MT 5 - Digestion and energy metabolism Flashcards

1
Q
  1. Food intake
A

•Cats: regularly, smaller amounts. Front-paws to grab food.
•Dogs: quickly, great amounts, one occasion. May use paws.
•Pigs: nose ring to nuzzle, grab food w. lower lip.
•Horses: use lips and bite w. corner teeth.
•Ru: pull w. tongue, and press it against lower incisors and dental plate to tear off.
-Chewing:
•Chewing muscles relaxed when mouth is empty by a reflex mechanism.
•Open mouth generates stretch receptors–stretch reflex.
•Mechanoreceptors in cortex stim. contraction and relaxation of tongue and cheek muscles.

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2
Q
  1. Swallowing
A

•Food->mouth->bolus->pharynx->esophagus
•Result of several contractions and relaxations of muscles
•Receptors in pillars of fauus, tonsils, soft palate and tongue
-Process of swallowing:
1.Bolus from oral cavity to pharynx:
a.Swallowing begins voluntarily. Food mixed with saliva forms bolus. Bolus is placed in the medial line bw. tongue and hard palate.
b.Soft palate rises and closes nasopharyngeal opening. Breathing is inhib., larynx rises and glottis closes.
c.Pressure pushes bolus to pharynx. Epiglottis is pushed back, pharynx is closed.
2.Bolus from pharynx to esophagus:
a.Muscle fibers contract around bolus and pushes it against esophagus.
b.At the same time, the pharyngoesophageal sphincter relax, and bolus enters esophagus.
3.Passing bolus in esophagus:
a.When bolus reaches upper part of esophagus, peristaltic movement begins, which pushes bolus towards stomach.
b.By effect of the peristaltic motion, tone of cardia decr., and bolus can enter stomach.

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3
Q
  1. Salivary secretion
A

•Bi-phasic process
•Primary secretion:
o Na+, Cl-, P and HCO3 (in Ru) are secreted into primary saliva by active secretion.
o Ptyalin and mucin is prod. and added by acini cells.
o Prim. saliva is prod. by diffusion and secretion.
•Secondary secretion:
o Electrolytes in prim. saliva is changed in the tubules
o Na+ and Cl- is partly reabs., while K+ and HCO3- is secreted.
o Ion reabs. is not followed by water reabs., due to that sec. saliva have lower osmolarity
o Ion exchange depends on the flow of saliva->more saliva secretion, less change in ion composition of prim. saliva.
-Regulation of salivary secretion:
•Parasymp: prod. high amount of saliva, poor in mucin
o Acetyl choline binds to muscarine receptors
o This incr. IC Ca2+ level, which incr. Cl- and Na+ secretion to lumen.
o High enzyme secretion is due to DAG and protein kinase C mechanism.
•Sympathetic: small amount of saliva, rich in mucin
o Cat: sympathetic activity incr. prod. of saliva
o By noradrenaline
o Stim. cAMP system.
•Aldosterone: Aldosterone conc. of blood significantly modifies Na+ abs. in the tubules.

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4
Q
  1. Electrophysiology of the gastrointestinal tract
A

-Slow wave potential: a rhythmic electrophysiological event in the GI tract
•Basic Electrical Rhythm (BER): el. activity generated by slow waves.
-Spike potential: the AP of GI SM cells.
•Slow waves triggers spike pot. when threshold level is reached
-Neurohormonal regulation
•Central neural regulation: chewing, swallowing, defecation
•Peripheral neural regulation: gastric, pancreatic, bile secretion,GI motility, intestinal juice prod.
-Extrinsic neuronal regulation
•Sympathetic: postganglionic
•Parasymp.: preganglionic
-Intrinsic neuronal regulation
•Plexus myentericus: efferent fibers of intrinsic regulation
•Plexus submucosae: afferent fibers and receptors of intrinsic regulation
-Gastrointestinal reflexes
•Intestines->prevertebral ganglion->intestines
o Gastic-colon reflex, Colon-gastric reflex, Colon-ileum reflex
•Intestines->spinal chord, brain stem->intestines
o Noiciceptive reflex, defecation reflex

