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metabolism Flashcards

pancreas, liver, metabolic adaptations, cellular metabolism

1
Q

pancreas structure

A

-sits below and behind stomach
-tapering structure consisting of three regions
-head -largest section near duodenum
-body -central section
-tail -tapering section
-connected to duodenum via two ducts [main pancreatic duct and accessory duct], main pancreatic duct joins common bile duct.

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2
Q

pancreas juice flow

A

-juice and bile flow are regulated by individual sphincter muscle
-entry into duodenum via hepatopancreatic ampulla
-flow of juice and bile through this duct in controlled by the sphincter of hepatopancreatic ampulla or sphincter of Oddi
-flows into intercalated ducts to the interlobular duct
-then drains into main pancreatic duct delivered into duodenum

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3
Q

pancreatic acini

A

-pancreas contains clusters of glandular epithelial cells
-acini makes up 99% of there clusters
-cells withing these acini produce and secrete components of pancreatic juice
-cells of acini secrete inactive versions of digestive enzymes [zymogens or proenzymes]
-cells also secrete bicarb ions [rases pH of chyme, also secreted by centroacinar cells]
[digestive enzyme secretion activated by cholecystokinin [CCK], bicard secretion activated by secretin]

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4
Q

enzymes of pancreatic juice

A

-carbohydrate digestion [pancreatic amylase]
-protein digestion [trypsin, chymotrypsin, carboxypeptidase, elastase]
-lipid digestion [pancreatic lipase and phospholipase]
-nucleic acid digestion [deoxy/ribonuclease]

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5
Q

pancreas secretory cells

A

-alpha islet cells [17%][secret glucagon]
-beta islet cells [70%][secret insulin]
-delta cells [7%][secrete somatostatin, inhibits secretion of glucagon and insulin]
-F cells [6%][secretes pancreatic peptide, inhibits somatostatin]

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6
Q

pancreatic hormone glucagon

A

-promotes glycogenolysis and gluconeogenesis [increase blood glucose conc., promotes release of fatty acids vis lipolysis]
-main target is liver and adipose tissue

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7
Q

pancreatic hormone insulin

A

-promotes glucose uptake into skeletal muscle and adipose tissue via GLuT4
-promotes glycogenesis in muscle and liver
-increases AA uptake and protein synthesis
-increases formation of triglycerides

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8
Q

liver functions

A

-metabolism [CHO, lipids, proteins]
-detoxification
-excretion
-synthesis
-storage [glycogen, vit A,B12,D,E,K, minerals including iron and copper]
-phagocytosis
-activation of vit D [converts inert vit D from sun exposure or foods to calcidiol, this is then processed by kidneys to form active form of vit did, calcitriol]

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9
Q

liver composition

A

-second largest organ
-composed of hepatocytes, bile canaliculi, hepatic sinusoids, stellate reticuloendothelial cells [hepatic macrophages that phagocytose ageing red and white blood cells and bacteria]

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10
Q

hepatocytes

A

-main cell of liver [80%]
-capable of performing many different tasks [metabolic, secretory and endocrine]
-form 3D layers called hepatic laminae
-network of ducts between laminae called bile canaliculi

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11
Q

bile canaliculi

A

-networks of ducts between hepatic laminae
-carry bile secreted by hepatocytes to bile ducts
-these ducts converge into common hepatic duct
-bile can be stored in gall bladder

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12
Q

hepatic sinusoids

A

-surround hepatic laminae
-very permeable blood cap
-convey oxygen rich blood from branches of hepatic artery to central veins
-also carry nutrient rich, oxygen poor blood from hepatic portal vein to central veins
-blood flows towards central vein while bile flows in opposite direction

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13
Q

key bile components

A

-bilirubin [main bile pigment derived from haem]
-bile salts [salts of bile acids, responsible for emulsifying lipids [breaking them down and suspending them]
also aid absorption via formation of micelles [allow for more efficient lipase action]

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14
Q

liver metabolic role -CHO

A

key role in maintaining blood glucose concentration
-stores glucose molecules as glycogen [driven by insulin]
-breaks down glycogen to glucose [driven by glucagon]
-conversion of some AA and lactic acid to glucose
-converts fructose and galactose to glucose

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15
Q

liver metabolic role -lipid

A

-triglycerides [excess energy store and use as fuel source for ATP production]
-converts excess CHO and protein to triglycerides
-synthesises cholesterol and phospholipids
-produces lipoproteins for transportation of triglycerides and cholesterol to other cells [VLDL, LDL, nascent HDL protein]

