Section IV Part 2 (Chapters 24-28) Flashcards
What is the mechanism by which re-oxidation of NADH + FADH2 via the ETC results in ATP synthesis?
ETC oxidizes NADH and FADH2 and donates e- to O2 while pumping protons across the inner mitochondrial membrane, the energy (electrochemical gradient) from the reduction of O2 to H2O is used to power ATP synthase/ F0F1-ATPase, which phosphorylates ADP to ATP
What phosphorylates ADP to ATP?
ATP synthase/ F0F1-ATPase
Where does ox phos occur?
Inner membrane of mitochondria
Components here: ATP synthase & ETC
Why does ox phos occur on the inner membrane of mitochondria?
To maintain a chemical gradient
How do electrons flow in ETC?
Electrons flow from NADH to NADH:CoQ oxidoreductase/complex I to coQ to cytochrome b-c1 complex (III) to cytochrome c to cytochrome c oxidase (IV)
How does oxidative phosphorylation occur?
Occurs from the reduction of O2 and generation of a chemical gradient that powers an ATP synthase to generate ATP
How does substrate-level phosphorylation occur?
Utilizes the release of high-energy bonds to phosphorylate an ADP molecule, accomplished without O2
What is the importance of iron, copper, and oxygen in the ETC?
The oxidation-reduction components of ETC = Complex I-IV, flavin mononucleotide (FMN) , Fe-S centers, CoQ, Fe in cytochrome b/c1/c/a/a3 and Cu in cytochrome a/a3
FMN accepts 2 e- from NADH and pass them to Fe-S centers that pass to CoQ
Fe atoms in cytochromes change from oxidated state (Fe3+) to reduced state (Fe2+)
Cu+ ions in cytochrome oxidase facilitate the collection of e- and reduction of O2
Proton motive force in ox phos: importance & generation
The movement of H+ across the impermeable membrane via action of the ETC ( chain of oxidation-reduction rxns with final e- acceptor = O2) creates an electrochemical gradient = proton motive force = potential energy of H+ reentering the matrix via ATP synthase = oxidative phosphorylation
What is 30% of energy from NADH/FADH2 oxidation by O2 used for?
ATP synthesis
What is 70% of energy from NADH/FADH2 oxidation by O2 used for?
Transport anion and Ca2+ into mitochondria
Released as HEAT
Glycerol 3-phosphate shuttle
In the cytosol, NADH is reoxidized to NAD+ by transferring e- to DHAP to make glycerol 3-P, which can be shuttled through the mitochondrial membranes via Glycerol 3-P shuttle; e- is donated to FAD and (eventually) donated to coQ
Malate-aspartate shuttle
NADH can transfer e- to cytosolic oxaloacetate to form malate which is transported via Malate-aspartate shuttle into matrix and malate is oxidized back to oxaloacetate to generate NADH; OA can convert to aspartate to pass back into cytosol
What hampers ETC & ATP production?
Deficiencies in iron, riboflavin, or niacin
What are iron, riboflavin, or niacin in terms of ETC & ATP production?
Coenzymes
Iron is necessary for…
Fe-S centers and redox reactions
Riboflavin is part of…
FAD, a coenzyme succinate DH, ETF-CoQ oxidoreductase & glycerol 3-phosphate DH
Riboflavin is also a
Electron acceptor that donates to the ETC
Niacin is a part of…
NAD, which is an E-acceptor that donates to ETC
Energy yield for glycolysis (aerobic v anaerobic)
BOTH produce 2 ATP, 2 NADH, and 2 pyruvates from one glucose molecule
Anaerobic glycolysis can … produce 2 ATP, since NADH is recycled to … and pyruvate is reduced to…
Only, NAD+, lactate
Aerobic glycolysis can continue to…
Oxidize pyruvate to acetyl CoA then to TCA
How much ATP can be formed via aerobic glycolysis
30-32 ATP
OXPHOS disease is caused by
Mutations in mitochondrial DNA
What is the mechanism for OXPHOS disease?
MtDNA codes for 13 subunits of the ETC complexes and mt mRNA/rRNA/tRNA; mutated mtDNA will hamper proper oxidative phosphorylation = OXPHOS diseases
What is the mode of inheritance of OXPHOS disease?
Mutated mtDNA comes from maternal inheritance, replicative segregation, threshold expression, high mtDNA mutation rate and accumulation of mutations with age
What does uncoupling mean in respect to ox phos?