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5
Q
  1. Motoric activity of the gastrointestinal tract
A

-Motility types: Passing-, mixing and villi movement
-Filling: SM become longer->intragastric pressure hardly changes (LaPlace law)
•Circular retraction - rolling-mixing contraction. Gastric content mixed with gastric secretion -> chyme
-Regulation of motor movements of stomach:
•Duodenal inhib. effects: Neuronal reflexes and hormonal (secretin, GIP, CCK)
•Gastric facilitating effects: V of foodstuff and gastrine
-Motor movements of ileum: Mingling, segmental movement, villi movement, proceeding: slow peristalsis
-Regulation of motor movements of ileum:
•N.splanchnicus: sympatheticinhibition
•N.vagus: parasympatheticexcitation
-Motor movements of colon: Responsible for microbial synthesis and reabs. of water and electrolytes.
•Ru: Retrograde flow
•Horses: 3 types of contraction
o Peristalsis + antiperistalsis->mixing in colon
•Ca:
o Small microbial synthesis
o Fast movement caused by an aboral-mass peristalsis
-Motor movements of rectum:
•Main role: evacuation (feces stored in colon)
•Defecation is under hypothalamic and cortical control.
•Efferentation: Pelvic nerves incr. contraction and peristalsis, relaxes sphincters.

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6
Q
  1. motility of the forestomachs
A

-Type of bolus:
*Light bolus (hay straw): Kept in dorsal sac of rumen for a longer period of time, until it becomes dense enough to sink down to the ventral sac->reticulum->omasum ->abomasum
*Heavy bolus: Enters directly to the ventral sac, then the reticulum shortly->omasum->abomasum
-Innervation:
•Parasympathetic vagus n. = incr. intensity and frequency
o Ventral vagus n. -> reticulum, omasum and abomasum, o Dorsal vagus n.-> rumen
•Sympathetic innervation = decr. forestomach motility.
-Ruminoreticulum cycle: synchronized, cyclic motility
•Sep. fermentation products according to density, and mix forestomach content and transport it to abomasum.

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7
Q
  1. Rumination
A
  • Digestion in ruminants
  • Result of a reflex mechanism, initiated by the mechanoreceptors in the ruminal mucosa, in the reticulum and the cardia.
    1) Regurgitation
    a. Bolus enters into cardia-esophagus
  • Saliva swallowing
  • Inspiration with closed glottis
  • Cardia opens reflexively
  • Regurgitation contraction
    b. Esophageal phase:
  • Bolus squeezed
  • Bolus is sep. and passed further by antiperistalsis
  • Bolus enters oral cavity
    2) Remastication and reinsalivation
    a. Remastication
    b. Mixing with saliva
    c. Swallowing with saliva (2-3 times)
    3) Redegutition
    a. Swallowing of the remasticated bolus
    b. Bolus is mixed in the rumen
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8
Q
  1. Eructation
A

•Gas production
•Gas location: on the top of the dorsal rumen sac
•Gas enters cardia:
o Stretch receptors of the dorsal rumen sac are stim. by distention of rumen wall due to gas accumulation.
o Dorsal sac, cranial and caudal ruminal pillars contract and press the gas cranially
o Simultaneously, reticulum dilates, which lets the cardia above the liquid level
• Antiperistaltic gas transport in the esophagus:
o The esophagus section bw the cardia and diaphragm is filled with gas
o Gas is passed towards the pharynx by antiperistalsis
•Gas leaves the rumen:
o A nasopharyngeal closure occurs->part of gas enters trachea and then lung, while the other part is emptied through nares.
o The gas-mixture in the lungs becomes balanced with the alveolar air->the compounds enter the circulation.

