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Phys > Week 12 - Nutrition and Metabolilsm > Flashcards

Week 12 - Nutrition and Metabolilsm Flashcards

1
Q

Metabolism

A

Sum of body’s chemical reactions. Series of enzyme-catalysed reactions, which include 4 basic processes

  1. Harnessing energy: in chemical bonds of molecules obtained from diet (nutrients); may be used to make adenosine triphosphate (ATP)
  2. Converting: one type of molecule into another for cell’s synthesis reactions
  3. Synthesising macromolecules: such as proteins, polysaccharides, nucleic acids, and lipids
  4. Breaking down macromolecules: into monomers or other smaller molecules
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2
Q

Catabolism

A
  • group of reactions where one substance is broken down into smaller parts
  • EXERGONIC reactions, which releases energy
  • cells can harness the energy released to drive other processes
  • energy released by catabolic processes in the form of ATP
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3
Q

Anabolism

A
  • group of reactions which case smaller molecules to be combined to make a larger molecule
  • ENDERGONIC reactions (USE energy)
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4
Q

Metabolic rate

A
  • total amount of energy expended by body to power all of its processes
  • sum of all anabolic and catabolic reactions occurring in the body
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5
Q

Basal metabolic rate (BMR)

A
  • The body continues to use energy even when at rest. BMR is the minimal rate of metabolism for an awake individual at rest

Resting conditions:

  • person has not eaten for the past 12 hours and has had a restful night of sleep
  • person is not performing physical activity and has not performed strenuous physical activity for at least 1hr
  • person is not under physical or emotional stress
  • temp surrounding person is constant and comfortable
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6
Q

Factors affecting total Metabolic rate and BMR

A
  • pregnancy, anxiety, fever, eating, thyroid hormones, depression
  • BMr varies between individuals, depending on factors such as gender and muscle mass ( skeletal muscle is a highly metabolically active tissue)
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7
Q

Metabolic reactions - energy requirements

A
  • energy is released from exergonic CATABOLIC REACTIONS
  • this energy can be used to SYNTHESISE ATP
  • when ATP is broken down, energy is released and is used to fuel endergonic ANABOLIC REACTIONS
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8
Q

NUTRIENTS

A

A molecule obtained from food that body requires for its metabolic processes

WATER- essential component for multiple metabolic processes in body. broken down by enzymes through HYDROLYSIS

MACRONUTRIENTS - carbohydrates, proteins, lipids.

MICRONUTRIENTS- vitamins and minerals

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9
Q

Carbohydrates

A

45-65%
humans cannot digest fibre

Polysaccharides:

  • starch
  • glycogen
  • cellulose (fibre)

Disaccharides:

  • lactose
  • maltose
  • sucrose

Monosaccharides:

  • glucose
  • galactose
  • fructose
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10
Q

Lipids

A

in diet includes triglycerides, cholesterol, certain vitamins

  • Fats, mostly unsaturated =30% daily intake
  • saturated fatty acids: mostly animal-derived products
  • unsaturated fatty acids: commonly found in plant- derived products
  • essential fatty acids: body is unable to sunthesize → must come from diet
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11
Q

Proteins

A

Proteins & 20 amino acids

  • 10-35% of daily intake is from protein-rich food
  • 11 nonessential amino acids : can be synthesised
  • 9 essential amino acids: must be obtained from dietary sources
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12
Q

Vitamins

A

Fat-soluble: hydrophobic compounds, structurally similar to cholesterol → Vit A, D, E & K

Water-soluble: hydrophilic compounds featuring polar covalent bonds → Vit C & B

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13
Q

Minerals

A

any element other than carbon, hydrogen, oxygen and nitrogen that is required by living organisms

  • 7 major minerals are ions (in moderate amounts_ → calcium, chloride, magnesium, phosphorus, potassium, sodium and sulfur

10 trace minerals are ions (v small amounts) →iodine, iron & selenium

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14
Q

ATP synthesis

A
  • cells harness ATP energy by removing the 3rd phosphate group in a HYDROLYSIS reaction, bond between 2nd and 3rd is broken w/ a water molecule, releasing free phosphate and ADP (adenosine diphosphate)
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15
Q

