Ch 12 - Bioenergetics, Metabolic Regulation Flashcards
1
Q
Gibbs free energy equation
A
deltaG = deltaH - T*deltaS
- negative deltaG is spontaneous
- deltaG = deltaGo + RT ln(Q)
2
Q
Energy derived from fat and carbs
A
- protein = 4 kcal/g
- carbs = 4 kcal/g
- ketones = 4 kcal/g
- fat = 9 kcal/g
3
Q
ATP
A
- adenosine triphospahte
- formed via substrate level phosphorylation or oxidative phosphorylation
- provides about 30 kJ/mol
- used due to high energy phosphate bonds
- ADP is stable by resonance
- ATP is less stable
- hydrolysis to AMP is also spontaneous
4
Q
ATP coupled reactions
A
- ATP cleavage and transfer phosphate group to another molecule
- activate or inactive other molecule
- phosphoryl group transfers
- coupled with unfavorable reaction
5
Q
high energy electron carriers
A
- NADH
- NADPH
- FADH2
- ubiquinone
- cytochromes
- glutathione
- proteins with iron-sulfur clusters are good electron transporters
6
Q
Flavoproteins
A
- have modified vitamin B2
- aka riboflavin
- nucleic acid derivatives
- FAD - flavin adenine dinucleotide
- FMN - falvin mononucleotide
- in mitochondria and chloroplasts as electron carriers
- coenzymes fro oxidation of fatty acids
7
Q
Postprandial state
A
- absorptive or well fed state
- greater anabolism
- nutrients into gut and hepatic portal to the liver
- lasts 3-5 hrs after eating
- blood glucose rises and stimulate insulin release
- insulin targets liver, muscles, adipose tissue
- promote glycogen synthesis
- excess glucose converted to fatty acid and triglycerols
8
Q
Insensitivity to Glucose (special cells)
A
- nerve cells - oxidize glucose to CO2, insentitive to insulin
- RBC - use glucose anaerobically
- insensitive to insulin
9
Q
Fasting State
A
- postabsorptive state
- counterregulatory hormones - oppose insulin
- glucagon, cortisol, epi, norepi, GH
- stimulate glucogenolysis in liver
- stimulate hepatic gluconeogenesis
- slower than glucogenolysis
- release amino acids from skeletal muscle
- release fatty acids from adipose tissue
- Amino acids and fatty acids carried to liver for gluconeogenesis
10
Q
Starvation
A
- prolonged fasting
- high glucagon and epi
- rapid degradation of glycogen in liver
- gluconeogenesis maintains glucose levels
- excess acetyl-CoA from lipolysis is used for ketone bodies
- Muscles use fatty acids
- Brain uses ketones
- RBC still use glucose
11
Q
Insulin
A
- peptide hormone
- made by Beta cells in pancreatic islets of Langerhans
- required by adipose and skeletal muscle to uptake sugar (glucose transporters)
- increases metabolism of carbs
- increase glycogen synthesis in liver
- increase amino acid uptake by muscles
- increase triclygerol uptake by fat cells
- directly controlled by plasma glucose level
- glucose enters beta cell, metabolized, increase intracellular ATP, Ca2+ release, exocytosis
12
Q
Insulin resistant cells
A
- nervous tissue
- kidney tubules
- intestinal mucosa
- RBC
- beta cells of pancreas
13
Q
Glucagon
A
- peptide hormone
- alpha-cells of pancreatic islets of Langerhans
- targets hepatocytes via second messenger
- increase liver glycogenolysis
- increase liver gluconeogenesis
- increase liver ketogenesis
- increase lipolysis in the liver
- promoted by low plasma glucose
- basic amino acids promote secretion
14
Q
Glucocorticoids
A
- from adrenal cortex
- Cortisol - secreted during stress
- promotes use of energy stores
- elevates blood glucose
- inhibit glucose uptake in most tissues - to increase availability in brain
- Increase hepatic output and gluconeogenesis
- enhance glucagon, epi, catecholamines
- long term causes hyperglycemia
- stimulate insulin
- promote fat storage
15
Q
Catecholamines
A
- secreted by adrenal medulla
- epi and norepi
- increase liver and muscle glycogen phosphorylase - glycogenolysis
- increase glucose output from liver
- increase glycogenolysis in skeletal muscle
- lacks enzymes, therefore does not reach bloodstream and is metabolized by muscle cells
- increase lipolysis via increase lipase
- increase BMR