Term
| What is the affect of high concentrations of Niacin on cholesterol levels? |
|
Definition
| Raises HDL and lowers LDL |
|
|
Term
| Where are Ketone bodies in synthethized? |
|
Definition
|
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Term
| What tissue types can consume ketone bodies? |
|
Definition
| Virtually any tissue can consume ketone bodies except for the liver |
|
|
Term
| What fuel source are Ketone bodies made from? |
|
Definition
|
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Term
| Why does beta oxidation not work very well in the absence of carbohydrates? |
|
Definition
| Oxaloacetate is removed for gluconeogenesis and is not as available for krebs cycle |
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Term
| Ketone body synthesis mirrors what other lipid metabolic pathway? |
|
Definition
| Cholesterol synthesis, HMG CoA though is instead catabolized by HMG CoA Lysase (instead of reductase) to form Acetoacetate |
|
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Term
| What are the by products of Ketone body synthesis? |
|
Definition
| Acetone (volatile) and Beta hydroxybutryate |
|
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Term
| How do Ketone Bodies work with the Krebs cycle to create ATP? |
|
Definition
| Ketone bodies are broken back down to Acetoacetate (via hydroxybutyrate dehydrogenase). Aceto acetate is then used in combination with a Krebs cycle step (succinyl-coA -> Succinate) to create Acetoacetyl-CoA via Succinyl-CoA acetoacetate transferase. This results in the production of 2 Acetyl-CoA |
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Term
| Diabeties has what affect on adipose tissue breakdown? |
|
Definition
| upregulates the breakdown of triglycerides into fatty acids (HSL is not inhibited) |
|
|
Term
| Diabetic patients have what effect on Beta oxidation? |
|
Definition
| upregulate beta oxidation by no longer inhibiting the carnitine pump (since glycolysis is not occuring). |
|
|
Term
| Diabetic patients have what effect on Beta oxidation? |
|
Definition
| upregulate beta oxidation by no longer inhibiting the carnitine pump (since glycolysis is not occuring). |
|
|
Term
| Why do diabetics have upregulated Ketone body formation? |
|
Definition
| Diabetes upregulates the breakdown of adipose triglycerides and hinders the ability of a cell downregulate Beta oxidation (Carnitine pump). Furthermore intermediates of the krebs cycle are being drawn off for Gluconeogenesis (Due again to the cells inability to uptake blood glucose). The result is a big buildup of Acetyl-CoA that favors synthesis of Ketone bodies |
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Term
| What is the function of Phospholipase A1, A2, C, D? |
|
Definition
A1: cleaves phospholipid at alpha 1 carbon
A2: cleaves phospholipid at Alpha 2 carbon
Phospholipase C: cleave a phospholipid and make an alcohol
Phospholipase D: cleave a phospholipid to regenerate a phospholipid and a sugar
all are used to make signal molecules |
|
|
Term
| What major signalling molecule is created by Phospholipase C? |
|
Definition
|
|
Term
| What major products are created by Phospholipase A2? |
|
Definition
| Arachodonic acid and Platelet-activating factor (immune response) |
|
|
Term
| What is DPCC important for? |
|
Definition
| major component of Surfactant |
|
|
Term
| From what lipids are Glycolipids synthethized? |
|
Definition
|
|
Term
| What enzyme is used to create Glycosphingolipids (ceramide)? |
|
Definition
|
|
Term
| Where are glycolipids found in relation to the membrane? |
|
Definition
|
|
Term
| Why are Glycosphingolipids important? |
|
Definition
Embryogenesis and differentiation of cells
Cell mediated immunity
Cell adhesion
Surface receptors for cholera and tetanus toxins
signalling |
|
|
Term
| Dsyfunction of Beta galactosidase gives rise to which disease? |
|
Definition
| Generalized gangliosidosis |
|
|
Term
| Dysfunction of the enzyme hexoaminidase-A results in which disease? |
|
Definition
|
|
Term
| Dysfunction in glucocerebrosidase results in which disease? |
|
Definition
|
|
Term
| Dysfunction in alpha galacto sidase A results in which disease? |
|
Definition
|
|
Term
| Dysfunction in hexoaminidase A and B results in which disease? |
|
Definition
|
|
Term
| Failure of the enzyme Sphingomyelinase results in which disease? |
|
Definition
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