triglycerides Flashcards

1
Q

sources of TG

A

dietary TG (processed in intestinal cells)
de novo TG (in liver hepatocytes)
de novo TG (in adipocytes)

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2
Q

lipases involved in breakdown of TGs in adipocyte

A

hormone sensitive lipase (HSL)
lipoprotein lipase
monoacylglycerol lipase

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3
Q

promote lipolysis in adipocytes by acting on hormone sensitive lipase (HSL)

A

glucagon (secreted in response to hunger)

epinephrine (secreted in response to exercise)

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4
Q

inhibit lipolysis in adipocytes by acting on hormone sensitive lipase (HSL)

A

insulin (secreted in response to high carb meal)

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5
Q

perilipins are..? Fx? how many types?

A

family of proteins coating lipid droplets in adipocytes and muscle cells

  • regulate lipolysis by controlling physical acces to HSL
  • humans have 5 members in the family
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6
Q

perilipin 1

A
  • overexpression inhibits lipolysis
  • knockout PROMOTES lipolysis
  • regulated by PKA (phosphorylation allows assoication with HSL and promotes lipolysis)
  • target of obesity treatment
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7
Q

what is olestra?

A
  • synthetic fat made of sucrose backbone with 6-8 FA
  • NOT absorbed in small intestine
  • no calories
  • excreted out in stool
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8
Q

issue with olestra

A

absorbs vitamins A, D, E, K

  • high amounts causes deficiency in these vitamins
  • abdominal cramps, bloating, diarrhea
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9
Q

serve as transport vehicle for cholesterol, TGs, fat soluble vitamins

A

lipoproteins

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10
Q

structure of lipoproteins

A

outer shell: monolayer of phospholipids, free cholesterol and apolipoprotiens (ALP)
inner core: packed with hydrophobic TGs, cholesterol esters

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11
Q

converts free cholesterol into extremely hydrophobic cholesterol esters stored in lipid droplets

A

Acyl CoA Acyl Transferase (ACAT)

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12
Q

different types of lipoproteins

A
chylomicrons
VLDL
LDL "bad cholesterol"
IDL
HDL "good choelsterol"
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13
Q

chylomicron properties

A
largest
least dense
high TG content
exogenous
formed from dietary fats
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14
Q

HDL properties

A

smallest
most dense
high protein and phospholipid content
“good cholesterol” particle

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15
Q

ALPs on chylomicron

A

ApoB-48
ApoE
ApoC-II

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16
Q

ALPs on VLDL

A

ApoB-100
ApoC-II
ApoE

17
Q

ALPs on IDL

A

ApoB-100

ApoE

18
Q

ALPs on LDL

A

ApoB-100

19
Q

ALP acting as co-factor to activate capillary lipase

A

ApoC-II

only present on VLDL, HDL and chylomicrons

20
Q

LDL has a high content of

A

cholesterol esters

21
Q

ALPs on HDL

A

ApoA-1
ApoE
ApoC-II

22
Q

swelling of lymph nodes found in

A

infections

cancer (non-Hodgkin lymphoma)

23
Q

Apoplipoprotein funcitons

A
  • structural (stabilize lipoproteins)
  • transport (redistribution of lipids between tissues)
  • cofactors for enzymes (e.g. activation of LPL by Apo-CII)
24
Q

cause and effects of Type I hlp: familial hyperchylomicronemia

A

C: deficiency in apoC-II (cofactor for LPL) or defective lipoprotein lipase
E: chylomicrons ^ and triacylglycerol ^

25
Q

cause and effects of Type IIa hlp: familial hypercholesterolemia

A

LDL receptor completely defective
E: cholesterol ^
TG: normal
LDL: ^

26
Q

cause and effects of Type IIb hlp: familial hypercholesterolemia

A
LDL receptor partially defective
E: cholesterol ^
TG: ^
LDL: ^
VLDL: ^
27
Q

Type I hlp: familial hyperchylomicronemia

issue, ages, blood sample, inheritence, clinical symptoms, treatment

A
  • inability to hydrolyze TAGs in chylomicrons and VLDL
    primary LPL def. - infancy
    ApoC-II def. - post adolescence
    plasma TAG levels > 1000 mg/dL
    creamy appearance of blood sample; overnight at 4 C separates into creamy and clear layer
  • both autosomal recessive
    s/s - abdominal pain, acute pancreatitis, cutaneous eruptive xanthomas (fat accumulating on skin)
    treatment: low fat diet
28
Q

Type II hlp: familial hypercholesterolemia (FH)

issue, inheritance, cholesterol levels for hetero/homo and their outcomes and treatments, physical symptoms

A
  • increased cholesterol in blood and subsequent atherosclerosis
  • impaired ability to recognize ApoB 100 on LDL
  • autosomal dominant inheritance
  • normal cholesterol 130-200 mg/DL [heterozygous; 300-500 mg/dL, homozygous >800 mg/dL]
  • untreated homozygous die of coronary artery disease (CAD) before teenage years; heterozygous develop CAD by 40
    physical symptoms: xanthomas, arcus senilis or corneal deposits in eye, angina pectoris
    heterozygous respond to diet, statins and bile acid binding resins
    homozygous need LDL apheresis and liver transplantation
29
Q

beneficial effects of HDL, whats its job? levels increased by which activities and drugs? HDL levels low in??

A
  • antioxidant and antiinflammatory properties
  • reverses cholesterol transport from peripheral tissues to liver
  • HDL levels increased by weight loss, exercise, smoking cessation and moderate consumption of alcohol
  • antihyperchoelsteremic drugs, fibrates, niacin, antidiabetic thiazolidine drugs, estrogens, omega-3 fatty acids, increase HDL-C
  • HDL levels low in smoking, progestins, androgens, beta blockers and high intake of PUFA (omega-6)
30
Q

statins mechanism of action

A

mimic the structure of HMG CoA and Mevalonate (substrate and product of HMG CoA reductase)

  • rate limiting enzyme in cholesterol biosynthesis
  • potent competitive inhibitors ==> cholesterol levels fall
  • enhances transcription of LDL receptor ==> more uptake into hepatocytes, lowers plasma levels
31
Q

use of statins also effects

A

production of heme a, dolichol, ubiquinone, prenylated proteins;
bisphosphonates (to treat osteoporosis) also working upstream of these