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9
Q
  1. Secretion and regulation of gastric juice
A

-Regions of the gastric mucosa:
•Aglandular region: microbial digestion (ru)
•Cardia: mucin–protection of gastric mucosa
•Fundus: HCl and pepsinogen synthesis
•Pylorus: mucin (protection), pepsinogen (digestion), gastrin (regulation)
-Type of cells:
*Parietal cells – HCl production
*Chief cells – Pepsinogen production
*Cells producing mucin
*G-cells - Gastrin prod., in mucosa in pylorus region.
-Gastrin: secreted to blood by effect of vagus n., and by chem. stim.
•H-cells - Histamine prod., in gastric mucosa
-Histamine: secreted by effect of vagus n. or gastrin.
-Pepsinogen: Stored in granules. Release stim. by n.vagus, or by low blood sugar induced by insulin.
•Degraded to pepsin at pH 2. (HCl)
•Histamine release incr. pepsinogen
-Pepsin:
•Hydrolyses peptide bonds which consists of Phe, Try and His aa, at pH 1,8-3,8.

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10
Q
  1. Regulation of gastric juice
A

•Regulation of parietal cells is usually divided into:
1.cephalic phase 2.gastric phase 3.intestinal phase
•Regulation of pepsinogen prod. cells occurs through an indirect way of HCl prod. by parietal cells.
•Parietal cells is regulated by acetylcholine, gastrin and histamine
1. Cephalic phase:
•The food in mouth stim. taste buds and then CNS.
•In CNS info. is gets to stomach->gastric juice secr.
•Vagus n.: incr. gastric secr. directly by stim. chief and parietal cells, and indirectly by stim. G-cells
-Gastric phase:
•Gastric content stim. stretch- and chemoreceptors in mucosa. Mechanical effects stim. chief and parietal cells, direct effect.
•Chem. stimuli activate G-cells, which indirectly incr. the prod. of gastric secr, until pH is 3.
•Gastrin stim. H-cells, which will indirectly incr. HCl prod.
•Pepsinogen prod. of chief cells is regulated by neurotransmitter of vagus n. and HCl.
•Regulation of CNS: parasympathetic vagus n. Mediator is acetylcholine, which binds to muscarine type receptors on G-cells, H-cells and parietal cells ->Incr. IC Ca2+ level.
-Intestinal phase:
•Substances get into duodenum->slight incr. in gastric juice secr->induce gastrin secr.

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11
Q
  1. The exocrine function of the pancreas
A

-Pancreas:
•Exocrine cells of pancreas is organized into acinar cells, with zymogen granules.
•Lumen is narrow, and form drainage tubules, which produces bicarbonate.
•Interlobular ducts are continued as extralobular ducts, which enters the pancreatic ducts that ends in duodenum.
-Function of pancreas: prod. pancreatic juice.
It has two main roles:
•Neutralize acidic gastric content getting into the duodenum
•Secretes enzymes essential for digestion of proteins, fats and carbs.

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12
Q
  1. Pancreatic enzymes
A
  • Pancreas secrete mainly enzymes in an inactive form, which are activated into the duodenum.
  • The activation is initiated by enteropeptidase, which produces trypsin (active) from trypsinogen.
  • Trypsinogen activates other proenzymes to active form.
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13
Q
  1. Regulation of pancreatic juice secretion
A

•By hormones and neurotransmitters.
oParasympathetic->vagal stimulus cause incr. enzymatic secretion, and slight incr. of electrolytes and water
oSympathetic->splanchnic stimulus cause decr. amount of pancreatic juice.
1) Cephalic phase
•High protein content, but small amount of juice is released
2) Gastric phase
•Parasympathetic effect dominates, gastrin appears in the blood. Enzyme secretion incr.
3) Intestinal phase
•Influenced by chyme in duodenum and jejunum.
•Slight acidity leads to high volume, much HCO3 and low enzyme content in the juice. Stim. by secretin.
•Presence of aa, FA or monoglycerides leads to pancreatic juice secretion that is rich in enzymes. Stim. by CCK.