ATP phosphorylation

A

Process where released energy can by used by a cell

process where ATP donates a phosphate group to a reactant → reactant becomes more reactive →favours conversion of reactant to desired product

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16
Q

Nutrients and ATP synthesis

A
  • carbohydrates (glucose and glycogen) is the preferred source for ATP production
  • breaking down glucose is a catabolic process known as GLYCOLYSIS resulting in the product PYRUVATE
  • if carbohydrates in the diet do not meet metabolic demands for glucose, the body can produce glucose through non-carn sources → amino acids (proteins) & fatty acids (lipids)
  • pyruvate can be used in the CITRIC ACID CYCLE (Kreb cycle) and the ELECTRON TRANSPORT CHAIN to yield more ATP molecules
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17
Q

Stores and function of carbohydrates

A
  • Stored in
    1. muscle glycogen
    2. liver glycogen
    3. blood glucose
  • Most carbohydrate serves as FUEL for the body (ATP SYNTHESIS)
    →Neurons, RBCs and kidneys depend on glucose
  • Sugars also serve as STRUCTURAL COMPONENTS
    → nucleic acids, glycoproteins and glycolipids, ATP
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18
Q

regulation of blood glucose levels - rise

A

Stimulus: BGL rises after carb rich meal
→beta cells of pancreas release insulin into the blood
→ body cells take up more glucose & liver takes up glucose and stores it as glycogen
→ BGL declines
→ Homeostasis: BGL (70-110 mg/100ml)

19
Q

regulation of blood glucose levels- fall

A

Stimulus: BGL falls after skipping meal
→ alpha cells of pancreas release glucagon into blood
→ liver breaks down glycogen and releases glucose into blood
→BGL rises
Homeostasis: BGL (70/110mg/100ml)

20
Q

Carbohydrates absorption

A
  • starts in oral cavilty when SALIVARY AMYLASE until pH drops to <4.5 in stomach
  • final steps in carbohydrate metabolism in the small intestine:
    →secretion of PANCREATIC AMYLASE
    → a number of enzymes from brush border of the small intestine breakdown carbohydrate into monosaccharides
  • in the liver excess glucose is stored as GLYCOGEN
21
Q

Glucose as a primary energy source

A
  • glucose is a small, soluble molecule that is easily distributed through body fluids
  • glycolysis provides a small amount of ATP ANAEROBICALLY
  • unlike ATP, glucose can be efficiently stored as GLYCOGEN
  • the break down of glycogen (GLYCOGENOLYSIS) occurs v quickly and involves only a single enzymatic step. mobilisation of other intracellular reserves involves much more complex pathways and takes considerable more time
22
Q

Glycolysis

A
  • GLYCOLYSIs glucose is broken down in a series of 10 enzyme-orchestrated reactions that takes place in cytosol of all cells
  • glucose is SPLIT into two 3-carbon sugar molecules called PYRUVATE
  • the 10 reactions which take place dyring glycolysis can be condensed into two phases
    1, energy investment phase
    2. energy pay off phase
23
Q

Glycolysis - first phosphorylation

A

Reaction 1

glucose is phosphorylated by ATP, yielding glucose-6-phosphate and ADP

24
Q

Glycolysis - second phosphorylation

A

Reaction 2&3

  • the carbon atoms in glucose -6-phosphate are rearranged and the molecule is then phosphorylated by another ATP, yielding fructose-1,6-biphosphate and ADP
25
Q

Glycolysis - Cleavage

A

Reactions 4&5

  • the six carbon fructose-1,6-biphosphate is split, and two three-carbon molecules are formed
26
Q

Glycolysis - oxidation

A

reaction 6&7

  • Glyceraldehyde-3-phosphate is phosphorylated and oxidised by NAD+ to hield NADH and 1,3-byphosphoglycerate, which then donates a Pi to ADP, producing ATP
27
Q

Glycolysis - ATP synthesis

A

Reaction 8-10

  • the carbon atoms in 3-phosphoglycerate are rearranged to form phosphoenolpyruvate, which donates a Pi to ADP, yielding ATP and pyruvate
28
Q