H+ leak back into matrix without going through ATP synthase, which dissipates the electrochemical gradient without ATP production
Physiologic uncouplers (UCPs)
Channels in membrane that conduct H+ from intermembrane space to matrix to generate HEAT
Chemical uncouplers (Proton Ionophores)
Hydrophilic compounds that transport intermembrane H+ back into the matrix, reducing the proton gradient, and reducing ATP synthesis
What is an example of the effect of physiologic uncouplers?
Thermogenin in brown fat
What is the mechanism of thermogenesis in brown fat?
Cold causes sympathetic nerves to release NE that activate lipase in brown fat
Brown fat expresses UCP1/thermogenin which can be activated to form channel which conduct H+ across membrane which generates HEAT via nonshivering thermogenesis
ETC inhibitors … the sequential e- flow from NADH/FADH2 to O2
Bind/block
Uncouplers…
Disturb the inner mitochondrial membrane, leading to leakage of H+ and loss of potential energy as heat
Rotenone, amytal inhibits
Transfer of electrons from complex I to coenzyme Q
Antimycin C inhibits
Transfer of electrons from complex III to cytochrome c
Carbon monoxide (CO) inhibits
Transfer of electrons from complex IV to oxygen
Cyanide (CN) inhibits
Transfer of electrons through complex IV to oxygen
Atractyloside inhibits
Inhibits the adenine nucleotide translocase (ANT)
Oligomycin inhibits
Inhibits proton flow through the F0 component of the adenosine triphosphate (ATP) synthase
Dinitrophenol inhibits
An uncoupler; facilitates proton transfer across the inner mitochondrial membrane
Valinomycin inhibits
A potassium ionophore; facilitates potassium ion transfer across the inner mitochondrial membrane
What situations may cause lactic acidosis?
EtOH consumption increases NADH levels = lactic acidosis
Hypoxia/anoxia/ischemia/cyanide/CO increase anaerobic glycolysis = more lactate
Deficient/inhibited TCA cycle enzymes prevent acetyl-CoA oxidation = increase pyruvate = lactate
mtDNA defects decrease ETC activity = more anaerobic glycolysis = more lactate
Lactic acidosis can result from inhibition of lactate use in gluconeogenesis
What is lactic acidosis?
Results from increased NADH/NAD+ ratio in tissue which directs pyruvate to LDH to generate lactate
Why can any functional impairment of ox phos cause lactic acidosis?
Impaired OXPHOS will push ATP production towards the anaerobic route = lactate production for NADH recycling
Inner mitochondrial membrane is
Impermeable to polar molecules
Outer mitochondrial membrane is
Permeable to small polar molecules
How can mitochondrial permeability cause cell death?
Increase Ca2+, phosphate, ROS, hypoxia lead to OPENING of mitochondrial permeability transition pore (MPTP) = large nonspecific pore through inner and outer mt membrane = H+, anions, cation flood in and mt swells and results in NECROSIS
What are examples of inner mitochondrial membrane transport?
Phosphate-malate exchange, citrate-malate exchange, aspartate-glutamate transporter
What allows small polar molecules to get through the outer mitochondrial membrane to get through?
Nonspecific pores = VDACs
Rotenone is a
Insecticide, fish poison
Amytal is a
Barbiturate
Antimycin is a
Bacterial product
Cyanide can be found in
Almond pits, other fruit pits, created by burning plastics
What are the indirect inhibitors of ETC?
Atractyloside: blocks transport of ADP from cytosol into mitochondrial matrix via Adenine Nucleotide Translocase (ANT, Fig. 21.14).
Oligomycin: blocks Fo proton channel; stops ATP formation
What compounds allow for inner mitochondrial membrane permeability?
Aspirin, pentachlorophenol (wood preservative), 2,4- dinitrophenol (DNP, by-product of TNT synthesis – and once used as a diet aid!)
Aspirin, pentachlorophenol, and DNP are what types of molecules?
hydrophobic weak acids!
Thyroid hormone increases…
Basal metabolic rate (BMR)
What does free radical mean?
Molecule with unpaired e-; free radical exists independently
What does reactive oxygen species (ROS)?