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16
Q

liver metabolic role - protein

A

-deamination of AA [removal of amino groups]
-transamination of AA [synth. of non-essential AA]
-conversion of ammonia to urea
-synth of most plasma proteins [albumin, alpha and beta globulins, prothrombin, fibrinogen]

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17
Q

liver detoxification pathways

A

phase 1
-driven by specific enzymes
-involved oxidation, peroxidation and reduction
-process produces less harmful substances
phase 2
-converts phase 1 metabolites into water-soluble form
-involved powerful antioxidants such as glutathione
-allows excretion in urine

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18
Q

absorptive vs postabsorptive state

A

absorptive
-recently digested and absorbed nutrients are available, including glucose for ATP production
postabsorptive state
-no new nutrients are available, metabolic needs of cells must be met by mobilising nutrients stored in body
we spend 12 hours per day in each state

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19
Q

absorptive state

A

-up to around 4 hours after a meal
-nutrients from GI tract enrich blood
-glucose and AA transported to liver via hepatic portal vein
-most absorbed lipids encased in chylomicrons [absorbed in lacteals, transferred to blood via thoracic ducts, arrive at liver via hepatic artery]
-nutrients can be used immediately or stored

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20
Q

absorptive state metabolic reactions -glucose

A

-50% is oxidised and used for ATP production via glycolysis, Krebs cycle and electron transport chain
-40% converted to triglycerides and stored mainly in adipocytes
-10% converted to glycogen in liver and skeletal muscle

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21
Q

absorptive state metabolic reactions - lipids

A

-most triglycerides and fatty acids are stored in adipocytes
-lipids delivered to adipocytes by chylomicrons from digestive system, VLDL from liver
-adipocytes also synth triglycerides from excess glucose

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22
Q

absorptive state metabolic reactions - protein

A

-AA absorbed for manufacture of proteins
-deaminated by liver to produce keto acids
-keto acids can either enter Krebs cycle for ATP production or be used to make glucose or fatty acids

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23
Q

absorptive state regulation

A

-insulin secretion increases after a meal
-driven by glucose-dependant insulinotropic peptide [GIP] and rising blood glucose

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24
Q

insulins many metabolic effects

A

-GluT 4 production and entry of glucose in skeletal muscle and adipocytes
-anabolism of glucose to glycogen
-formation of triglycerides in adipocytes and liver
-AA absorption and protein synthesis [also requires thyroid hormones and insulin like growth factor [IGF]]

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25
Q

maintaining blood glucose concentration

A

around 5 mmol/L [90 mg/dL] is essential
-range 3.9-6.1 mmol/L or 70-110 mg/dL
-glucagon can promote glucose release from liver glycogen stores
-cortisol and glucagon promote gluconeogenesis

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26
Q

postabsorptive state metabolic reactions - glucose production

A

-glycogen catabolised to free glucose molecules
-triglycerides broken down to permit the conversion of glycerol to glucose
-gluconeogenesis [lactic acid produced, glycolysis can be converted to glucose in liver, AA can be used for glucose production by the liver]

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27
Q

postabsorptive state metabolic reaction - glucose sparing

A

-reactions that help preserve the body
processes include
-fatty acid oxidation for ATP production
-oxidation of lactic acid by cardiac muscle
-oxidation of AA by liver to produce ATP
-oxidation of ketone bodies for ATP production

28
Q

postabsorptive state regulation

A

-driven by hormones and sympathetic division of ANS
-glucagon [stimulates glycogenolysis and gluconeogenesis]
-cortisol [promotes gluconeogenesis, stimulates protein catabolism and lipolysis for use as fuel for ATP production]
-epinephrine and norepinephrine [stimulate lipolysis and glycogenolysis]

29
Q

ketone bodies

A

-major alteration to normal metabolic processes during fasting and starvation is production of large quantities of ketone bodies
-produced mostly by hepatocytes [constantly produce small quantities, once glucose has been exhausted, production is increased]

30
Q

ketogenesis

A

-fatty acids undergo beta oxidation to produce acetyl-CoA
-large quantities of acetyl-CoA skip Krebs cycle and are used to for ketone bodies
-production triggered by low insulin conc.
-can be upregulated by glucagon, cortisol, T3 and T4, catecholamines [increase release of fatty acids]

31
Q

leptin

A

-produced by adipocytes [proportional to amount of adipose tissue]
-acts on hypothalamus to decrease feeding stimulus

32
Q

catabolism

A

-process that breaks down complex molecules to simpler one
-exergonic [releases more energy that they consume]

33
Q

anabolism

A

-process that builds larger structures from simpler ones
-endergonic [consume energy]

34
Q

metabolic reactions are balanced between?

