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Chapter 26: Nutrition and Metabolism
Terms in this set (60)
Body weight seems to have stable, homeostatic set point that varies among individuals: heredity explains ~30-50% of the variation.
What explains the rest of the variation among individuals?
diet and exercise habits
Short-term regulators of appetite:
Peptide YY (PYY)
Long-term regulators of appetite:
-secreted by parietal cells in the gastric fundus
-produces the sensation of hunger and stimulates the hypothalamus to secrete growth hormone-releasing hormone
-Stimulates NPY center to drive sensation of hunger.
Peptide YY (PYY)
-secreted by enteroendocrine cells in the ileum and colon
-signals satiety and terminates eating
-secreted by enteroendocrine cells in the duodenum and jejunum
-stimulates secretion of bile and pancreatic enzymes but also stimulates the brain and sensory fibers of the vagus nerves, producing an appetite-suppressing effect
-signal to stop eating
-secreted by adipocytes throughout the body
-levels are proportional to one's fat stores
-secreted by the pancreatic beta cells
-stimulates glucose and amino acid uptake and promotes glycogen and fat synthesis
-regulates appetite; in hypothalamus
-2 neural networks: 1) neuropeptide Y (NPY) and 2) melanocortin
Neuropeptide Y (NPY)
-stimulated by ghrelin
-inhibited by insulin, PYY, and leptin and CCK
-stimulated by leptin
Leptin & insulin inform the brain of how much ___________ tissue the body has and activate mechanisms for adding or reducing ____________.
Which cell types produce and secrete the hormone ghrelin, and where are they found?
found in the gastric fundus
Ghrelin stimulates the hypothalamus to secrete ________________, which, in addition to stimulating the sensation of hunger, primes body cells to take up soon-to be absorbed nutrients.
growth hormone-releasing hormone
source of substrates for catabolism & anabolism, consisting mostly of fatty acids, glucose & amino acids (all come from triglycerides, glycogen, and proteins)
Catabolic vs Anabolic Pathways:
Catabolic those in which energy rich large (bio) molecules are broken down, so energy can be siphoned off and put to use. Consequence: biomolecules broken to constituent components, can be used in anabolic pathways.
Anabolic pathways synthesize large energy rich biomoleules from their constituent components.
tiny droplets with a core of cholesterol and triglycerides and a coating of proteins and phospholipids; transport hydrophobic lipids
4 major categories of lipoproteins
chylomicrons, high-density lipoproteins (HDLs), low-density lipoproteins (LDLs), and very low-density lipoproteins (VLDLs)
-the higher the proportion of protein to lipid, the higher the density
-produced in the absorptive cells of small intestine lining.
-Lipoprotein lipase attached to surface of endothelial cells is responsible for hydrolizing the lipids into monoglycerides and free fatty acids
Very low-density lipoproteins
VLDL/ LDL Pathway
Liver produces VLDLs --> 1) triglycerides removed and stored in adipocytes or 2) VLDLs become LDLs containing mainly cholesterol --> Cells absorb LDLs by receptor-mediated endocytosis
produced in the liver; empty shells when produced, circulate through body and pick up cholesterol from cells (removal mechanism that the liver is responsible for!), once returned to liver, two major processes that occur (we have learned about)
-vehicle for removing excess cholesterol from the body
Liver produces empty HDL shells --> HDL shells pick up cholesterol and phospholipids from tissues --> filled HDLs return to liver --> liver excretes excess cholesterol and bile acids
What is the mechanism by which exercise lowers blood cholesterol levels?
Exercise reduces the sensitivity of the right atrium of the heart to blood pressure, so the heart secretes less natriuretic peptide. Consequently, the kidneys excrete less sodium and water, and the blood volume rises. This dilutes the lipoproteins in the blood , and the adipocytes therefore consume more blood triglycerides. This shrinks the VLDL particles, which shed some of their cholesterol in the process, and HDLs pick up this free cholesterol for removal by the liver.