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14
Q
  1. Function of bile
A

-Bile components: bile salts, cholesterol and lecithin, which form micelles
o Conjugated bile acids form salts with different cations=bile salts
o Lecithin has an amphiphatic character, found at the borders
o Cholesterol is hydrophobic, found inside the micelle
•Bile also contains pigments and electrolytes
•Lecithin incr. solubility of cholesterol, but if cholesterol level incr., extra amount may form a crystal
•Bile salts take part in emulsifying fat (secretory)
•Metabolic end-products and antibodies (excretory)

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15
Q
  1. Production of bile
A
  • Ba are synt. from cholesterol, and forms 50% of dry mass of bile
  • Prim. ba: cholic acids and chenodeoxycholic acid
  • Prim. ba can be conjugated with taurine and glycine in liver cells: glyco- or taurocholic acid
  • Prim. ba are dehydroxylated and deconjugated by bacteria in terminal end of ileum, and sec. ba are generated: deoxycholic acid (from cholic acid) and lithocholic acid (from chenodeoxycholic acid)
  • 95-98% of bile salts are abs. actively in ileum, and gets into liver via portal v., where hepatocytes take them up, conjugate them again, or hydrolyses the sec. ba and secrete them into bile.
  • A smaller portion (5%) is abs. passively from jejunum
  • Bile salt transp. to liver by the enterohepatic circ. inhibit ba synt. from cholesterol-> repression mechanism
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16
Q
  1. Regulation of bile
A

•N. vagus: PS effect cause fall bladder to slightly contract
•Secretin: Stim. bile secretion to intestine, but not bile prod. by parenchyma cells itself. Result in bile salt dilution, containin high HCO3 conc.
*Main role: buffering acetic intestinal content.
•Cholecystokinin: Secretion by intestinal cells is stim by high lipid content of chime.
*Contraction of gall bladder, and relaxation of sphincter-> incr. gall release to intestines-> emulsifies lipids so they get abs.
•Bile salts: Inhib. synt. of ba from cholesterol, but incr. prod. of bile
•Gall bladder: Not present in horse, giraffe, camel, elephant, pigeon and rat. The continuously prod. liver-bile is stored here, and extensively conc. Results in bladder bile, which contains the conc. bile components.

17
Q
  1. Catabolism of carbohydrates
A

-Startch:
•Oral cavity: Saliva ptyalin cleave straight chains
•Smaller and branched mol. are prod.->maltose, maltotrase, dextran
•Stomach: effect of salivary amylase last until gastric content is mixed.
•Later the low chem. reaction denaturises the enzyme.
•Small intestines: bi-phasic process: α-amylase of pancreatic juice hydrolyses starch to di- and oligosaccharides
•Brush border digestion:
o Small mol. bind to specific receptors having enzymatic effect, located on surface of enterocytes.
o Monosaccharides are generated this way, and can enter blood circ. by abs.
-Cellulose: Fibrous carbohydrate
•Can’t be digested my mammalian enzymes, must be cleaved by microbial enzymes.
•Horse:
-End-product is VFA
-Occurs in the colon
•Ca:
•Doesn’t digest large amount of cellulose, but microbial fermentation in colon is still important
•Carb molecules which are not abs. represent a significant osmotic P in colon, which would cause loss of water
-Ruminants:
•Microflora of rumen: competition bw protozoa and bacteria -> good
•Fermentation: end products is mostly VFA
•A part of the microbes, effectively deaminate aa, prod. branched FA
•Part of them prod. urease, by hydrolyzing carbamine, and release NH3