O-containing highly reactive free radicals/compounds that readily convert to free radical
What are the reactive oxygen species (ranked from most to least reactive)
Hydroxyl radical (OH●) > superoxide (O2-) > hydrogen peroxide (H2O2)
How is ROS generated in the body?
- O2- is made by CoQ in ETC
- Oxidases, oxygenases and peroxidases
- Cytochrome p450 enzymes “leak” ROS
- OH● : made by O2- + Fe2+/Cu2+, Fenton rxn or Haber-Weiss rxn
What are the Fenton/Haber-Weiss rxns?
What are examples of reactive oxygen species (ROS)?
Superoxide anion, hydrogen peroxide, hydroxyl radical, organic radicals, peroxy radical, hypochlorous acid, singlet oxygen, nitric oxide, peroxynitrite
How can ROS react with cellular components to cause deleterious effects?
ROS can oxidize/extract electrons (hydrogen atoms) from cellular components (damage DNA, peroxidate lipids, digest proteins), promote mutation, injury, cell swelling and necrosis
What is the synthesis & normal function of nitric oxide?
NO synthase convert arginine to gaseous NO, which acts as a NT/hormone (vasodilator) at low levels
What is the toxic effect of nitric oxide
Directly, NO combines with Fe compounds that also have single electrons affecting Fe-S centers in ETC, or Fe-heme proteins in hemoglobin and cytochromes (usually little damage because of low concentration, but more pronounced in OXPHOS diseases)
At high levels, NO combines with O2(-) to form RNOS and cause neurodegeneration (Parkinson dz) and inflammation (RA)
How are ROS & RNOS produced during phagocytosis and inflammation?
During infection, phagocytic cells increase consumption of O2 = respiratory burst:
- NADPH oxidase generate free radicals from O2-,
- SOD makes H2O2; myeloperoxidase use H2O2 to make HOCl (extremely TOXIC to bacteria)
- NO reacts with O2- to form RNOS
- Free radicals destroy invading microorganism/tumors and other targeted cells
What are antioxidant-scavenging enzymes?
SOD (#1 defense) convert O2- to H2O2 + O2
Catalase (peroxisome) reduce H2O2 to H2O
Glutathione peroxidase (cytosol/mt; requires dietary Se & NADPH via PPP) reduce H2O2 to H2O, lipid peroxide to alcohol
What are antioxidants/free-radical scavengers?
Typically donate H & have conjugated DB-system
In terms of dietary antioxidants…
vitE/α-tocopherol inhibit lipid perox-idation;
vitC/ascorbic acid redox/reduce to form vitE,
carotenoid/previtA/B carotene quench singlet O2 (contains empty outer orbital)
flavonoids inhibit oxidases, chelate Fe/Cu, donate e- or complex with free radical
In terms of endogenous antioxidants…
Uric acid/protein thiol & Melatonin: donate H to trap free radicals
Cellular compartmentalization defense system
Contain ROS generation (ex: peroxisomes)
Metal sequestration via…
Proteins in blood or cell
DNA repair mechanism
Remove oxidized fatty acids & degrade oxidized AA/protein
What is the protective efficacy of dietary supplements as antioxidants?
Vitamin E = most potent antioxidant; Carotenoids (zeaxanthin/lutein) decrease incidence of age-related macular degeneration (AMD) & flavonoids do a lot!
What occurs in Parkinson’s disease with ROS & RNOS?
Parkinson dz = degenerate nigrostriatal neurons = DOPA depletion; pt with Parkinson exhibit: increased O2- production & Fe = free radicals, decreased glutathione and mitochondrial dysfunction, increasing oxidative damage and neuronal degeneration
What are patients with Parkinson’s disease treated with?
Monoamine oxidase B inhibitor
This drug inhibits monoamine oxidase (which inactivates dopamine and produces H202) therefore preventing/slowing the degradation of dopamine
What is the proposed role of ROS in ischemia-reperfusion injury?
Reperfusion with O2 works similar to respiratory burst, ischemic tissue now using O2 on overdrive = increase free radical production = tissue injury:
- In the mitochondria/ET, O2- production occurs via CoQ and xanthine oxidase; OH● can damage ETC and mitochondrial lipids;
- Macrophages from blood enter tissue and release NO and O2-, which creates more radicals (RNOS) and exacerbates tissue damage
What are these diseases associated with?
Free-radical injury
What is the structure & function of glycogen in the liver & muscle?