What environmental, lifestyle factors, contribute to elevated LDL levels?
saturated fats, cigarette smoking, coffee and stress
What effect does high blood cholesterol level have on arteries?
-cholesterol can build up on artery walls and eventually block blood flow to the heart (so heart can't receive oxygen)
Why is a high HDL:LDL ratio healthier than a high LDL:HDL ratio?
HDL removes cholesterol from the arteries and transports to liver for disposal.
Carbohydrates are absorbed as glucose, galactose, and fructose; the latter two are rapidly converted to ______________.
Cells convert the energy stored in glucose to energy stored in __________.
1) Glycolysis - splits a glucose molecule into 2 pyruvic acid molecules
2) Anaerobic fermentation - reduces pyruvic acid to lactic acid without using oxygen
3) Aerobic fermentation - requires oxygen and oxidizes pyruvic acid to carbon dioxide and water
The role of enzymes and coenzymes
Enzymes remove electrons; Coenzymes donate them to other compounds
What's the functional significance of removing electrons and donating them to rxns in later pathways?
produces a reduced coenzyme with a higher free energy content than it had before the reaction; coenzymes can act as temporary carriers of the energy extracted from glucose metabolites
NAD+ + 2 H --> NADH + H+
FAD + 2 H --> FADH2
What are the sources of coenzymes?
removal of H+ from enzymes
H+ & e- transfers result in reduced/oxidized coenzymes with higher/lower free energy content than before the reaction.
Glycolysis: major steps
1) Phosphorylation: hexokinase transfers inorganic phosphate from ATP to ADP to produce glucose-6-phosphate (G6P).
2) Priming: G6P is rearranged to form fructose-6-phosphate (F6P). F6P is phosphorylated to form fructose 1,6-phosphate, providing actiavtion energy. (step uses another ATP)
3) Cleavage: F1,6P splits into two 3C sugars, generating 2 PGAL (phosphoglyceraldehyde aka glyceraldehyde-3-phosphate)
4) Oxidation: removal of pair of hydrogen atoms from PGAL; converts NAD+ to NADH and H+. Phosphate group is also added to each 3C sugar from cell's pool of free phosphate ions.
5) Dephosphorylation: In 2 steps, phosphate groups are taken from the glycolysis intermediates and transfered to ADP, producing ATP. The 3C sugar becomes pyruvic acid.
End products of glycolysis
2 pyruvic acid + 2 NADH + 2 ATP + 2 H+
Of all the energy in the initial glucose molecule, at the end of glycolysis, most of that energy is where?
What are the effects of phosphorylation of glucose to G6P?
-keeps the intracellular concentration of glucose low, maintaining a concentration gradient that favors the continued diffusion of more glucose into the cell
-prevents the sugar from leaving the cell (phosphorylated compounds cannot pass through the plasma membrane); irreversible in most cells
-when oxygen isn't present
-used by cells without mitochondria, such as erythrocytes
-NADH donates a pair of electrons to pyruvic acid, reducing it to lactic acid and regenerating NAD+ (which can then be used to convert glucose to pyruvic acid during glycolysis)
What happens to the lactic acid produced by anaerobic fermentation?
-travels through the bloodstream to the liver
-when oxygen becomes available again, the liver oxidizes lactic acid back to pyruvic acid (oxygen needed for this contributes to the excess postexercise oxygen consumption)
-liver can also convert lactic acid back to G6P where it can be polymerized to form glycogen for storage or can remove the phosphate group and release free glucose into the blood.
-when oxygen is present
-forms 32 ATP
Matrix Reactions: controlling enzymes are in the fluid of the mitochondrial matrix
Membrane Reactions: controlling enzymes are bound to membranes of the mitochondrial cristae
After glycolysis, conversion of pyruvic acid to acetyl-CoA:
-pyruvic acid is decarboxylated to form a 2C sugar
-NAD+ removes hydrogen atoms from 2C to form acetyl group
-acetyl group binds to coenzyme A, forming acetyl-CoA
Citric Acid Cycle (CAC or Krebs Cycle)
1) CoA hands off acetyl group (2C) to oxaloacetic acid (4C compound), forming citric acid (6C).