18
Q
  1. Absorption of carbohydrates
A

-Startch:
•Fru: facilitated by GLUT-5 transporter, NO E needed
•Glu/galactose: Sec. transport, need a special receptor
-Luminal receptor take up glu/gal only if Na+ binds before. Glu/gal and Na+ are diffused into cytoplasm.
•Here glu/gal is taken up by GLUT-2 transporter, and molecules are transp. to basal membrane. It enters interstitium by facilitated transport
-Ruminants:
•VFA: can diffuse through mucosa into blood.
If pH in the rumen decr., abs. of VFAs incr. to maintain optimal pH in rumen.
•Lactic acid: products of easily digestible carbs as grains. Usually low conc. in rumen, but sudden incr. can cause damage to mucosa, and leads to acidosis.
•Ammonia: big amount released from fermentative digestion of urea and protein, abs in rumen. Goes to liver via portal v., where urea is synt. from it.
•Low pH decr. ammonia abs., and high pH leads to a significant abs. (toxic)

19
Q
  1. Catabolism and absorption of lipids: lipids
A

-Lipids: majority of lipids in food is triglyceride, but also contains sterine, sterine-ester and phospholipids in a smaller amount.

20
Q
  1. Catabolism of lipids
A

-Begins through the luminal digestion with proteolytic enzymes prod. by stomach and pancreas. Proenzymes are cleaved to form activated enzymes.
•Pancreatic lipase: water-soluble molecule which can digest lipids at the lipid-water interphase.
o The surface of this interphase is extremely enhanced by emulsification
•Bile acids: can emulsify lipids inefficiently by itself, but with the help of lecithin, the emulsification is appropriate.
•Fat digestion results in 2 FA and one 2-monoglyceride which forms micelles combined with bile salts.
o In this form the digested products get to the brush border, where they can easily get through fat-soluble membrane.

21
Q
  1. Catabolism and absorption of lipids: Transport
A

•Products that enter enterocyte is transp. into sER.
o FA in sER are re-esterified, in which process sp. specific triglycerides are synt. by binding appropriate FA to 2-monoglyceride.
o The re-synt. triglyceride aggregates in sER, abs. cholesterol and phospholipid in a way to place the hydrophilic part towards the environment (chylomicrons).
•Apolipoproteins emerge onto surface of chylomicrons and direct its further transport and metabolism.
o Chylomicrons with the attached apolipoproteins get out of cell by exocytosis though basolateral side to IC space, where they get into lymphatic capillaries, and are transp. by lymph into blood

22
Q
  1. Catabolism of protein
A

•Cleavage of proteins may happen at inner regions (endopeptidases), or at terminal aa (exopeptidases). The result is peptides with 2-6 aa, appearing in small intestines. Some free aa are also present here.
•Further catabolism proceeds by brush border digestion, when peptidases of enterocytes catabolize peptides to tri- and dipeptides, as well as free aa.
-Stomach:
•Peptide digestion starts in the stomach.
•Chief cells prod. pepsinogen, which is cleaved by HCl into active pepsin. Pepsin will activate other pepsinogens in an autocatalytic way.
•Pepsin can hydrolyse bonds consisting of Phe, Tyr and His, at pH 1,8-3,8.
-Small intestines
•Peptide digestion primarily in proximal region
•Luminal membrane of duodenal and jejunal enterocytes contain large amount of peptidases. These enzymes catabolize polypeptides into aa and oligopeptides.
•Carboxypeptidases: cleaves free terminal aa from C-terminal of the polypeptide.
•Trypsin: hydrolyses carbonyl bonds with Arg and Lys.
•Chymotrypsin: cleaves carbonyl bonds with Tyr or Phe.
-Luminal and brush border digestion finish the digestion
o Amino peptidases: Cleave aa from N-terminal
o Dipeptidases: Cleave dipeptides into aa.
o Dipeptidil-aminopeptidases: Cleave dipeptides from N-terminal

