Adipose tissue Flashcards

1
Q

What are the 4 functions of adipose tissue?

A

1- Mechanical cushioning
2- Thermal insulation
3- Energy store
4- Endocrine organ

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2
Q

Brown adipose is 1/2 of the two types of fat.

1- What does it contain a lot of? Relate to function
2- Why is it important in children? How much is found in adults?
3- What does it develop from?

A

1- Many mitochondria and multiple fat droplets; = metabolism generates heat

2- Their high surface area/body mass ratio
> No significant levels in adults

3- Develops from muscle cell progenitors

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3
Q

White adipose is 1/2 of the two types of fat.

What does it contain a little of? Relate to function.

A
  • Fewer mitochondria and a single fat droplet= Controlled storage and release of fat
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4
Q

What type of adipose tissue has relatively low oxygen consumption and is an integral part of whole body carbohydrate and fat metabolism?

A
  • White adipose tissue
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5
Q

How are Triglycerides synthesised? Name the molecules that make it up.

A
  • 1 molecules of glycerol to which three fatty acids have been esterified.
    > The fatty acids present in triacylglycerols are predominantly saturated.
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6
Q

What does HDL do? What protein does it usr to chive its function?

A
  • “scavenge” cholesterol and TAG from tissues, atheromas, even VLDL and chylomicrons via cholesterol ester transfer protein
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7
Q

Describe the 4 main ways Lipids are transported?

A

LIPOPROTEINS: bind to specific receptors on the cell surface, allowing the exchange of lipids between the lipoprotein particles and the cells.

  1. Chylomicrons:
    > Largest and least dense
    > Transport dietary triglycerides from the intestines to various tissues throughout the body, including adipose tissue and muscle.
  2. VLDL (Very Low-Density Lipoprotein):
    > Produced in the liver and carry endogenously synthesized triglycerides. They transport triglycerides from the liver to other tissues, where they can be used for energy or stored as fat. As VLDL particles lose triglycerides, they transition into IDL (Intermediate-Density Lipoprotein) and then further into LDL (Low-Density Lipoprotein).
  3. LDL:
    > Delivering cholesterol to various tissues in the body. LDL is often referred to as “bad cholesterol” because if LDL levels are too high, it can lead to the accumulation of cholesterol in the arteries, increasing the risk of atherosclerosis.
  4. HDL: They are synthesized in the liver and small intestine. HDL is often referred to as “good cholesterol” because it removes excess cholesterol from the tissues and carries it back to the liver for excretion.
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8
Q

Describe the carbohydrate major metabolic pathway in a fed state inside an adipocyte.

A

Carbohydrate metabolism in FED state:

(1) Increased glucose transport —
Elevated insulin levels in fed state leads to influx of glucose through insulin-sensitive transporter.

(2) Increased glycolysis — Increased intracellular glucose results in enhanced glycolysis. Glycolysis supplies glycerol phosphate for triglyceride synthesis.

(3) Increased hexose monophosphate pathway (HMP)—Metabolism of glucose through this pathway produces NADPH, which is essential for fat synthesis.

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9
Q

Describe the fat major metabolic pathway in a fed state inside an adipocyte.

A

Fat metabolism in a FED state:

(1) Increased fatty acid synthesis — De novo synthesis from acetyl CoA is a major source of fatty acids in human adipose tissue only when re-feeding after a fast.

(2) Decreased triglyceride hydrolysis — Elevated insulin levels favors the dephosphorylated (inactive) state of hormone-sensitive lipase, preventing TG degradation and promoting storage.

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10
Q

Describe the carbohydrate major metabolic pathway in a fasting state inside an adipocyte.

A

Carbohydrate metabolism in FASTING state:

Glucose transport and metabolism are depressed due to low insulin levels. This leads to a decrease in fatty acid and triglyceride synthesis.

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11
Q

Describe the fat major metabolic pathway in a fasting state inside an adipocyte.

A

Fat metabolism in a FASTING state:

(1) Increased triglyceride hydrolysis — The activation of hormone-sensitive lipase via phosphorylation leads to hydrolysis of stored TG. This activation is enhanced by noradrenaline released from sympathetic nerve endings in adipose tissue.

(2) Increased fatty acid release — Fatty acids liberated by TG hydrolysis are released into the circulation and transported to other tissues for use as fuel. The glycerol released by TG hydrolysis is used by liver for gluconeogenesis.

(3) Decreased fatty acid uptake — In the fasting state, lipoprotein lipase activity in adipose tissue is low, and lipoprotein TG is not available for TG synthesis in adipose tissue.

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12
Q

How is a fat cell developed?

A

1- Fibroblast-like precursor cells receive hormone signals that trigger differentiation into adipocytes

2- Cells alter gene expression pattern and begin to accumulate lipid droplets.

3- As the lipids accumulate, they merge together and form a mature fat cell (triglyceride droplet and nucleus).

4- Mature fat cells cannot divide, but the early stages are reversible (see arrows).