A

-catabolic and anabolic
-ATP produced by anabolic reactions
-when ATP is broken down to ADP+P, energy is released
-energy is used to re-attach a phosphate group to ADP to form ATP [phosphorylation]

35
Q

ATP and ADP meaning

A

-adenosine triphosphate
-adenosine diphosphate

36
Q

ATP - cellular energy

A

-provides energy required for metabolic reactions in the cell
-each cell contains around 1 billion molecules of ATP
-each molecule lasts less than 1 minute

37
Q

oxidation

A

-results in a change to original molecule or substance
-can occur in 3 ways: addition of oxygen, removal of electrons from an atom or molecule, removal of hydrogen
-exergonic - releases energy
-occur simultaneously with reduced states [redox cycle]

38
Q

reduction

A

-result in a change in original molecule or substance
-occur in three ways: removal of oxygen, addition of electrons to a molecule [known as high energy electrons], addition of oxygen
-endergonic -require and store energy
-occurs simultaneously with oxidative states [redox cycle]

39
Q

NAD and FAD

A

-nicotinamide adenine dinucleotide [from vit B3 - niacin]
-flavin adenine dinucleotide [from vit B3 -riboflavin]
-both have oxidation/reduction states
-both cofactors that are crucial for energy production
-can be reduced by accepting hydrogen and electrons/oxidised and the released of hydrogen and electrons used to produce ATP

40
Q

NAD redox states

A

-oxidised NDH[+] is reduced to NADH+H+
-gains a hydride ion [hydrogen atom with additional electron]
-2 hydrogen ions [2H+] and 2 electrons [2e-]
-1 of hydrogen ions is released

41
Q

FAD redox states

A

-oxidised FAD is reduced to FADH2
-gains 2 hydrogen ions [2H+] and 2 electrons [2e-]

42
Q

what is preferred energy substrate for ATP production

A

-glucose oxidised to form ATP
-dietary CHO are hydrolysed to monosaccharides [mostly glucose 80%, also fructose and galactose, liver converts galactose and most-fructose to glucose]
-additional metabolic pathways for glucose [formation of AA, glycogen [glucose polysaccharide], synth of triglycerides by liver]

43
Q

glucose entry into cells

A

-GluT = glucose transporters
-enter via GluT molecules on most cells of the body [facilitated diffusion]
-neurons and hepatocytes posses GluT 2&3 respectively
-skeletal muscle and adipose cells produce and insert GluT 4 molecules in response to high insulin conc. [these two cell types make up a larger portion of us as organisms >60%]

44
Q

glucose catabolism and stages

A

-glucose is phosphorylated once inside the cell [prevents glucose from leaving cell]
-4 stages in glucose catabolism
1-glycolysis
2-formation of acetyl coenzyme A
3-Krebs cycle reactions [aka citric acid cycle or tricarboxylic cycle]
4-electron transport chain reactions

45
Q

glycolysis

A

-pathway of 10 reactions in cytosol of cells
-one molecule of glucose [C6H12O6] is oxidised to produce 2 molecules of ATP, 2 molecules of pyruvic acid, 2 molecules of reduced NAD [NADH] [contains energy]

46
Q

Acetyl coenzyme A formation

A

-intermediate stage that oxidises pyruvic acid for entry into Krebs cycle
-in mitochondria pyruvic acid produces 1 molecule of CO2, 1 molecule of reduced NADH+H+ [contains energy] and molecule of acetyl coenzyme A

47
Q

the Krebs cycle

A

-acetyl CoA oxidised in mitochondrial matrix
-primary aim to produce NADH and FADH2 [used in electron transport chain]
-also produces ATP and CO2

48
Q

oxidative phosphorylation

A

-O2 involved in final step of electron transport chain
-oxidative phosphorylation involves two connected processes [passage of electrons along electron transport chain, pumping hydrogen ions -chemiosmosis]
-why we need to breathe oxygen

49
Q

electron transport chain

A

-series of electron carriers on the inner mitochondrial membrane [1000s of transport chains per mitochondrion][due to folded inner membrane increasing surface area]
-carriers are systematically reduced and oxidised [exergonic reactions produce energy]
-last electron acceptor is O2
-electron carriers are proteins found in inner mitochondrial membrane [known as protein complexes I-IV
-also contain two key additional factors [coenzyme Q10, cytochrome C complex]
-electrons are supplied by two main products of the Krebs cycle -high energy electron carriers [NADH/FADH2]

50
Q

NADH in electron transport chain

A

-NADH is oxidised and donates 2 electrons to protein complex I, these electrons passed between other complexes
-as this happens each protein complex pumps hydrogen ions [protons] into intermembrane space [ten in total]
-complex I pumps out of 4 protons
-complex III pumps out 4 protons
-complex IV pumps out 2 protons

