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38 Cards in this Set
- Front
- Back
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Diabetes T1 T2
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T1- problem w/ pancreas producing insulin
T2 - problem w/ peripheral cells using or responding to insulin |
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diabetes symptoms
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hyperglycemia
thirst - polydipsia excessive urine production rapid wt loss |
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Metabolic effects of diabetes
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body acts as if 'starved' of CHO
body fat mobilized - broken down - produce ketones - acidosis protein catabolized - ammonia released to buffer ketones |
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pancreatic islet B cell failure
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due to autoimmune disease
viral destruction of B cells |
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Glucokinase genetic mutation
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insulin release requires pancreatic glucose-sensing enzyme glucokinase & GLUT 2
mutations of either cause insulin release problems |
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T2
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insulin resistance in muscle and adipose cells
takes unusually lg amts of insulin to regulate or control blood glucose w/in normal limits |
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Insulin Receptor
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proteins
mutations in receptor |
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GLUT problems
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interrupted insulin signal - T2
blocked insulin signal in cell - failure of vesicles to move to cell surface - reduced GLUTs - reduced glucose uptake |
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fat cells and diabetes
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adipocytes show marked depletion of mRNA that encodes for GLUT 4 transporter protein = take in less glu
lg fat cells more insulin resistant - distorted cell membrane abdominal obesity = incr. visceral fat - associated w/ insulin resistance - release FA that inhibit glu metabolism and insulin receptor fxn |
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GI Index
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effect dif CHO foods have on blood glu levels
quantitative comparison b/w foods reference food assigned value of 100 - white bread |
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GI load
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blood glu response after 50g of test food / 50g pure glu x 100
uses more realistic / typical serving sizes for CHO foods reflection of CHO foods effect on blood glu levels |
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Glycogenolysis
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purpose: release of indiv. glu mol for further oxidation and use as fuel
glycogen phosphorlase debranching enzyme hexonase & gluconase Triggers: glucagon + epinephrine + insulin |
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Glucogenesis
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Purpose: provide glu to store as glycogen in muscle/liver
hepatocytes & muscle cells Glu enters - hexokinase / glucokinase extract IP from ATM and attach to glu making G-6-P glu G-6-P Glucogenesis - or - glucolysis |
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# ATP needed to add 1 Glu to glycogen chain
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1 ATP
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Key Metabolic Pathways of Nutrients
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Mitochondria: focus of CHO, lipid, AA metabolism
Citric Acid / Krebs cycle, Beta Oxidation of FA, ketogenesis, respiratory chain, ATP synthesis Cystosol: glycolysis, pentose phos pathway, FA synthesis Ribosomes: protein synthesis Endoplasmic Reticulum: Triglyceride synthesis |
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Why store E as glycogen and not Fat
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can't breakdown fat as quickly as glycogen
fat cannot be burned/used in the absence of O2 Fat cannot be converted to glucose glycogen takes too much space in cells and attracts lot of water |
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w/o G-6-Phosphatase
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only glucose in liver
can't dump glucose in blood hypoglycemic |
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w/o debranching enzyme
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cannot move glu to break 1,6 bond & release glu to make G-6-P & release glu to blood
only break down so far |
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w/o glycogen phosphorylase in liver
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can't break down glycogen at all
key step in breaking off glucose |
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ETC & Oxidative Phosphorylation
BIG PICTURE |
Simple Combustion/oxidation:
glucose + fire = Co2 + H2O + Heat Cellular Oxidation: glucose [via metabolism] = Co2 + H2O + Heat + ATM CHO, Fat, Pro oxidized to: CO2, H2O, ATP, Heat ETC - 4 complexes (3 are pumps) overall driving force behind ETC = NADH2 wants to give up e- and O2 wants e- |
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oxidative phosphorylation
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MAJOR means of making ATP - indirect
