Lipoprotein Metabolism (end of cholesterol) Flashcards
(56 cards)
What cholesterol importer is located on enterocytes in the ileum and to a lesser extent in the colon and kidney?
ASBT
What cholesterol exporter is located on enterocytes in the ileum and to a lesser extent in the colon and kidney?
OST-alpha/beta
What is phase I bile composition?
-Bile is a micellular liquid
Composition:
- Bile Salts: Moderate amount (40-90%)
- Cholesterol: Low ( 85%)
What is the precursor for all steroid hormones?
Cholesterol
Where are glucocorticoids made (be specific)?
- Adrenal Cortex (zona fasciculata and zona reticularis)
* Cortisol = glucocorticoid
Where are mineralcorticoids made (be specific)?
- Adrenal Cortex (zona glomerulosa)
* Aldosterone = mineralcorticoid
Where are sex hormones made (be specific)?
- Made in testis and ovary
* Androgens and estrogens = sex hormones
When is cortisol released?
- regulation
- effects
- Released in response to stress
- MOST POTENT glucocorticoid
effects:
- Gluconeogenesis, and glycogen synthesis stimulated
- Protein Catabolism
- ANTI-inflammatory
- Inhibits leukocyte migration
- Na+ retention (swelling)
What result does cortisol have on an infection?
Infection may persist because it prevents leukocyte migration
What disease state might result from cortisol stimulating gluconeogenesis and glycogen synthesis?
Diabetes
Estradiol
- Where is it produced?
- What does it do?
- Produced in ovarian granulosa cells
- Has an affect on bone turnover
- This is why post menopausal women are more susceptable to osteoporosis
What is the precursor for estrodiol?
Testosterone
What disease results from a 21-hydroxylase deficiency?
Congenital Adrenal Hyperplasia
What causes the ambiguous genitalia in patients with Congenital Adrenal Hyperplasia?
21-hydroxylase Deficiency leads to build up of 17-hydroxyprogesterone that is converted to testosterone
- This masculinizes female infants
Why is microgenitalia not the biggest issue for patients with Congenital Adrenal Hyperplasia?
- Along with not being able to make estrodiol they also don’t make CORTISOL and ALDOSTERONE
- No aldosterone means you pee all your Na+ (and thus H2O) out and get dehydrated
What needs to happen for Vitamin D to get activated?
- name of activated species
1 C-25 hydroxylation in the liver
2 Hydroxylations
Final METABOLICALLY ACTIVE product = 1,25-dihydroxycholecalciferol
What the sources of Vitamin D?
- biggest contributor
MAJORITY made by Malpighian layer of the epidermis by SUNlight
Small amounts also come from the diet
What does the active form of Vit D. (1,25-dihydroxycholecaliferol) do?
(3 things)
- Stimulates expression of genes involved in intestinal absorption of calcium
- Recruits stem cells to make osteoclasts that mobilize Calcium form bone
- MAJOR EFFECT is to get correct Ca2+ and phosphate balance
Where is Vitamin D synthesis most highly regulated?
- Renal Hydroxylation by 1 alpha-hydroxylation
liver hydroxylation is only loosely regulated
What are the regulators of 1 alpha-hydroxylase in the kidney?
(+) PTH (induced by low Ca2+ in blood)
(+) Hypocalcemia
(+) Hypophosphatemia
(-) Fibroblast Growth Factor 23 from osteocytes
What does vitamin D deficiency lead to in adults and in children?
- causes
Children - Rickets
Adults - Osteomalacia
Causes:
- no sunlight
- Liver or Kidney Disease
- Genetic defects of Vit D receptor
Why would liver or kidney disease cause osteomalacia?
- You can’t complete one of the two hydroxylation steps needed to get to the active form
What is Rachitic Rosary?
- swelling of costochondral junctions resulting from rickets
What is the cause of biliary rickets?
- Lack of bile production
- Vit D. is fat solubule so it can’t be absorbed without bile
- Lack of vitamin D = bad
