lecture 3 lipid metabolism Flashcards
Adipose tissue as an _____ and _____ organ
endocrine and secretory
There were two things that Dr. Williams underlined that adipocytes contribute to
Leptin, adiponectin, Resisting
-molecules regulating energy homeostasis
Molecules regulating innate immune system
-TNF a and IL-6
Fatty acids are taken up by ____, where they may serve as precursors in the synthesis
cells
after fatty acids are taken up by the cell, what are the different paths it can go
synthesis fatty acids for storage or export
mitochondria for energy or ketone bodies (export energy)
What is the major form of energy storage?
fat
what is the distribution fuel reserves in a typical individual
Fat: 100,000 kcal
Protein: 25,000 kcal
carbohydrate: 650 kcal
What are the intermediated if fatty acid metabolism
phospholipid (in membranes)
Eicosanoids, including prostaglandins and leukotrienes which play a role in physiological regulation
What are the diseases for fatty acid metabolism?
Diabetes mellitus
specific disorders of fatty acids oxidation like SIDS, Reye syndrome which might be related to a deficiency of medium chain acyl CoA, dehydrogenase, an important enzyme of fatty acid oxidation
For SIDS AND Reye syndrome, what might that be related to
related to a deficiency of medium chain acyl CoA, dehydrogenase, an important enzyme of fatty acid oxidation
What are two precursors of acetyl coA?
amino acids and glucose
Acetyl coA makes what?
Fatty acids
triglycerides
phospholipid
eicosanoids
CO2, H2O,ATP
Cholesterol–> steroid hormones
Ketone bodies
What is the structure of acetyl coA
1.Acetyl group
2.Coenzyme A
-Beta-mercaptoethylamine
-Pantothenic acid (not synthesized in man – an essential nutrient)
-Phosphate
-3’, 5’-adenosine diphosphate
What is the structure of fatty acid
A long hydrocarbon chain
A carboxylic acid group
What is the chain length and structure of fatty acids
Ranges from 4 to 30 carbons
Most common: 12-24 carbons
LINEAR
EVEN NUMBER OF CARBONS
What is one system of fatty acid classification
based on the number of double bonds
How many db are in saturated fatty acids
ZERO
What is an example of saturated fatty acid
Stearic acid
How many bonds are in monounsaturated fatty acids
ONE
what is an example of monounsaturated fatty acid
oleic acid
What does db in fatty acids cause and what is the result
db cause steric hinderance which affects the melting point
More dbs = lower melting point
The db in natural unsaturated fatty acids are in ____ configuration
CIS
Fatty acids with ____ double bond are the most prevalent in the human body
one
in saturated fatty acids, why is the melting point higher?
Hydrophobic interaction with packed tightly
Solid
More double bonds=
lower melting point
LISTEN TO LECTURE TO ADD QUESTION
What are the five common fatty acids that we need to remember
palmitic acid
stearic acid
oleic acid
linoleic acid
linolenic acid
For the five common fatty acids, list them with their carboxyl reference
palmitic acid—> 16:0
stearic acid—>18:0
oleic acid —> 18:1▵ 9
linoleic acid–> 18:2 ▵9, 12
linolenic acid–> 18:3 ▵9,12,15
The first carbon numbers in the fatty acid is what?
The carboxyl carbon will always be one
What is the carbon next to the the carboxyl carbon
alpha, then it goes to beta, gamma
What is ALWAYS the last carbon, regardless of how many carbons we have
omega, ⍵
Instead of starting with the carboxyl carbon for greek letters, what is the other way?
omega (⍵) subtracted by the number of carbons until we hit the db
Example: ⍵-3–> the db is 3 carbons from the end
Where does fatty acid synthesis occurs primarily in ?
CYTOPLASM of these tissues:
-liver
-adipose (fat)
-central nervous system
-lactating mammary gland
What are the major lipogenic tissues?
liver
adipose
CNS
lactating mammary gland
What is the starting molecule of the de novo synthesis of fatty acids
glucose to pyruvate to then make acetyl coA
What is the fatty acid created with the De Novo synthesis
palmitate (16:0)
What is the process of glucose
Glucose is degraded to pyruvate by aerobic glycolysis in the cytoplasm.
Pyruvate is transported into mitochondria, where pyruvate dehydrogenase oxidatively decarboxylates pyruvate, forming acetyl CoA which can serve as a substrate for citrate synthesis.
Citrate transported out of the mitochondria to the cytoplasm (where fatty acid synthesis occurs), and split to generate acetyl CoA for fatty acid synthesis.
what is another pathway that citrate can take besides fatty acid synthesis?
Citrate can be oxidized by TCA cycle in mitochondria to get energy
What is the next step with acetyl CoA in fatty acid synthesis
Acetyl CoA + bicarbonate+ ATP with acetyl CoA carboxylase (biotin) to create malonyl CoA
What is the RLS for de novo synthesis in fatty acid synthesis?
acetyl CoA carboxylase (biotin)
What are the short term ways of regulating acetyl coA carboxylase?
Phosphorylation (inactive)
-mediated by AMP-dependent protein
-kinase and protein kinase A
Dephosphorylation (active)
-mediated by phosphoprotein phosphatase
Allosteric regulation
-citrate is a positive effector
-long chain fatty acids are negative effectors
Increase insulin, decrease glycogen activates what
Phosphoprotein phosphatase
decrease insulin, increase glycogen activates what
protein kinase A
How do we long term regulate fatty acid synthesis in liver
Carbohydrate-responsive element binding protein (chREBP)
What is Carbohydrate-responsive element binding protein (chREBP)
is a major glucose responsive transcription factor
When is the expression of chREBP gene is induced in the liver?
in response to increased glucose uptake
ChREBP acts _____ with ____
ChREBP acts synergistically with Sterol Response Element Binding Protein (SREBP)
What happens when ChREBP acts synergistically with Sterol Response Element Binding Protein (SREBP)
to induce lipogenic genes such as acetyl CoA carboxylase and fatty acid synthase.
What happens to ChREBP under low (basal) glucose concentration?
ChREBP is phosphorylated and resides in the cytosol.
What happens to ChREBP when glucose concentration raise?
dephosphorylated and translocated to the nucleus where it binds to Carbohydrate Response Elements (ChoREs) to stimulate transcription of lipogenic genes
Where does the dephosphorylated ChREBP translocate and cause?
translocated to the nucleus where it binds to Carbohydrate Response Elements (ChoREs)
stimulate transcription of lipogenic genes
Besides ChREBP what also translocated to the nucleus
insulin, increases pSREBP-1c to bind to SRE for the stimulation of transcription of lipogenic genes