ADP + P = ATP H collected and pumped through membrane space of mitochondria 1 NADH2 = 3 ATP via ATPase 1 FADH2 = 2 ATP |
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How to Make ATP
BIG PICTURE |
Addition of P molecule in phosphorylation
2 ways: substrate level phosphorylation; oxidative phosphorylation phosphate anhydride bond holds onto bonds of ATP splitting of P bond is exothermic and releases E Adenosine - P~P~P -P = ADP + 7300cal/mol -2P = AMP + 7300cal/mol GLucose + P + 4000cals/mole = G-6-P 7300cal-4000cal to put P on G6P precursor = 3300 calories to maintain 98.6 temp |
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Harvesting Hydrogens for NADH
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NAD+ + e- = NAD
NAD + H = HADH NADH + H = NADH2 |
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1 spin of Krebs cycle w/ 1 Acetyl CoA
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1 ATP
8H 2Co2 |
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1 molecule of glucose through Krebs cycle =
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w/ 2 pyruvate to begin
2 ATP 16 H 4 Co2 |
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Krebs cycle
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aerobic metabolism
final catabolic pathway of fat, protein, CHO - complete oxidation to Co2, H20, E oxidative rxns are dehydrogenations enzymes catalyze removal of 2H to an acceptor molecule FAD or NAD H's are source of E for formation of ATP in ETC |
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steps in Krebs
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Pyruvate (2)
Acetyl CoA Citrate Isocitrate NADH2 Ketoglutarate NADH2 Succinyl CoA ATP Succinate FADH2 Fumarate Malate Oxaloacetate |
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Controls for Krebs cycle
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After Isocitrate: isocitrate dehydrogenase stops ATP/NADH2 production
After Ketoglutarate: ketoglutarate dehydrogenase stops ATP/NADH2 Succinyl CoA stops also |
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controls for mechanism b/w pyruvate and Acetyl CoA
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Pyruvate dehydrogenase
+ Insulin & Epinephrine - NADH2, Acetyl CoA, ATP |
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phosphorylase
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breaks down glycogen & turns on glycogenolysis
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Glycogenolysis
BIG PICTURE |
glucose cleaved 1 at a time from glycogen branches
def: breakdown of glycogen to glucose fxn: designed to liberate glucose from stored form as glycogen for use in muscle cells and exported to blood BRAKE: insulin inhibits glucogenolysis SPEED UP: epinephrine (muscles) / glucagon (liver) turned on by hormones: glucagon & epinephrine w/ lot of ATP, no need to break down glycogen |
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Glycogen
BIG PICTURE |
storage form of CHO in humans
liver and muscle (75%) Liver - purpose to provide glucose to blood muscle - purpose provide glucose to working muscles - can't leave muscle cell Takes 1 ATP to add glucose to glycogen chain |
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Glucose Uptake and liver
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glu phosphorylated = G6P upon entering cells
glucokinase in liver hexokinase in muscle |
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Glycolysis
BIG PICTURE |
all cells in human body
major pathway for utilization of glucose & is found in the cytosol of the cell Can operate when ample O2 is available (aerobic) and fxn w/o O2 (anaerobic) O2 and mitochondria necessary to complete end stage of glycolysis Glucose broken down into 2 molecules of pyruvate Fxn: initial set of rxn necessary for eventual complete oxidation of glucose via kreb's cycle and ETC Fxn: ability of glycolysis to provide ATP (E) in absence of O2 glycolysis dependent tissues: RBC (lack mitochondria; Eye (ltd. blood supply); Kidney, testis, leukocytes, white muscle fibers; BRAIN ~120 g glucose/day |
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Pentose Phosphate Pathway (PPP)
BIG PICTURE |
generate important metabolic intermediates not produced in other pathways
products: ribose (pentose) needed for synthesis of nucleic acids and DNA NADPH needed for synthesis of FA, Steroids (Chol) and some AA active in liver, adipose, adrenal corex, thyroid gland, testis, lactating mammary glands G6P starts end w/ ribose-5-phosphate - used in cmpds that need ribose |
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Missing G6P
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RBC hemolysis (RBC burst open) - hymolytic anemia
provides NADPH2 needed for activation of enzyme glutathione peroxidase (RBC) - protects cell membranes from free radical damage |
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Summary of CHO Pathways
Glycogenesis Glycogenolysis Clycolysis Gluconeogenesis Critic Acid/TCA/ Krebs Cycle Hexosemonophosphate Shunt (PPP) |
glucose - glucogen
glycogen - glucose glucose - pyruvate non-cho stuff - glucose acetyl CoA - Co2 and H's GLucose - Ribose |
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3 Metabolic Pathways
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Anabolic - synthesis of compds constituting body's ss and machinery
Catabolic - Oxidative process that release E, usually E-phosphate mol or reducing equivalents Amphibolic - more than 1 fxn and can occur at "crossroads" of metabolism acting as links b/w anabolic and catabolic pathways |