2) Water is removed and citric acid molecule rearranges.
3) Hydrogen atoms are removed and accepted by NAD+, forming NADH + H+
4) Another CO2 is removed, forming 5C chain.
5) 6) repeat steps 3 and 4. Generate another CO2, leaving a 4C chain. (all 3 carbon atoms of pyruvic acid have now been removed as CO2)
7) Phosphorylate GDP to GTP. GTP transfers the phosphate to ADP to make ATP.
8) 2 hydrogen atoms are removed and accepted by FAD to form FADH2.
9) Water is added.
10) 2 final hydrogen atoms are removed and accepted by NAD+ to form NADH + H+, generating oxaloacetic acid.
purpose of the membrane reactions
1) oxidize NADH and FADH2 and transfer their energy to ATP
2) to regenerate NAD+ and FAD and make them available again to earlier reaction steps
Electron Transport Chain
Flavin mononucleotide (FMN), Iron-sulfur (Fe-S) centers, Coenzyme Q (CoQ), Copper (Cu) ions, and Cytochromes (b, c1, c, a, a3)
3 enzyme complexes; CoQ and Cytochrome C shuttle electrons between complexes
ATP synthase transports H+ from intermembrane space to mitochondrial matrix
ATP synthase harnesses this energy to drive ATP synthesis; "push" created by the electrochemical H+ gradient
the synthesis (anabolism) of fat from other types of molecules
Intermediates in carbohydrate metabolism can be used in lipogenesis:
PGAL --> Glycerol
Acetyl-CoA --> fatty acids
the breakdown of fat for fuel
-Begins with the hydrolysis of triglyceride to glycerol and fatty acids and subsequent oxidation by separate pathways for glycerol and fatty acids
-removes 2 carbon atoms at at time from the fatty acid, making an acetyl group each time
-Acetyl groups bond to coenzyme A to make acetyl-CoA, which can enter the citric acid cycle
-Excess acetyl groups can be metabolized in the liver via ketogenesis
How does ATP yield from fatty acid chains compare with ATP yields from glucose?
eat fat molecule generates 3 fatty acids; ATP from fatty acids chains is greater than that from glucose
metabolism of excess acetyl groups by the liver, forming ketone bodies
-acetoacetic acid, beta-hydroxybutyric acid, and acetone
-Some cells can convert acetoacetic acid back to Acetyl-CoA for entry in TCA
-During high rates of fat oxidation, ketone bodies accumulate; blood ketone levels rise (ketosis) which can cause ketoacidosis
-Amino acids in the dietary pool can be converted to other amino acids, converted to glucose or fat, or directly used for fuel.
-Pathways for these variously involve deamination, amination, & transamination
amino acids used for fuel
1) deaminate them, creating a keto acid
2) keto acid may be converted to pyruvic acid, acetyl-CoA, or one of the acids of the CAC depending on which amino acid is involved
amino acids in gluconeogenesis
keto acids are used to synthesize glucose through reversal of the glycolysis reactions
-protein--> aa --> keto acids --> pyruvic acid --> glucose
amino acids in transamination, ammonia and urea
When an aa is deaminated, it's -NH2 group is transfered to CAC intermediate alpha-ketoglutaric acid, converting it to glutamic acid
-goes to liver where -NH2 group is removed to reform alpha-ketoglutaric acid. The -NH2 group become ammonia (NH3) and enter urea cycle.
the liver combines ammonia with carbon dioxide to produce urea, which is excreted in urine
amino acids in protein synthesis
-transamination reactions of CAC intermediates and from other aa in the liver can form all aa except the essential aa, which must be obtained from the diet
transamination of alanine to make pyruvic acid and glutamic acid
alanine + alpha-ketoglutaric acid --> pyruvic acid + glutamic acid
When is the peak bone mass?
A weight loss program should include what lifestyle changes?
What is the function of pepsinogen?
What is the relationship between biotin and alopecia?
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