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13
Q

What happens to white adipose tissue during long-term positive energy balance? (energy intake exceeds expenditure )

A
  • Cells increase in size (hypertrophy) and number (hyperplasia)
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14
Q

In white adipose tissue there is no upper limit to the amount that can be stored…

  • Why is this a problem for dieters, explain this using the term “Thrifty genes”
A

“Thrifty genes” – permit more efficient food utilisation and fat deposition in times of abundance, resulting in better survival in times of subsequent famine - HISTORICAL… Now causes obesity and diabetes

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15
Q

How do adipocytes change during obesity?

A
  • Modest weight gain = increase in cell size up until maximum size
  • Further weight again = recruitment of pre-adipocytes to differentiate into adipocytes
  • In weight loss, cell number does not decrease but cell size decreases.
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16
Q

Why is white adipose tissue considered to be an organ?

A

> Has metabolic integration achieved by endocrine activity including production of:

  • Steroid hormones e.g. oestrogen and cortisol
  • Proteins of energy metabolism, blood clotting and the complement pathway
  • Cytokine signalling
  • Peptide hormones including leptin.
17
Q

What satiety hormone is missing causing obesity?
What causes the hormone to be missing?

A
  • LEPTIN
    > Caused by 2 recessive mutations in the genes ob (obese) and db (diabetic)
    > Leptin not produced when these genes are present
18
Q

Where is leptin produced?
> What does 3 things does leptin treatment result in?

A
  • Primarily in adipose tissue, in proportion to adipose tissue mass.
    > Reduces food intake,
    > Increases energy expenditure,
    > Reverses obesity in ob/ob mice
19
Q

Why is leptin not an anti-obesity drug to everyone?

A
  • Effective only in individuals who are obese because of leptin deficiency

> Most obese subjects have high leptin concentration but fail to respond normally – a condition known as leptin resistance.

20
Q

Adipocytes secrete 6 hormones.
Name them and describe their function.

A
21
Q

What two regions in the hypothalamus dramatically influence feeding behavior?

A

Lateral hypothalamus (hunger center): animals with lesions in this area become anorectic and lose weight.

Ventromedial hypothalamus (satiety center): animals with lesions in this area overeat and become obese.

> Not the whole story

22
Q

What hormones are used as appetite signals when individuals are hungry AND fed?

A

Green = hunger
Ghrelin from the stomach

Red = fed
Glucose, insulin other gut hormones and sensors

23
Q

What does stored energy release in response to appetite?

A
  • Products of adipose = Leptin and RBP4 in proportion to fat content.
24
Q

What does RBP4 do?
> What does adiponectin do to RBP4?

A
  • RBP4 reduces tissue insulin sensitivity. *Adiponectin antagonises RBP4 but falls in obesity
25
Q

What effect do the following hormones have on appetite?

1- NPY = Neuropeptide Y

2- AgRP = Agouti-related peptide

3- POMC = Pro-opiomelanocorticon

A

1- Neurotransmitter (Brain + ANS)
INCREASE Food intake (orexigenesis), DECREASE physical activity.

2- Neuropeptide (Brain)
INCREASE Appetite, DECREASE metabolism.

3- Hormone precursor (Pituitary) regulates melanocyte stimulating hormone
REGULATES appetite and sexual behaviour

26
Q

Hormones that regulate appetite act on the hypothalamus.

1- How do leptin and insulin decrease appetite?
2- How does ghrelin increase appetite?

A

1- Inhibitory actions on NPY/AgRP neurons. They signal the well-fed state

2- Ativates NPY/AgRP neurons.

27
Q

Endocrine signalling differs depending on size of fat cells

1- What do “Fat” fat cells promote?
2- What do “Thin” fat cells regulate?

A

1- Promote insulin resistance; trigger low-grade chronic inflammation;
= Type 2 diabetes, high BP, cardiovascular disease and increased cancer risk

2- Benignly regulate metabolic interplay between tissues.
> They release adiponectin that promotes glucose uptake into tissues.

28
Q

Fat in different locations has different effects on the body

1- Where is visceral fat found? What effect does it have on the body?

2- Where is subcutaneous fat found? What effects does it have on the body?

A

1- Surrounds the abdominal organs, is particularly problematic.
> Its signals go straight to the liver.

2- Under the skin,
> Metabolically less active and seems to produce fewer signalling molecules

29
Q

Describe what type of obesity Android, Ovoid and Gynoid are.

A

Android - Upper body obesity
Ovoid - Overall obesity
Gynoid - Lower body obesity.

30
Q

Who is android obesity common in?
What does android obesity increase the risks of?

A

More common : in men and post-menopausal women,

Greater risk for diabetes and hypertension, larger fat cells, more easily mobilised fat stores.

31
Q

Who is Ovoid obesity more common in?

A

Most common in people genetically predisposed to obesity.

32
Q

Who is Gynoid obesity common in?
What does Gynoid obesity increase the risks of?

A

More common in pre-menopausal women,

Fat stores not easily mobilised, more difficult to lose weight, relatively benign health-wise except for arthritis and varicose veins.

33
Q

What are the messenger, translation and effector systems involved in the regulation of body weight?

A
  • Long term regulation of body weight results from a complex integration of hormonal, metabolic and neural signals