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Phys II Unit II > 7 Fat > Flashcards

7 Fat Flashcards

(53 cards)

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1
Q

What is the “old view” of fat?

A

Fat is a passive organ that is a DEPOT for fat storage

“Fat” refers to lipids and cells/tissues that store lipids

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2
Q

What is the “modern view” of fat?

A

Fat is a DYNAMIC organ

Energy conversion and storage
Regulates energy balance and nutritional homeostasis
Generates heat (“brown fat”)
Cushions organs
Affects body shape and appearance
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3
Q

What is adiposity?

A

How fat deposition occurs in the body

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4
Q

How is BMI calculated?

A

BMI = weight (kg) / height (m^2)

Or

BMI = weight (lbs) x 703 / height (inches^2)

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5
Q

BMI>30

A

Obese

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6
Q

BMI = 25-29.5

A

“Overweight”

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7
Q

BMI = 18.5 - 24.9

A

Health lean

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8
Q

BMI<18.5

A

Underweight

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9
Q

What happens to BMI with age?

A

Increases

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10
Q

What is the definition of obesity

A

Clinical state of excessive accumulation of body fat

Usually based upon BMI (>30)

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11
Q

The condition of abnormal lipid levels and/or their lipoproteins

A

Dyslipidemia or hyperlipidemia

Can be elevated cholesterol and triglycerides or elevated chylomicrons and LDL

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12
Q

White adipose tissue can be subdivided into …

A

Visceral vs subcutaneous white adipose tissue

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13
Q

Which is more dangerous: visceral or subcutaneous fat

A

Visceral

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14
Q

Obesity is associated with…

A

Heart disease
Stroke
Diabetes
Cancers

36.5% of US adults are obese

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15
Q

What groups are disproportionally obese?

A

Non-Hispanic blacks (48.1%)

Middle age (40.2% vs young adults 32.3%)

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16
Q

What are the three types of adipocytes?

A

White, Brown, Beige

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17
Q

What are the two types of fat deposits?

A

White adipose tissue (WAT)

Brown adipose tissue (BAT)

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18
Q

What types of cells are found in WAT?

A

Adipocytes (~50% of cells)
Pre-adipocytes (~2% of cells) - these are adipo stem cells
Fibroblasts - connective tissue
Endothelial cells - circulatory
Nerve cells
Macrophages (M1 pro-inflammatory vs M2 anti-inflammatory)

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19
Q

Brown fat is a _______ organ

A

Heat-generating

Hormone dependent - requires UCP1 transcription and G-protein second messenger

Daily heat production: 27 kcal/kg body weight

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20
Q

What allows brown adipose tissue to directly transfer food energy into heat energy?

A

Uncoupling Protein 1 (UCP1)

Dependent upon both Epi and TSH

T4 enters, converted to T3, binds to receptor and transcription —> UCP1 production; UCP1 enters mitochondria and generates heat.

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21
Q

Brown fat is found predominantly in _______.

A

Infants

It decreases with age but adults still have some concentrated around neck, shoulders, lungs (F>M)

BAT contains numerous small lipid droplets, uncoupled mitochondria, and myoglobin

BAT activity can be increased in response to cold exposure or epi

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22
Q

What is Beige Fat?

Study These Flashcards
A

Occurs in WAT, has INTERMEDIATE mitochondria, UCP1 and lipid droplets, heat production compared to BAT

Possible induction by T3 and epi, cold, hepatic bile acids, and ANP/BNP, skeletal muscle hormone Irisin

23
Q

What hormone promotes storage of fats into adipocytes and stimulates anti lipolysis effect (FA—>TG)?

Study These Flashcards
A

Insulin

Stimulates lipoprotein lipase to convert TG to FA
Stimulates GLUT4 to increase glucose uptake into adipocytes
Inhibits hormone-sensitive lipase

Results:
Lower fatty acids and increased storage
Increased glucose uptake into adipocytes
Increased enzymes that produce fatty acids
Increased fatty acid uptake
Decreased lipolysis
24
Q

What hormones stimulate a lipolysis effect (TG —> FA)?

Study These Flashcards
A

Epinephrine, cortisol, glucagon, and GH

Epi acts via HSL and adipose tissue triglyceride lipase (ATGL)

Thyroid hormone also has some indirect effect:
Doesn’t directly regulate fuel metabolites b/c onset is too slow to rapidly adjust blood levels of nutrients