23
Q
  1. Catabolism and absorption of protein: Protein absorption
A

•Aa and small peptides can get into enterocyte by facilitated diffusion or by active transport. The more hydrophobic and conc. an aa. is, the more significant diffusion is on its abs.
•Luminal side:
o Na+ symport systems is active transport of neutral aa, phenylalanine, methionine, proline and hydroxyproline.
o By facilitated transport: Hydrophobic neutral aa and alkaline aa.
•Basolateral side:
o From among the transport mechanisms operating with Na-symport, two are important:
-Small hydrophilic aa
-Structure dependent uptake of neutral aa
o Facilitated transport plays a role only in the transport of hydrophobic neutral aa

24
Q
  1. Electrolyte cycle of the intestinal canal
A

•Important function of GI-tract: reabs. of digestive secretion delivered into prox part of intestines.
•The sum of GI secretion forms a substantial fraction of ECF from which they are derived.
oThese compounds must return to ECF in order to maintain homeostasis
•Reabs. starts in distal section of small intestines, and ends in first part of large intestines.
•Water will follow transport of osmotically bound active subst.
•Glucocorticoids (small and large intestines) and aldosterone (only colon) regulates Na+ level by incr. its reabs. When Na+ is abs., K+ secretion incr..

25
Q
  1. Water transport
A
  • Enters with food and GI secretion
  • Small intestine water transport is mainly regulated by osmosis.
  • By abs. of digested luminal contents, contents in lumen become hyperosmotic, and water reabs. rapidly occurs.
26
Q
  1. Iron transport
A

•Abs. according to the need of the animal
•Iron transported to the animal by food is generally in water-nonsoluble complexes, which abstract abs.
o These complexes dissociate at low pH, with help of gastric HCl secretion.
o The destruction of complexes reduces Fe3+ to Fe2+.
o Transferrin, secr. by enterocytes in duodenum and jejunim, binds two iron ions and forms a Tf-Fe complex.
o Receptors at the surface of brush border bind the complex, and take them up by endocytosis
o In the cytoplasm, the receptor is released, and the complex moves to the basolateral side where iron is released.
o Free transferrin mol. are secr. back to intestinal lumen.
o Ferritrin will bind to excess Fe molecules

27
Q
  1. Digestion in the colon
A

-Carbohydrate:
•Microbial digestion happens in colon in simple stomach herbivores.
•Microbial digestion of cellulose is important because:
o Some carbs are not abs. in small intestines
o Carbs not abs. represents osmotic P in colon, and would cause water loss if not digested down to VFA
o They also neutralize acetic products, ensure long retention time, and dilute fermentation products.
-Protein
•Common features with ruminant forestomach.
•Bacteria in colon receive urea from blood to balance N-metabolism
•Rabbit: Microbial digestion occurs in cecum.
•In order to not loose microbial vitamins and proteins, rabbit digest their food two times.

28
Q
  1. Faeces formation
A

-Motions of the colon:
•Slow waves of colon arise from circular muscle layer and extend from there to longitudinal fibers.
•The stimuli from pacemaker areas spread both directions, which makes retrograde motions and mixing of intestinal content possible (antiperistalsis).
Peristalsis + antiperistalsis = mixing
•Dog and cat: aboral mass peristalsis
-Lieberkühn glands in colon prod. mucin for mechanical protection as well as feces formation, and HCO3- for buffering of VFA.
-Composition, dry mass and pH of feces vary greatly among the domestic species.
-Its color is based on stercobilin
-Contain organic indigestible subst. only to a small degree
•Proteins in feces originate from detached epithelium of large intestines, and from microbial origin.

