topic 10 insulin resistance Flashcards

1
Q

how many lessons?

A

Lesson1:glucose hemostasis
Lesson2:Insulin &insulin resistance
Lesson3:obesity and insulin dysregulation

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2
Q

interactions between different organs and tissue in glucose homeostasis

A
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3
Q

somatostatin is produced which 3 places?

A
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4
Q

pancreatic hormones

A

glucagon
amylin
insulin
somatostatin
ghrelin

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5
Q

where does ghrelin produced?

A

stomach and ?

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6
Q

full name of GIP?

A

Gastric inhibitory polypeptide (GIP)

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7
Q

full name for GLP-1?

A

glucagon‐like peptide‐1 (GLP‐1)

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8
Q

what are GIP and GLP-1 function?

A

stimulate insulin secretion from pancreatic β cells.

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9
Q

where are GIP and GLP-1 produced?

A

two primary incretin hormones secreted from the intestine on ingestion of glucose or nutrients

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10
Q

what is CCK?

A

cholecystokinin

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11
Q

where is CCK produced?

A

small intestine(SI)

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12
Q

what triggers the release of cholecystokinin?

A

When cells in the mucosal lining of your duodenum (called I-cells) detect the presence of proteins and fats to digest, they trigger cholecystokinin to release into circulation.

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13
Q

what’s the function of cholecystokinin?

A
  1. It stimulates your gallbladder to contract and release bile into your small intestine.(“Cholecystokinin” means to “move the gallbladder.”
  2. It stimulates your pancreas to release pancreatic enzymes. (This is what its other name, “pancreozymin,” means.)
  3. cholecystokinin suppresses gastric emptying so your stomach won’t deliver any more food until the first batch is done.
    4.It also suppresses your appetite while you’re digesting, by making your stomach feel physically full and by activating vagal nerves in your stomach wall.
    5.Finally, it triggers peristalsis, the muscle contractions that move food along through your intestines to continue the digestive process.
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14
Q

glycolysis?

A

糖酵解,释放能量

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15
Q

glycogenesis?

A

糖原生成,消耗能量

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16
Q

glycogenolysis?

A

糖原分解,释放能量

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17
Q

gluconeogenesis

A

糖异生,消耗能量

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18
Q

insulin, glucagon and energy related process?

A

insulin: glycolysis+, glycogenesis+, glycogenolysis-, gluconeogenesis-
glucagon: glycolysis-, glycogenesis-, glycogenolysis+, gluconeogenesis+

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19
Q

why insulin, glucagon have such a relationship with those energy related process?

A

insulin is produced when body met a high blood sugar level, so to decrease blood level and reserve energy
glucagon is produced when a low blood sugar level, to use any means to raise blood sugar level, verse vasa with insulin

20
Q

what is GLUT?

A

glucose transporter

21
Q

how is GLUT-4 translocation stimulated?

A

insulin and exercise

22
Q

How Does IR(insulin residence) develop?

A

hyperglycemia
physical inactive
genetic factors
Oxidative Stress
Dyslipidemia
Adipocytokine induced IR
Inflammation

23
Q

what is IR?

A

Insulin-dependent cells fail to respond properly to normal circulatory concentrations of insulin—-Higher levels of insulin required for normal response

24
Q

where would IR effect human body?

A

skeletal muscle, adipocytes and liver tissue

25
Q

which part of human body has most GLUT-4

A

Muscle & adipocytes account for ~ 60-70% of insulin-stimulated glucose uptake via GLUT4 receptors

26
Q

How would IR effect skeletal muscle

A

IR impairs损害 glycogen synthesis & protein catabolism in skeletal muscle

27
Q

How would IR effect adipocytes?

A

IR impairs lipoprotein lipase LPL activity in adipocytes leading to increase in FFA and inflammatory cytokines

28
Q

how would IR effect liver

A
  1. IR impairs glucose output & fatty acid metabolism
  2. Increasing VLDL & triglycerides
29
Q

liver insulin-stimulated glucose uptake?

A

Liver accounts for ~ 30% of insulin-stimulated glucose uptake

30
Q

which glucose transporter is insulin dependent?

A

GLUT-4

31
Q

how does oxidative stress lead to IR?

A

↓ insulin signal transduction
↑adipokine dys`regulation
IR degradation
Excess free radicals suppress GLUT4 localization by impairing insulin signaling cascade and reducing GLUT4 expression

32
Q

what would cause oxidative stress?

A

Overnutrition increases cellular load of glucose & FFAs

33
Q

why oxidative stress will cause insulin resistance

A

Peripheral & adipose tissue protect themselves from damaging effects of oxidative stress by producing insulin resistance to prevent penetration of glucose & FFA into cells

34
Q

Peripheral fat vs Visceral fat

A

Visceral fat: fat besides organs
Peripheral fat : under skin subcutaneous fat)

35
Q

what is CEPT

A

cholesterol ester transfer protein

36
Q

what are the Most important adipose-derived
mediators

A

FFAs(free fatty acids) & adipokines

37
Q

how is insulin resistance induced by adipocytokine?

A
38
Q

what are adipokines?

A

Adipokines are a family of polypeptides synthesized by adipocytes that include over 100 different molecules: leptin and adiponectin are the most commonly ones.

39
Q

what are the pro-inflammatory mediators

A

leptin, TNF-α, IL-6 & apelin

40
Q

what could leptin do?

A

a hormone produced by fat cells. It plays a role in regulating appetite and metabolism. However, it can also have pro-inflammatory effects.

40
Q

what would TNF-a(Tumor Necrosis Factor-a) do? (FYI)

A

TNF-α is a cytokine involved in systemic inflammation. It is produced by various cells of the immune system and plays a role in the body’s response to infection and inflammation.

40
Q

what would IL-6 do?(FYI)

A

IL-6 is another cytokine that has pro-inflammatory properties. It is produced by various cells, including immune cells, and is involved in the regulation of the immune response.

41
Q

what would apelin do?

A
42
Q

Adipokines responsible for local inflammation in adipocytes but may also induce system inflammation after entering circulation
yes or no

A

yes

43
Q

Adiponectin vs Adipokines

A

adiponectin 脂联素
adipokine(adipocytokine)脂肪因子

44
Q

what would adiponectin do?

A

Adiponectin may ameliorate negative effects
* Positively associated with insulin sensitivity
* Downregulated in obesity(在肥胖的情况下,脂联素的水平往往会降低。)

45
Q

GIP and GLP-1

A

促进胰岛素,但机制不同