25
Women tend to have more ________ fat depots, whereas men tend to have more ________ fat depots
Women = Subcutaneous (Gynecoid Adiposity) Blood drains to skeletal muscle and free fatty acids are utilized for energy during exercise Men = Visceral (Android Adiposity) Mental and messenteric Blood drains to hepatic portal and free fatty acids are cleared by the liver
26
How does testosterone affect adiposity?
It decreases subcutaneous depots and increases visceral depots, particularly in men
27
How does insulin affect adiposity differently in men v women?
Higher whole body insulin sensitivity in women (increases adiposity) Men are less sensitive to anti-lipolysis effects of insulin Estrogens and androgens lower body fat and improve insulin sensitivity in both sexes
28
How does metabolic activity differ in different types of WAT?
Subcutaneous WAT in lean people —> active metabolic activity Gluteal-femoral WAT tissue —> least active metabolic activity Visceral WAT —> most active metabolic activity
29
How does sensitivity to sex hormones vary between the different types of WAT?
Subcutaneous WAT in lean people is LEAST sensitive Gluteal-femoral WAT is ESTROGEN sensitive Visceral WAT is TESTOSTERONE sensitive
30
How does macrophage activity vary between different types of WAT?
Subcutaneous WAT: 10-15%, mostly M2 anti-inflammatory Gluteal-femoral WAT: 10-15%, mostly M2 anti-inflammatory Visceral WAT: 40-60%, mostly M1 pro-inflammatory*** This is why visceral fat is the most dangerous
31
What is the difference between hypertrophy and hyperplasia of adipose tissue?
Hypertrophy = increase in volume Can but by up to 1000x REVERSIBLE Hyperplasia = increase in the number of adipocytes Generally occurs during first year of life, late pregnancy, and beginning of puberty NON-REVERSIbLE Cells derived from pre-adipocytes
32
Visceral obesity results from deposit in the ...
Mental, mesenteric, and retroperitoneal fat depots Visceral obesity is usually a sign that lipids are also being deposited ectopically (muscle, liver, pancreas), which could aggravate DM
33
What are the hormones of the adipose organ called?
Adipokines - Leptin and Adiponectin
34
Adipokines that is a metabolic regulator and feedback signal on appetite
Leptin
35
Adipokine that is for insulin sensitizing and anti-inflammatory hormone
Adiponectin Promotes the uptake of beneficial lipids
36
Other than Leptin and Adiponectin (the two main adipokines), what other adipokines regulate glucose metabolism?
Resistin: associated with T2DM and elevated LDL Omentin: plays crucial roles in the maintenance of body metabolism and insulin sensitivity, and has anti-inflammatory, anti-atherosclerotic, and CV protective effects Visfatin: released from visceral fat, binds the insulin receptor and exerts a hypoglycemic effect (promotes insulin function)
37
Visceral or Subcutaneous: Leptin
SC>V Stimulated by increased adiposity, targets hypothalamus to decrease appetite, protects body from too much lipid
38
Visceral or Subcutaneous: Adiponectin
SC>V Stimulated by weight loss, targets muscle, liver, heart, and vessels to increase oxidation of FFAs and has anti-inflammatory effects Beneficial effects on insulin resistance
39
Visceral or Subcutaneous: Tumor necrosis factor alpha
V>SC Stimulated by engorgment of adiposites, acts on liver, muscles, adipocytes etc to decrease adipocyte mass and opposes insulin signaling
40
Visceral or Subcutaneous: Interleukin-6
V>SC Stimulated by inflammatory cytokines, targets liver, muscle, and adipose tissue to oppose insulin signaling
41
What are the beneficial effects of Adiponectin?
Improves insulin sensitivity Anti-inflammatory Anti-atherogenic Targets resting skeletal muscle to increase GLUT4 Has CV protective effects Stimulates liver to promote glucose uptake and energy storage ***Autocrine signaling in adipose promotes adipogenesis and insulin-directed glucose transport
42
In mouse studies, over expression of Adiponectin in fat tissue leads to ...
An increase in SC fat, and yet it protects against diet-induced insulin resistance
43
What are the pro-inflammatory adipokines?
TNFa Interleukin-6 Interleukin-1 (regulatory, promotes tumor growth)**** One of the theories as to why obesity is associate with a higher cancer risk
44
What happens when fat gets inflamed?
Constraints on extracellular matrix and diffusion limited hypoxia —> necrotic conditions Macrophages increase 10% to 50% of cells M1 macrophages increase proinflammatory cytokines (ie TNFa), which inhibit insulin action Chronic low-grade inflammation —> increased ROS Associated with elevated risk of cancer and can exasperate T2DM
45
Where does Leptin signaling occur in the brain?
In the arcuate nucleus of the hypothalamus
46
Anorexigenic or Orexigenic: Melanocortins
Melanocortins (POMC) suppress appetite —> anorexigenic
47
Anorexigenic or Orexigenic: Neuropeptide Y (NPY)
Potent appetite stimulus —> orexigenic Also decreases metabolic rate and suppresses fertility
48
Anorexigenic or Orexigenic: Agouti-related protein (AgRP)
Potent appetite stimulant —> orexigenic Also decreases metabolic rate and suppresses fertility
49
Anorexigenic or Orexigenic: Ghrelin
When released from the stomach, it stimulates NYP and inhibits the action of Leptin and POMC —> Orexigenic
50
What are the anorexigenic inputs to the hypothalamus?
Leptin (secreted from adipose tissue, weight loss in obese individuals reduces Leptin) Insulin inhibit NYP cells Amylin slows gastric emptying and signals satiety Peptide PTT produced by small and large intestine inhibits NPY neurons Cholecystokinin (CCK) released from the mucosal lining of the small intestine in response to a meal signals satiety
51
What are the orexigenic inputs to the hypothalamus?
Ghrelin, the hunger hormone released by the stomach, peaks before food is eaten and falls immediately after a meal
52
Explain why Leptin resistance is now an alternative theory as to the cause of obesity
Normally, Leptin inhibits insulin secretion in a classic negative feedback regulation Leptin stimulates liver gluconeogenesis by vagal stimulation, and muscle, heart, BAT glucose uptake via ANS-sympathetic NS When the feed back is lost, hyperinsulinemia increases weight gain, aggravates DM, and elevates Leptin levels In Leptin resistant over-weight individuals, the permeability of the BBB to Leptin is decreased, leading to increases in appetite
53
Why do Biggest Loser contestants have a much reduced metabolic rate
Leptin levels crashed by the end of the season, and only recovered to ~50% of normal after six years (the never get back up to normal metabolic rate levels because of Leptin resistance)

Phys II Unit II (9 decks)

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