impact lipid trafficking/metabolism, inhibiting mitochondrial function and increasing ROS.

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16
Q

What are M2 macrophages?

A

Macrophages that enhance lipid handling, mitochondrial function, anti-inflammatory cytokine production and inhibition of ROS

17
Q

How does macrophage activity differ in healthy vs dysfunctional adipose tissue?

A

M2 predominates in healthy adipose, and M1 predominates in dysfunctional tissue

18
Q

Outline the main differences between dysfunctional and healthy adipose tissue in terms of metabolic/immune/hormonal function:

A

Healthy: M2 Macrophages predominate, very little M1 activity. Decreased leptin and increased adiponectin
Dysfunctional: M1 macrophages predominate, increased leptin and decreased adiponectin

19
Q

What did Frayn 2018 find about the relationship between BMI and bf%?

A

reliable relationship between BMI and bf% at a population level

20
Q

Fat people are not necessarily in energy surplus. They could have been in surplus a long time ago and now are in balance. This is a reminder, not a question.

A

Yes.

21
Q

What is the biggest differentiator between any individuals energy expenditure? Give evidence

A

Physical activity. According to Thompson et al 2009, there is a difference in over 500,000kcal per year between the most and least active individuals in the sample, which is explained by differences in physical activity

22
Q

What is the primary observational evidence to show that obesity is determined by physical activity rather than energy expenditure?

A

-Prentice and Jebb 1995 found that there is a correlation between obesity increasing and physical activity decreasing, but energy intake has not changed in the same time. So physical activity is more important than diet

23
Q

What did the systematic review by Franz et al 2007 on intervention studies for obesity?

A

Exercise least effective both in impact and adherence
Diet alone more effective, Diet and exercise most effective.

Weight loss medication and meal replacements seemingly as effective as diet and exercise in first 12 months.

24
Q

Name a systematic review in opposition to exercise interventions for weight loss

A

Thorogood et al 2011

25
Q

Name a systematic review giving mixed results for exercise and diet interventions for weight loss, with some detail

A

Schwingshackl et al 2014: Diet and exercise is moderately supported to be useful for long term obesity management. Diet is slightly more important than exercise

26
Q

Why is it that physical activity interventions may not be effective for obesity? 2 main reasons

A
  • Substitution effect

- PA compensation effect

27
Q

what is the substitution effect and how does it impact the effectiveness of exercise interventions for weight loss?

A

The effectiveness of a physical activity intervention depends on the level of physical activity that the planned exercise is replacing/substituting. If the exercise is planned for a time when one would normally be active, it will be less effective than if planned for a time where one would usually be totally sedentary, resulting in a lower deficit

28
Q

What is PA compensation and why does it impact the effectiveness of an exercise intervention for weightloss?

A

Individuals may be less physically active for the rest of the day after exercising, resulting in the same overall energy expenditure

29
Q

What compensation can exist outside of PA compensation that can impact the effectiveness of exercise for weight loss?

A

Dietary compensation. Eating more after exercising more.

30
Q

How does weight loss impact your BMR? How does this impact energy balance on a diet?

A

As you lose weight you lose mass, which means you lose total metabolically active mass, so your BMR decreases. With the same energy deficit, your weight loss will eventually plateau,

31
Q

Is there any evidence to suggest that obesity is genetic?

A

-Stunkard et al 1986 found that BMI of adoptive children are associated with those of their bio-parents, not adoptive parents.

32
Q

Does the environment ‘expose’ the effects of genetic predisposition to obesity? Give evidence.

A

Walter et al 2016 found that in more recent observational studies, individuals with a higher genetic risk for obesity were more likely to be obese than individuals with the same risk several decades before

33
Q

Is there any evidence to support the concept of ‘fat but fit’?

A

Francisco B Ortega et al., found that CV fitness can offset the risks of CVD and all cause mortality associated with obesity. A fit obese person may have less risk of CVD than normal weight but unfit people.

34
Q

Is there any evidence to support the concept of ‘fat but fit’?

A

Francisco B Ortega et al., found that CV fitness can offset the risks of CVD and all cause mortality associated with obesity. A fit obese person may have less risk of CVD than normal weight but unfit people.

35
Q

Which type of white adipose tissue increases the risk of chronic diseases more?

A

Visceral moreso than subcutaneous.