Glycogen = glucose units linked by α-1,4-glycosidic bonds & α-1,6-branches @ every 8-10 residue
Storage form of glucose/energy
What is glycogen metabolism in muscle?
G1P to G6P to Lactate, CO2, ATP via glycolysis
What is glycogen metabolism in the liver?
Glycogen converted to G1P by glycogen phosphorylase G6P in liver is converted by glucose 6-phosphatase (only in liver and kidney) to free glucose that enter blood
What are the steps for the synthesis of glycogen from G6P? Describe the mechanism for adding branches to the glycogen molecule
Phosphorylation of glucose => G6P => G1P => UDP-G => α-1,4-bond to glycogen primer via glycogen synthase; once the chain gets about 11 molecules in length (extra long) cleave section 6-8 residues long by amylo-4,6-transferase/branching enzyme & reattached by an α-1,6-bond (both continue to lengthen and branch)
What regulates the synthesis of glycogen from G6P?
Glycogen synthase
What are the steps in the breakdown of glycogen to G6P?
Glycogen cleaved @ nonreducing end by glycogen phosphorylase releasing G1P, down to last four of a chain (steric hindrance)
How are glycogen branches are removed?
Debrancher enzyme (transferase/α-1,6-glucosidase) removes three glucose residues and adds to longer chain by a-1,4 bond and one glucose residue is then removed, breakdown continues after this
What is Type O disease?
Enzyme: Glycogen synthase/liver
Manifestation: Hypoglycemia, hyperketonemia, fail to thrive, early death
What is Von Gierke disease?
Enzyme: G6-phosphatase/liver
Manifestation: Hepato/Renomegaly, growth failure, hypoglycemia, lipemia, thrombocyte dysfunction
What is Pompe disease?
Enzyme: Lysosomal α-glucosidase/ ALL
Manifestation: Infant = muscle hypotonia, heart failure & death by 2 yrs
Juvi = cardio/myopathy ; Adult = limb-girdle muscular dystrophy
What is McArdle disease?
Enzyme: Muscle glycogen phosphorylase
Manifestation: Exercise-induced myalgia, cramps, progressive weakness & myogloburia
What is Hers disease?
Enzyme: Liver glycogen phosphorylase
Manifestation: Hepatomegaly & mild hypoglycemia
What is Tarui disease?
Enzyme: PFK-1/muscles & RBC
Manifestation: Same as McArdle + enzymopathic hemolysis
What is Fanconi-Bickel syndrome?
Dysfunction: GLUT-2 transporter
Manifestation: Glycogen accumulation in kidneys/liver = rickets, growth restriction, glucosuria
How does glucagon regulate glycogen metabolism?
Glucagon => cAMP => PKA phosphorylates glycogen phosphorylase (a-active) and glycogen synthase (b-inactive) = glycogen degradation
How does insulin regulate glycogen metabolism?
Insulin = principle regulator by reversing/inhibiting glucagon effects; insulin can activate phosphodiesterase that converts cAMP to AMP = inactivate PKA of glucagon
What is glucose mean in insulin regulation?
Glucose is an allosteric inhibitor of glycogen phosphorylase and stimulate dephosphorylation, leading to glycogen phosphorylase b (inactive) and glycogen synthase a (active)
How does epinephrine regulate glycogen regulation?
EPI increase demand for glucose/glycogenolysis by binding to 2 receptors:
- α-agonist-R in hepatocytes = G-protein => PLC => DAG + IP3 => PKC and increase Ca2+-cam => phosphorylase kinase => glycogen phosphorylase a/glycogen synthase b
- β-agonist-R = G-proteins => adenylyl cyclase => cAMP => PKA kinase => glycogen phosphorylase a/glycogen synthase b
What does calcium do in regulation of glycogenolysis in liver?
In liver, EPI => IP3=> Ca2+ release => bind calmodulin & activate phosphorylase kinase => glycogenolysis => supply blood
What does calcium do in the regulation of glycogenolysis in muscles?
In muscles, contraction => AMP from muscle energy usage activates glycogen phosphorylase b (inactive) causing anaerobic glycolysis to occur first (onset of exercise) => Ca2+ released from SR after neural stimulation binds to calmodulin which activates phosphorylase kinase => phosphorylase kinase converts glycogen phosphorylase b to a (active) = glycogenolysis
What does epinephrine stimulation do for glycogenolysis?
