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CSP > Adipokines > Flashcards

Adipokines Flashcards

1
Q

what is obesity

A

abnormal or excessive fat accumulation that presents a risk to health.

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2
Q

describe the histology of adipose tissue

A

Connective tissue
Several cell types:
Adipocytes (white/brown/beige)
Stromal vascular cells
(pre-adipocytes, fibroblasts, endothelial
cells and monocytes/macrophages)

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3
Q

what are the traditional roles of adipose tissue

A

Store energy
Cushion organs
Insulation

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4
Q

what are adipokines

A

adipokines are immunomodulatory cytokines secreted by adipose tissue that include acute phase reactants, growth factors and other inflammatory mediators, adipose tissue hormones such as leptin; and have an autocrine, paracrine, and endocrine mechanism of action.

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5
Q

how many adipokine proteins are there

A

347 protein components

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6
Q

what are the major adipokine classes

A

Metabolic adipokines
Pro-inflammatory adipokines
ECM components
Mitogenic/angiogenic adipokines

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7
Q

what cell factors do metabolic adipokines come from

A

leptin : white adipose tissue (WAT)

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8
Q

what cell factors do pro-inflammatory adipokines come from

A

visfatin : macrophages

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9
Q

what cell factors do ECM components come from

A

fibronectin : fibroblasts

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10
Q

what cell factors do mitogenic/angiogenic adipokines come from

A

Adiponectin: WAT

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11
Q

name some metabolic adipokines

A

Adiponectin
Leptin
Visfatin (PBEF, NAMPT)

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12
Q

name a pro-inflammatory adipokine and does it provide a mechanism for the pro-inflammatory phenotype of obesity

A

Visfatin

it provides a pro-inflammatory phenotype for obesity but the adaptive response morphs into a maladaptive one over time.

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13
Q

name some Extracellular matrix (ECM) components

A

Fibronectin

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14
Q

what does long-term obesity have on the extracellular matrix?

A

in long-term obesity, the extracellular matrix builds up around adipokines and thickens (fibrosis) causing the adipokine to shrink

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15
Q

name some Mitogenic/angiogenic adipokines

A

Adiponectin

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16
Q

name the three key adipokines

A

leptin
adipokines
visfatin

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17
Q

describe the genetic characteristics of leptin

A

16.7 kDa hormone
product of ob gene

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18
Q

where is leptin secreted

A

mainly from white adipose tissue (subcutaneous fat (beneath skin) > visceral fat (surrounds organs)

Also secreted by BAT, placenta, muscle, stomach etc…

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19
Q

what molecule has a satisfactory role

A

leptin (by giving fullness feeling)

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20
Q

what molecule is found in excess in obesity and type 2

A

leptin

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21
Q

what is leptins physiological role in as a satiety factor

A

Inhibits hunger by:
- counteracting the effects of (neuropeptide Y) NPY and anandamide (responsible for hunger)

promoting the synthesis of α-MSH (inhibits appetite

22
Q

what is the effect of prolonged leptin release?

A

Over time, leptin resistance becomes a factor (individuals w/ obesity)

23
Q

what is leptin’s physiological role in reproduction

A
  • Required for fertility

-Levels can affect egg quality and in vitro fertilisation success

-Stimulates GnRH released by the hypothalamus to release FSH AND LH

24
Q

what is leptin’s physiological role in NUTRIENT METABOLISM

A

-Enhances lipid oxidation in muscle

-Inhibits glucose-induced insulin secretion

25
Q

describe the general characteristics of adiponectin

A
  • 30kDa peptide hormone, multiple forms and segments
  • Implicated in glucose and lipid homeostasis
  • has anti-inflammation and anti-atherogenesis effects

-Levels drop with increased adiposity

  • May be increased in older adults (>70), especially centenarians
  • circulates as a multimer
26
Q

is adiponectin levels increased or decreased in obesity?

A

decreased

27
Q

true or false adiponectin counteracts leptin

A

true

28
Q

why does adiponectin circulate in different forms

A

circulates in different forms in different diseased states

29
Q

what forms can adiponectin be found in

A
30
Q

what bonds hold tetramers of adiponectin together

A

di-sulphate bridges

31
Q

how many adiponectin receptors are there

A

3 receptors

32
Q

what are the three adiponectin receptors and where they are expressed?

A

AdR1 – ubiquitously expressed, most abundant in skeletal muscle, globular

AdR2 – liver, full length

T-cadherin – in myoblasts, not liver.