51
Q

FADH2 in electron transport chain

A

-oxidised and donates 2 electrons to protein complex II, these are passed to coenzyme Q10 and then on to complex III and IV
-protons are pumped but complex I is missed so only 6 protons are pumped into intermembrane space
-complex III pumps out 4 protons
-complex IV pumps out 2 protons

52
Q

ATP production

A

-protons pumped by protein complexes collect in intermembrane space
-this creates high concentration gradient of H+
-these pass down their electrochemical gradient and into matrix through final protein [ATP synthase/synthetase]
-ATP synthase acts as a generator and the flow of protons powers the phosphorylation of ADP to ATP

53
Q

glycogenesis

A

-formation of glycogen -polysaccharide
-stored version of glucose
-total storage is around 500g [skeletal muscle 75% and liver 25%]
-glycogenesis is driven by hormone insulin
-when glucose is needed glycogenolysis occurs

54
Q

gluconeogenesis

A

-when glycogen stores depleted, body creates new glucose molecules [occurs mainly in liver]
-proteins and lipids are catabolised
-to make new glucose molecules we use glycerol from triglycerides, lactic acid, certain AA mostly alanine and glutamine

55
Q

gluconeogenesis hormones

A

-initiated by two hormones
-cortisol is a major glucocorticoid [also initiates catabolism of proteins, increasing available pool of AA]
-glucagon from pancreatic a cells
-[also involved release of thyroid hormones [T3/T4], mobilise proteins, stimulate mobilisation and degradation of lipids]

56
Q

lipid metabolism

A

-primary energy storage molecules
-98% of stored energy reserves are in the form of triglycerides [over twice as energy dense per gram compared to CHO or proteins, hydrophobic -cells do not exert osmotic pressure]
-packed into adipocytes and found in subcutaneous layer [50%] and as visceral fat

57
Q

lipolysis

A

-fatty acid from triglycerides can be oxidised and used to produce ATP
-first step is removing fatty acids from glycerol molecule [lipolysis]
-glycerol is converted into glyceraldehyde 3-phosphate
[converted into glucose if cellular ATP is high, catabolised to pyruvic acid if ATP is low]

58
Q

beta oxidation

A

-after lipolysis
-fatty acids are essentially long hydrocarbon chains [energy dense]
-catabolism starts in mitochondrial matrix
-beta oxidation involves removal of 2 carbon atoms from the fatty acid at a time
-these are attached to coenzyme A to form acetyl CoA

59
Q

fatty acid catabolism

A

-after beta oxidation
-acetyl CoA then enters Krebs cycle
-very high energy content
-palmitic acid contains 16 carbon atoms
-if fully oxidised through Krebs cycle and electron transport chain can yield 129 ATP molecules

60
Q

fatty acid - length of carbon chain

A

-short chain - 5 or fewer
-medium chain - 6-12 carbons
-long chain - 13-21 carbons
-very long chain - 22 or more carbons

61
Q

lipogeneses

A

-synth of lipids
-takes place in liver and adipocytes
-initiated by insulin
-occurs in response to a positive energy balance [more energy consumed than used]
-CHO, proteins, and fats are all converted into triglycerides and stored

62
Q

lipid transport

A

-lipids are non-polar and hydrophobic
-must be encased in a hydrophilic shell before transportation in blood can occur
-this occurs in 2 locations: Intestines form chylomicrons for dietary lipid transport and Liver produces very low density and low
density lipoproteins [VLDL and LDL] [liver and intestine produce nascent high density lipoprotein, becomes HDL]

63
Q

protein metabolism

A

-dietary protein is broken down into AA
-which is not stored, is used to build proteins or oxidised to make ATP
-excess AA are converted to glucose or triglycerides

64
Q

protein catabolism

A

-driven mainly by glucocorticoid cortisol
-broken down proteins into AA
-AA can then be converted into different AA, used to construct new proteins, converted to fatty acids, ketone bodies or glucose, oxidised to make ATP [via conversion to acetyl CoA]

65
Q

complete dietary proteins

A

supply all 20 AA in sufficient quantities

66
Q

human proteome

A

-humans can produce between 80,000 to 400,000 different proteins
-many are variants of same protein
-coded for by gene variants known as alleles
-this is form around 20,400 protein coding genes
-not all proteins produced at any one time [some only due to disease]

67
Q

transamination

A

-nitrogen is required for protein and nucleic acid production
-transamination involves recycling nitrogen to produce non-essential AA and to prevent ammonia production and excretion of nitrogen from kidneys
-use enzymes called transaminases
-transfer an amino group to a keto acid

biomed (9 decks)

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