Epinephrine stimulation in skeletal is similar to liver, activates phosphorylase kinase more, increasing glycogenolysis
What does not impact glycogen in muscle?
Glucagon
What is the importance of adequate liver glycogen stores in the neonate? How will anorexia impact that?
Fetus receive glucose from maternal blood to synthesize glycogen in their little fetal liver, which would allow them to survive up to 12 hours of caloric deprivation. Poor Gretchen suffered because her liver glycogen store was not enough, due to her anorexic mom
What do the extreme dangers of insulin injections cause?
Individuals could end up in comatose state from extreme hypoglycemia
What are the two phases of pentose phosphate pathway?
Oxidative phase and non oxidative phase
What is the oxidative phase of PPP?
Oxidative phase: Glucose 6-P => 2 NADPH + ribose 5-P
-NADPH is for reductive pathways like fatty acid synthesis, detoxification of drugs and glutathione defense vs ribose-5-P for DNA/RNA
What is the nonoxidative phase of PPP?
Reversible interconversion of ribose 5-P to G3P + F6P which are intermediates of glycolysis
What pathways require reduced NADPH?
FA/Cholesterol biosynthesis, NT synthesis, DNA synthesis, O2- synthesis; detox by CP450 monooxygenases & reduction of oxidized glutathione
What is the general purpose of NADPH?
Generally used in pathways that require electrons for reductive reactions because NADPH/ NADP+ ratio is higher than NADH/NAD+ (NADH is rapidly oxidized back to NAD+ by NADH dehydrogenase in ETC)
What is the role of thiamine in transketolase activity?
Thiamine (TPP) is a coenzyme for transketolase, acting as a transferase
How can transketolase activity in RBC be useful to measure thiamine status?
Addition of exogenous TPP & observation of transketolase catalytic rate can determine thiamine deficit
Transketolase transfer two carbon fragments of keto sugars to other sugars
What is the consequence of a deficiency in glucose 6-phosphate dehydrogenase? Why are RBCs are affected?
Glucose-6-P DH generates NADPH, the reducing agent for glutathione (ROS defense enzyme); so G6PDH deficiency will lead to accumulation of oxidized glutathione (GSSG) => ROS build-up & Heinz bodies (cross linked hemoglobin) that distort/stress RBC => hemolysis
What is the consequence of a deficiency in glucose 6-phosphate dehydrogenase? Why are RBCs are affected?
Glucose-6-P DH generates NADPH, the reducing agent for glutathione (ROS defense enzyme); so G6PDH deficiency will lead to accumulation of oxidized glutathione (GSSG) => ROS build-up & Heinz bodies (cross linked hemoglobin) that distort/stress RBC => hemolysis
What is the metabolic routes of UDP-glucuronate?
Glucuronides add (-) charge to compounds (such as bilirubin, morphine, T3/4, progesterone & estrogen) to increase their solubility for excretion
What is conjugated bilirubin?
Conjugated bilirubin has 2 glucoronate residues = more soluble than unconjugated
Indirect is measuring nonconjugated form bound to albumin
Direct is measuring conjugated form which is water soluble
Total is sum of both
What is unconjugated bilirubin?
Neonatal jaundice is caused by normal increased destruction of RBCs but immature bilirubin conjugating system in the liver, leading to elevated non-conjugated bilirubin deposits
can treat with phototherapy or biliblanket, causing bilirubin to absorb light and undergo changes to become more water soluble
What is the synthesis of lactose in the mammary gland? Mention the role of alpha-lactalbumin.
G1P converted to UDP glucose by UTP and UDP galactose by epimerase
Post-parturition, the hormone prolactin causes α-lactalbumin secretion which is a subunit of lactose synthase with galactosyltransferase (a lactalbumin lowers Km of galactosyltransferase) = catalyzes UDP-galactose with D glucose to make LACTOSE
What is the function, structure, and synthesis of glycoproteins?
Short carb chains link to Ser/Thr/Asn residue of proteins via O-/N-glycosylation using transferase enzyme specific for the sugar moiety and donating nucleotide of UDP/CMP/GDP-sugars; act hormones antibodies, enzymes, structural components of ECM
What is the function, structure, and synthesis of glycolipids?