29
Q
  1. Defecation:
A

-Rectum: main activity is regulation of storage and evacuation of feces.
-Most domestic mammals are unable to voluntarily regulate defecation, but e.g. in the dog a conditioned response can be developed.
-Defecation is under hypothalamic and cortical control.
1. Empty rectum
•A feces evacuation can be used if 15-20 mmHg P is exerted on the wall of rectum, and therefore feces are pushed from previous intestinal section, to the rectum.
•Spontaneous evacuation prevented by closing of inner and outer sphincter.
2. Feces gets into the rectum
•Afferent nerve fibers reach the S1-S4 segments of spinal cord
3. Feces evacuation reflex
•From medullary center, efferent stimulus incr. the contraction of rectum and peristalsis, and relaxes the tone of sphincter.
•Simultaneously with this the stimulus of somatic pudendal nerve causes the relaxation of external sphincter.
•During feces evacuation reflex caused by dilation and stretching of the wall of rectum, longitudinal muscles also contract. The consequence of this is shortening of rectum, and processing of its content in the aboral direction.

30
Q
  1. Avian digestion
A

-Food intake:
•Center of food intake is the hypothalamus
•High temp and protein in food decr food intake
•Low temp and egg prod. incr. food intake
•Beak is adapted for food-intake, no teeth, no soft palate, no parotid gland, unified oral-pharyngeal cavity.
-Esophagus:
•Peristalsis passes food to the crop or directly to stomach.
•Crop: temporal storage of food, and softening of it.
-Glandular stomach:
•Primary function is secretion of gastric enzymes.
*Mucous glands - mucin
*Complex glands - HCl, pepsinogen, mucin prod.
-Muscular stomach
•The inner layer is a ceratinoid layer, consisting of secretion of gizzard glands, detached epithelial cells and fragments of food.
•Motility is synchronized with the glandular stomach
-Duodenum: peristaltic and segmented contraction.
-Ileum: Fermentation occur
-Liver: Bile neutralizes the chyme and emulsifies lipids, and in some species it contains amylase.
-Pancreas: Pancreatic enzymes digest into the lumen, enterocyte enzymes digest in small intestines at brush border
-Cecum: two kinds of contractions:
1.Mixing: less powerful, but more frequent
2.Propulsive: stronger, but less frequent
•Small contractions mix the content, stronger ones pass it along by peristalsis and antiperistalsis.
-Colon, cloaca:
•Almost permanent anti-peristalsis passes urea from cloaca to colon/ceca, thus filling up the ceca.
•To recollect important end-products of microbial digestion, birds ingest parts of their feces. They are coprophagia. Significant because of vitamin supply.

31
Q
  1. Combustion heat of nutrients
A
  • Unit of (heat) energy: Calorie
  • 1 kcal = 1000 cal (heat)
  • 1 cal = 4.184 J
  • 1 calorie: amount of E required to raise the temp. of 1 gram of water by 1o Celsius.
  • Combustion of heat of a nutrient is equal to the amount of heat yielded by burning 1g of that nutrient.
  • Heat content of nutrients is measured by a bomb calorimeter.
  • The amount of heat measured by the bomb calorimeter is the maximum amount of heat that can be yielded by that nutrient in the body.
  • Combustion heat of carbohydrates and fats is equal to their physiological caloric value.
  • Proteins are not entirely combusted in the body. Some metabolites of proteins appear in the urine, which contain further combustible E
32
Q
  1. Utilisation energy of nutrients in the body
A

-Total Energy – Gross Energy (GE) (E excreted in faeces)->Digestible Energy (DE)(Fermentative E, E in urine)->Metabolizable Energy (ME)(Heat production, specific dynamic action)

33
Q
  1. Basal and resting energy metabolism, factors affecting metabolic rate
A
  • BMR – Basal Metabolic Rate: the energy production measured in an individual in complete resting state
  • RMR – Resting Metabolic Rate: measured in animals, and is very difficult to satisfy all criteria necessary for measurement
  • Components: specific dynamic action and continous utilisation of E
  • Diff. bw. BMR & RMR: the amount of E needed by the animal above the E used for vital processes during measurement of E in resting state.
34
Q
  1. Factors Affecting Metabolic Rate
A