Citric acid cycle (krebs)

A

2nd part of glucose metabolism

  1. Citrate synthesis: Acetyl-CoA combines with oxaloacate to form citrate and CoA (reaction 1)
  2. First oxidation: citrate is rearranged, then oxidized by NAD+ generating CO2 and NADH (reactio 2-4)
  3. ATP synthesis: succinyl-Coa is converted to succinate and CoA, while forming ATP (reaction 5)
  4. Second oxidation: succinate is oxidised by FAD and NAD+, generatinf FADH2 and NADH, and is converted back to oxaloacetate (reaction 6-8)
29
Q

Protein function

A
  • muscle contraction:movement of body, cells, cell structures
  • cell membranes (receptors, cell identity, pumps)
  • fibrous proteins (collagen, keratin): structural
  • globular proteins (antibodies, myoglobin, enzymes) : functional
  • plasma proteins: blood osmolarity and viscosity
30
Q

protein absorption

A

In stomach:
- HCL denatures and unfolds proteins preparing them for easier chemical digestion, PEPSIN breaks proteins into small peptides

In Duodenum:
- PANCREATIC ENZYMES (trypsin, chymotrypsin and carboxypeptidase) continue breaking proteins into small peptides

In jejunum and ileum of small intestine:
- various PEPTIDASE ENZYME in intestinal lining brush border finish digestio of peptides into amino acids

31
Q

amino acid catbolism

A

Dietary proteins are broken down into amino acid subunits in digestive tract; absorbed into bloodstream and delivered to liver

  • AA consist of a carbon skeleton bound to a nitrogen containing amino group
  • nitrogen is not used for energy so amino group is removed by TRANSAMINATION and the remaining carbon skeleton can be oxidised for fuel
32
Q

Lipids - sources and finctions

A
  • adipose tissue: helps protect tissues and organs and also provides fuel source
  • plasma membrane and myelin sheath: composed of phospholipids and cholesterol
  • cholesterol: precursor of steroids, bile salts and VIT D
  • fatty acids: precursor of prostaglandins and other eicosanoids
  • fat-soluble vits (ADEK)
33
Q

Lipid absorption

A
  • Begins in mouth with inguale LIPASE breaking down triglycerides into monoglycerides and fatty acids. continues in the stomach
  • BILE SALTS from gallbladder emulsifies the large lipid droplet into smaller ones → greater access of PANCREATIC LIPASE
  • most fats exist as triglycerides which contain three long hydrocarbon chains (FATTY ACIDS) linked to a modified sugar, (GLYCEROL)
34
Q

Cholesterol

A

lipid which is not oxidised for duel; important to many anabolic processes in body

  • Modified to produce Vit D, steroid hormones and bile salts
  • Important structural molecule in plasma membranes

Packaged along w/ other lipids and proteins into stucutres called lipoproteins → provide transportation for cholesterol and other lipids in bloodstream

35
Q

lipoproteins

A

Hydrophobic so protein carriers needed for transport in blood; complexes of lipids and proteins in blood.

categorised into 4 groups by DENSITY. the more protein content to lipid = higher density
1. chylomicrons: used for transport of dietary lipids to adipose tissue

  1. v low-density (VLDLs): made in liver to transport triglycerides to all tissues; converted to LDLs after removal of some triglycerides
  2. Low-density (LDLs): remnants of VLDL; carry cholesterol to cells; after they give away cholesteral they are repackaged into VLDL in liver as they are rich in cholesteral ‘bad lipoproteins’
  3. High-density (HDLs): HDL remove excess cholesterol from peripheral tissues and transport to liver for disposal ‘good lipoproteins’
36
Q

fatty acid catabolism, beta oxidation

A

LIPOLYSIS: enzyme-catalyzed process that liberates fatty acids and glycerol

  • both fatty acids & glycerol can be used for energy generation, but overwhelming amount of energy is derived from fatty acid BETA OXIDATION
  • glycerol is converted to clyceraldehyde-3-phosphate and enters glycolysis
  • fatty acids are catabolides to acetyl-CoA by BETA OXIDATION and to KETONE BODIES by KETOGENESIS
37
Q