Subclass of sphingolipids including cerebrosides and gangliosides; UDP-sugar + ceramide are cerebrosides and oligosaccharide + CMP-NANA are gangliosides; involved in cellular communication/recognition (ABO blood types)
What is the role of mannose-6-phosphate in targeting lysosomal hydrolases to the lysosome?
Mannose-6-P acts as a marker for proteins/enzymes intended for lysosome; lack of the marker will lead to an accumulation of substrates in lysosomes = lysosomal storage dz (I- cell)
Basis and clinical consequence of I-cell disease
I-cell = defective enzyme for adding mannose-6-P marker onto proteins
Causes build up of debris/waste in lysosomes and cell, leading to infection and eventual cell death
What is the membrane lipid used for the formation of glycolipids?
Glycolipids lipid component comes from the membrane of golgi apparatus/secretory vesicle
Upon binding to cell membrane, the lipid component remains in the outer layer of the cell membrane and carbohydrate component extends into extracellular space
What is the difference between ABO blood types in transfusion therapy?
Sugar component of glycolipid/protein on RBC membrane determine blood antigens:
Type O = defective transferase = H (fucose+galactose);
A = N-acetylgalactosamine transfrase = H + N-acetylgalactosamine attached
B = galactosyltransferase = H + galactose;
AB produces both A and B transferases
O is the universal
Donor
AB is the universal
Receiver
What is sphingolipidoses?
Diseases with accumulation of gangliosides, primarily in brain, skin, liver and spleen
Gaucher disease is associated with
Beta-glucosidase
Tay-Sachs Disease
An autosomal recessive disorder often seen in Ashkenazi Jews; defective in enzyme that hydrolyzes gangliosides = gangliosidoses (Hexosaminidase A)
sx: abnormal psychomotor development, muscle weakness, blindness, respiratory infections
What are the sources of blood glucose in fed, fasting, and starved state?
Fed (food), Brief fast (liver glycogenolysis > gluconeogenesis); Starved (gluconeogenesis)
What is the physiological significance of gluconeogenesis?
Low blood glucose levels/ high glucose demands, liver makes glucose by gluconeogenesis
What are the gluconeogenic substrates? How do they enter into the gluconeogenic pathway?
Glycerol => Glycerol-3-P => DHAP;
Ala, amino acids, & Lactate => Pyruvate
Odd number of FA => Proprionate => Glucose
Gluconeogenesis is the reverse reaction for
Glycolysis
What are the three reactions in gluconeogenesis that are different that are “reverse glycolysis”
(1) Pyruvate (pyruvate carboxylase)=> Oxaloacetate (PEPCK + GTP) => phosphoenolpyruvate + CO2
(2) Fructose-1,6-bP (F-1,6-bisphosphatase)=> Fructose-6-P + Pi
(3) Glucose-6-P (G-6-phosphatase)=> free glucose + Pi
Gluconeogenesis is regulated by…
Substrates such as glycerol, lactate, AA, enzymes
What is the effect of excessive intake of alcohol on gluconeogenesis and blood glucose levels?
Ethanol metabolism elevates NADH/NAD+ ratio: favors lactate production from pyruvate and prevent conversion of glycerol (requires NAD+) to DHAP = hypoglycemia
What happens to levels after high carb meal?
↑blood glucose; ↑↑↑insulin; ↓↓glucagon
What happens to levels after high protein meal?
Stable blood glucose; ↑insulin ↑↑glucagon
Which processes are responsible for maintaining blood glucose levels in the fed state?
Dietary glucose/uptake into cells for glycolysis; storage as glycogen
Describe which processes are responsible for maintaining blood glucose levels in the fasting state
Glycogenolysis > gluconeogenesis & lipolysis/proteolysis
Describe which processes are responsible for maintaining blood glucose levels in the starved state
Gluconeogenesis; lipolysis >proteolysis; later using only lipolysis to spare protein, creating ketones for energy
Summarize glucose levels at different time periods
12h: glycogen > gluconeogenesis via AA > glycerol/lactate
16h: glycogen < gluconeogenesis via glycerol/AA/lactate
30h: gluconeogenesis via glycerol/lactate > AA
What occurs in type 1 diabetes?
Cannot secrete insulin in response to meal due to defect in β-cells; Dianne cannot uptake dietary glucose after a meal without exogenous insulin
What occurs in type 2 diabetes?
Experience delayed insulin release and insulin resistance; Deborah does not efficiently uptake dietary glucose after a meal