33
Q

what part of adiponectin activates AdR1

A

globular area

34
Q

what part of adiponectin activates AdR2

A

any part of the molecule activates it

35
Q

what is adiponectin physiology?

A

Suppresses TNF-α and IL-6
Suppresses hepatic gluconeogenesis
Stimulates FFA (fatty acid) oxidation
Stimulates glucose uptake in muscle
Stimulates insulin secretion
Anti-cancerous (opposes leptin)

36
Q

Who is adiponectin beneficial too and why

A

Mostly beneficial effects – mostly lost in obesity (as levels drop)
Possibly due to changes in adipocyte size and deposition

37
Q

what are the possible therapeutic uses of adiponectin

A
  • anti-hyperglycemic
  • anti- anthropogenic
  • anti- inflammatory
  • could have important implications when developing new therapies for preventing/ treating obesity and obesity-related diseases
38
Q

where is visfatin secreted from

A

exclusively visceral tissue

39
Q

what is visfatin also known as

A

Also known as pre-B-cell colony-enhancing factor 1 (PBEF1) and Nicotinamide phosphoribosyltransferase (eNAMPT) -> produces nicotine mononucleotide

40
Q

what is visfatins known roles

A

+ Known to be nicotinamide mononucleotide (NMN) biosynthesisER (NAD precursor)
+involved in oxidative phosphorylation
+aging and cancer
+ acts as an enzyme extracellularly to produce NMN which converts to NAD

41
Q

What is the importance of visfatin secreted by macrophages?

A
  • Visfatin is secreted by neutrophils & macrophages in response to inflammatory stimuli
  • Obesity and metabolic syndrome are multifactorial diseases which includes chronic inflammation.
  • Visfatin is implicated, perhaps at early stages of the development of obesity and metabolic syndrome, to reduce inflammation.
  • Intracellular NAD+ concentrations correlate with visfatin protein expression upon PPARγ ligand activation
42
Q

what is the link between Visfatin and NAD+ in disease

A

NAD+ boosting was also efficient to improve glucose homeostasis in obese, prediabetic, and T2DM animals

43
Q

explain the Adipokine theory of obesity

A

development of metabolic disorders such as obesity and insulin resistance is a result of adipokines circulating and reduced levels or adiponectin

44
Q

explain the storage Storage deficit theory obesity

A

there is max safe level of lipids that can be stored in adipokines before lipids get stored elsewhere ex, pancreas and kidney

45
Q

explain the insulin secretion pathology of leptin

A

leptin decreases GLUCOSE STIMULATED INSULIN SECRETION (GSIS) (U SHAPED) so can act as a pro-diabetic

46
Q

Explain leptins cardiovascular pathological effects

A

Role in endothelial dysfunction as it causes endothelial cells to become more inflammatory adding more adhesion molecules to drive atherosclerosis(
-> arteries become narrowed and hardened due to fat build up)

47
Q

explain the pathology of leptins in cancer

A

In vitro – increased proliferation (breast, colorectal, prostate, ovarian and lung) and decreased apoptosis (colorectal and prostate),

48
Q

Can adipokines drive cancer? How would you test this?

A

There is evidence to suggest that adipokines can promote cancer cell growth and metastasis. However, more research is needed to understand the exact mechanisms by which adipokines contribute to cancer progression.

In vitro experiments involve growing cancer cells in a laboratory setting and exposing them to different concentrations of adipokines to observe their effects on cell growth and proliferation. In vivo, experiments involve administering adipokines to animal models with cancer and observing the effects on tumour growth and metastasis.

experiments are not definitive of adipokine involvement in cancer

49
Q

visfatin’s association w/ disease

A

*Extracellular visfatin can exert various deleterious effects on vascular cells, including inflammation and proliferation.
*The vasculature of visceral fat, is unique in that it drains into the hepatic portal vein (secretions of visceral fat is drained into liver).
* Plasma PBEF/visfatin can be increased in response to a sustained (90-240 minute) blood glucose elevation.
* Clinical studies are mixed, however, but suggest an association between increased circulating PBEF/visfatin with diabetes mellitus.
* visfatin activates insulin receptors and increases secretion however elevated visfatin for a long period of time can have opposing effect

50
Q

what are the various adiponectin levels effects if therapeutic?

A

*Lifestyle correction can increase adiponectin levels (<1 week)
*Anti-diabetic therapy increases adiponectin levels
*Cannot be oral because its a peptide – stomach
*Administration w/ injections - reduces visceral adiposity, adipocyte size and body weight (mice)
But… does not lower blood glucose in diabetic animals

CSP (5 decks)

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