Term
| when fatty acid synthesis is maximal |
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Definition
| when carbohydrates and energy are plentiful and when fatty acids are scarce |
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|
Term
| enzymes that play essential roles in fatty acid synthesis and degradation |
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Definition
| acetyl CoA carboxylase 1 and 2 |
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Term
|
Definition
| catalyzes the production of malonyl CoA (the active 2 C donor), which is the committed step in fatty acid synthesis |
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|
Term
| how acetyl CoA carboxylase 1 is activated |
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Definition
|
|
Term
| how acetyl CoA carboxylase 1 is deactivated |
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Definition
|
|
Term
| when fats are not synthesized |
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Definition
|
|
Term
| depiction of how acetyl CoA carboxylase 1 is regulated |
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Definition
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|
Term
| when the level of citrate is high |
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Definition
| when both acetyl CoA and ATP are abundant, signifying that raw materials for fatty acid synthesis are available |
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Term
|
Definition
| facilitates the citrate induced polymerization of inactive dimers into active filaments |
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|
Term
| function of palmitoyl CoA |
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Definition
-counteracts the stimulatory effect of citrate on the carboxylase -causes the filaments to disassemble into inactive subunits -inhibits some other enzymes |
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|
Term
| when palmitoyl CoA is abundant |
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Definition
| when there is an excess of fatty acids |
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|
Term
| depiction of the citrate-induced polymerization of inactive dimers into active filaments |
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Definition
|
|
Term
| when malonyl CoA is abundant |
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Definition
| when fuel molecules are abundant |
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Term
| the role of mitochondrial malonyl CoA in the regulation of fatty acid synthesis |
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Definition
| it inhibits carnitine acetyltransferase I, preventing the entry of fatty acyl CoA's into the mitochondrial matrix in times of plenty |
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|
Term
| depiction of the dependence of the catalytic activity of acetyl CoA carboxylase on the concentration of citrate |
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Definition
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|
Term
| some things that can regulate fatty acid synthesis and degradation |
|
Definition
-glucagon -epinephrine -insulin -diet |
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|
Term
| when glucagon and epinephrine are present |
|
Definition
| under conditions of fasting and exercise |
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|
Term
| stimulatory effect of glucagon and epinephrine on fatty acids |
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Definition
| they stimulate the mobilization of fatty acids from triacylglycerols in fat cells such that they can be used as fuel |
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Term
| inhibitory effect of glucagon and epinephrine on fatty acids |
|
Definition
| inhibit fatty acid synthesis |
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|
Term
| how glucagon and epinephrine inhibit fatty acid synthesis |
|
Definition
by inhibiting acetyl CoA carboxylase 1
this augments the inhibition by the AMP-activated kinase |
|
|
Term
| how glucagon and epinephrine regulate acetyl CoA carboxylase 1 |
|
Definition
| they switch off fattyb acid synthesis by keeping the carboxylase in the inactive phosphorylated state |
|
|
Term
| effect of insulin on fatty acids |
|
Definition
| inhibits the mobilization of fatty acids and stimulates their accumulation as triacylglycerols by muscle and adipose tissue |
|
|
Term
| effect of insulin on fatty acid synthesis |
|
Definition
|
|
Term
| how insulin stimulates fatty acid synthesis |
|
Definition
| by activating acetyl CoA carboxylase 1 |
|
|
Term
| how insulin activates acetyl CoA carboxylase 1 |
|
Definition
| by enhancing the phosphorylation of AMPK by Akt, which inhibits AMPK, as well as by stimulating the activity of a protein phosphatase that dephosphorylates and activates acetyl CoA carboxylase |
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|
Term
| the 2 steps of ethanol metabolism |
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Definition
1: conversion of ethanol to acetaldehyde; this happens in the cytoplasm 2: conversion of acetaldehyde to acetate; this happens in the mitochondria |
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|
Term
|
Definition
| catalyzes the conversion of ethanol to acetaldehyde |
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|
Term
| depiction of the function of alcohol dehydrogenase |
|
Definition
|
|
Term
|
Definition
| catalyzes the conversion of acetaldehyde to acetate |
|
|
Term
| depiction of the function of aldehyde dehydrogenase |
|
Definition
|
|
Term
| ethanol consumption leads to accumulation of... |
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Definition
|
|
Term
| effect of NADH accumulation |
|
Definition
| inhibits gluconeogenesis by preventing the oxidation of lactate to pyruvate |
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|
Term
| how NADH accumulation inhibits gluconeogenesis |
|
Definition
| by preventing the oxidation of lactate to pyruvate |
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|
Term
| NADH accumulation will cause this to accumulate |
|
Definition
|
|
Term
| these could happen as a result of lactate accumulation |
|
Definition
-hypoglycemia -lactic acidosis |
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|
Term
| how too moch NADH affects fatty acid metabolism |
|
Definition
| inhibits fatty acid oxidation |
|
|
Term
| the metabolic purpose of fatty acid oxidation |
|
Definition
| to generate NADH for ATP generation by oxidative phosphorylation |
|
|
Term
| why alcohol consumption leads to fatty liver |
|
Definition
| because the excess NADH from alcohol consumption is a signal to synthesize tiaclyglycerols |
|
|
Term
| liver mitochondria can convert acetate into... |
|
Definition
| acetyl CoA in a rxn requiring ATP |
|
|
Term
| function of acyl CoA synthetase in the context of alcohol metabolism |
|
Definition
| converts acetate into acetyl CoA |
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|
Term
| depiction of the function of acyl CoA synthetase in the context of alcohol metabolism |
|
Definition
|
|
Term
| why alcohol consumption leads to the accumulation of acetyl CoA |
|
Definition
| because further processing of the acetyl CoA by the citric acid cycle is blocked because of NADH inhibiting 2 important citric acid cycle regulating enzymes |
|
|
Term
| some consequences of acetyl CoA accumulation |
|
Definition
1: ketone bodies form and get released into the blood, exacerbating the acidic condition already created by high lactate concentration 2: processing of acetate in liver becomes inefficient, leading to buildup of acetaldehyde, which impairs proteins by forming covalent bonds with them |
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|
Term
| effect of ketone body accumulation in bloodstream |
|
Definition
| they exacerbate the acidic condition already created by high lactate concentration |
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|
Term
| how acetaldehyde messes with proteins |
|
Definition
| by forming covalent bonds with them |
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|