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

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
cause and effects of Type IIa hlp: familial hypercholesterolemia
LDL receptor completely defective E: cholesterol ^ TG: normal LDL: ^
26
cause and effects of Type IIb hlp: familial hypercholesterolemia
``` LDL receptor partially defective E: cholesterol ^ TG: ^ LDL: ^ VLDL: ^ ```
27
Type I hlp: familial hyperchylomicronemia | issue, ages, blood sample, inheritence, clinical symptoms, treatment
- 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
Type II hlp: familial hypercholesterolemia (FH) | issue, inheritance, cholesterol levels for hetero/homo and their outcomes and treatments, physical symptoms
- 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
beneficial effects of HDL, whats its job? levels increased by which activities and drugs? HDL levels low in??
- 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
statins mechanism of action
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
use of statins also effects
production of heme a, dolichol, ubiquinone, prenylated proteins; bisphosphonates (to treat osteoporosis) also working upstream of these