Ketogenesis

A
  • when body uses beta-oxidation of fats to make glucose, a by-product of incompletely oxidised fates is KETONES
  • during extreme caloric restriction, carbohydrate restriction, or full starvation, liver begins to rapidly oxidise fatty acids for energy; leads to production of large quantities of ketone bodies
  • ketone bodies cannot be further metabolised by liver cells to be appreciable amount enter bloodstream
  • accumulation of ketone bodies in blood is cakked KETOSIS; can lead to a dangerous lowering of blood pH called KETOACIDOSIS
  • people w/ diabetes who do not closely control BGL are at high risk of ketoacidosis. w/o insulin cells will switch fat oxidation for glucose production in order to meet metabolic demands
38
Q

Metabolic absorptive state

A

occurs right after feeding and can last up to 4 hrs when ingested nutrients enter bloodstream

processes occur as nutrients are being absorbed from small intestine:

  • OXIDATION: of nutrient molecules which provide energy to cells
  • GLYCONEOGENESIS: stores excess glucose in skeletal muscle and hepatocytes
  • LIPGENESIS: stores triglycerides in adipocytes and hepatocytes
  • PROTEIN SYNTHESIS: provides structural materials for cells
39
Q

Absorptive state regulation

A

pancreatic hormone INSULIN orchestrates many absorptive state processes
- Release of insulin is triggered by inc BGL

  • oxidation of glucose, small amounts of AA & FA generates ATP for cells
  • AA enter cells for protein synthesis; excess glucose enters muscle and liver cells and is stored by glycogenesis
  • excess glucose, AA and FA are converted to triglycerides.
  • lipgenesis stores triglycerides in adipocytes and hepatocytes
40
Q

postabsorptive state

A
  • body usually instate in late morning, late afternoon and most of night
  • most body tissues switch from carbohydrate sources for energy to using FA ( stoed in adipose tissue)

processes in PAS:

  • break down of proteins in muscle cells, releases glucogenic AA into blood
  • KETOGENESIS in hepatocytes, converts fatty acids to ketone bodies and releases into blood
  • GLUCONEOGENESIS & GLYCOGENOLYSIS in hepatocytes release glucose into blood → crucial for brain
  • LIPOLYSIS in adipocytes releases fatty acids into blood
  • oxidation of molecules such as Fa provides most cells w/ fuel
41
Q

Pstabsorptive state regulation

A

Maintaining normal BGL is a challenge → gluvose enters blood from two major sources

  • glycogen breakdown in liver
  • gluconeogenesis using AA and glycerol

co-ordinated by:

  • GLUCAGON: released from pancreas and stimulates glycogenolysis and gluconeogenesis in liver
  • EPINEPHRINE: stimulates glycogenolysis in skeletal and cardiac muscle and liplysis in adipocytes
  • GLUCOCORTICOIDS: stimulate mobilisation of lipid and protein reserves; enhanced by GH
  • pancreatic hormone GLUCAGON released when BGL drops; triggers glycogenolysis & gluconeogenesis
42
Q

neural regulation of feeding

A

Hypothalamus houses two nuclei that ontrol homeostatic variables associated w/ feeding

  • SATIETY CENTRE: elicits feeling of fullness and inhibits desire to eat
  • HUNGER CENTRE: (feeding centre)elicits feelings of hunger and stimulates desire to eat
43
Q

endocrine regulation of feeding : long-term

A

primarily hormonal:

  • LEPTIN: produced by adipocytes; stimulates satiety centre and inhibits neurons in hunger centre
  • GHRELIN: produced by stomachl stimulates neurons in hunger centre to promote hunger
44
Q

endocrine regulation of feeding: short term

A

can also inhibit or stimulate feeding

  • INSULIN → decreases food intake
  • feeding stretches stomach walls and initiates release of gastrointestinal hormones → both stimulate vagus nerve to indirectly suppress hunger centre

Phys (14 decks)

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