•Somatic NS: Skeletal muscle
•Sympathetic autonomic NS: Metabolic processes
•Malnutrition: decr. MR to a fifth of their normal values.
•Endocrine system: incr. in metabolic rate:
oEpinephrine, Norepinephrine
oGrowth hormone
oThyroid hormone
•Specific dynamic action: 1–3 hours after food intake, the BMR incr.
•Temperature:
oInternal temp. changes alter metabolism by changing the velocity of chem. reactions in the body (van’t Hoffs law).
oEnvironmental temp. changes, under low critical/over high critical temp. incr. metabolism.
•Persistent changes in environmental temp.–acclimatisation mechanisms of thyroid hormones.
•Muscular activity: Incr. in metabolism
•Production: Requires higher E, above RMR, depends on type of product

35
Q
  1. Calorimetric methods, the definitions
A

-Direct - Lavoisier & Laplace’s Direct Calorimetry
*Chamber containing the animal is surrounded by ice. The amount of ice melted and water prod. was used to estimate heat generation.
*Disadvantages: Expired air and evaporation off the body are not measured. Animal is in a chamber of high humidity.
-Direct- Complex Direct Calorimetry: emission of water vapour from the body is also taken into account.
•Water of known temp. enters the outer casing of the heat isolated chamber
•Heat emitted from the animal heats up the water and so the temp. of the water leaving the casing is measured. From this value and the velocity of the flow, heat production can be calculated
•Advantages: E turnover can also be measured during motion or work
-Direct- Compensation Calorimeter:
•2 chambers of identical thermal capacity are connected, and in a space of constant temp.
•Animal in one chamber, electric bulb of known output in the other.
•Animal heats up its chamber, the bulb will warm up its chamber to keep the temp. equal in both chambers.
•E used by the bulb will be the same as the output of heat produced by the animal.
-Direct - Gradient Calorimeter:
•Double walled chamber: inner wall is a good heat conductor, outer wall keeps a constant temp..
•The heat diff. bw. the two walls is measured to calculate the amount of heat dissipated.
•Quick, simple and reliable calorimetric measurement
-Indirect Calorimetry:
1.Open system (Douglas bag): Environmental/atmospheric O2 inspired, expired air is measured.
2.Closed system (Krogh’s device): No atmospheric O2 inhaled. Oxygen is added to the system. Indicator directly shows amount of consumed O2.
*Disadvantage: Restricted ability to measure the O2-dependant E prod. only.
-Direct & Indirect Calorimetry : O2 consumption and CO2 prod. of the animal can also be determined.
*Gives exact and reliable data.

36
Q
  1. Importance of the respiratory quotient
A

-RQ=CO2(vol./time)/O2(vol./time)
•Hyperventilation: RQ incr.
•Metabolic acidosis: RQ incr. – respiratory compensation of acidosis increases the amount of expired CO2.
•After exercise: RQ falls (0.5) – paying back of O2 debt
•Fattening: RQ > 1
•Starving: RQ < 0.5
•RQ values can provide information about the qualitative composition of E sources

37
Q
  1. Neurohormonal regulation of food intake
A

-Hunger: lateral nucleus
o Lesion: aphagia (loss of ability to swallow)
o Stimulation: hyperphagia (abnormally incr. apetite)
-Satiety (being full): ventromedial nucleus
o Lesion: hyperphagia
o Stimulation: aphagia
• Appetite: amygdale and prefrontal cortex
• Nutritional regulatory signals:
o Glucostatic:
 Increased glu level->satiety
 Decreased glu level->hunger
o Aminostatic: Incr. free aa. in EC-fluid inhibits eating, and vice versa
o VFA effect: Incr. free VFAs in the blood->food intake is decr. or terminates
-Effects of GI tract:
•Hormonal effects
•Gastric and intestinal filling
•Temperature – high temp decr food intake
•Estrogen – low estrogen level incr sensation of hunger
•Volemia – hydrated organs leads to incr food intake, while dehydrated do not
•Density of the population
•Hierarchy hormonal effects on hunger
•Night-day cycle