Nutritional Requirements for Animals. for fuel (chemical energy) organic materials used in biosynthesis essential nutrients (substances that animals can’t make for themselves). The 8 essential amino acids must be obtained from food. Essential fatty acids are unsaturated.
Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author.While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server.
2. Digestion—food is broken down mechanically and chemically into small molecules
3. Absorption—small molecules are absorbed
4. Elimination—undigested material is eliminated
Intracellular Digestion—After food is engulfed by a cell, food is hydrolyzed by enzymes inside vacuoles
Animal Feeding Mechanisms
Extracellular Digestion— Occurs in a compartment continuous with the outside of the body
Animals without a full digestive tract have a gastrovascular cavity where food is broken down into smaller pieces. Cells can then engulf smaller particles.
Complete digestive tract (alimentary canal)—digestive tube connecting the mouth and anus
Alimentary canal = mouth, esophagus, stomach, small intestine, large intestine, rectum, anus
Accessory glands = salivary glands, gall bladder, liver, pancreas
Peristalsis is the rhythmic waves of contraction
of smooth muscles that push food along.
Salivary amylase breaks down food in the mouth.
The bolus goes down the esophagus by peristalsis.
(Swallowing is voluntary, but after that, everything’s involuntary.)
contain pepsin to digest proteins. HCl (also secreted) converts pepsinogen into pepsin. Pepsin can also
All the stuff
esophagus. The pyloric sphincter regulates the
flow of chyme into the small intestine.
Small intestine is long! (Small diameter) This is
where most of the digestion & absorption happens.
The duodenum is the first section of the small
intestine—chyme mixes with digestive juices from
the pancreas, liver, gallbladder and intestine.
The liver produces bile that’s stored in the gallbladder.
Bile helps to digest fats.
The inactive forms are
secreted from the pancreas
The small intestine has a large surface area for absorption. Villiproject into the lumen. Absorption takes place in the microvilli.
Cecum—ferments ingested material (mostly plants)
Appendix—extension of the cecum—thought to play a minor role in immunity
Many bacteria live in the human colon. Some produce vitamins that supplement our dietary intake.
Intestinal Adaptations—plants are harder to digest than meat since plant cells have cell walls.
Mutualistic Adaptations—many animals have large populations of microorganisms in their alimentary canals to digest cellulose and other macromolecules. Both the host and the microorganism benefit from the products of this digestion.
Ruminants are herbivores. They have four chambered stomachs to get the most nutrients from their diets.
Digestion is controlled by the enteric division of the autonomic nervous system. The presence of food stimulates peristalsis in the stomach and intestines.
The endocrine system also controls digestion by regulating energy storage, glucose levels, and appetite.
If energy taken in > needed excess is stored in liver and muscle cells as glycogen. Once glycogen stores are full, additional excess energy is stored in fat in adipose tissue.
The pancreas detects blood glucose levels.
Insulin decreases blood glucose levels.
Glucagon increases blood glucose levels.
Gastrin stimulates gastric juice secretion when food is present.
Secretin stimulates pancreas to secrete bicarbonate when chyme is in duodenum.
CCK (cholecystokinin) stimulates gallbladder to release bile when aa or fatty acids are in duodenum.
Appetite is regulated by hormones that affect the satiety center of the brain.
Ghrelin triggers feelings of hunger.
Insulin suppresses appetite after eating.
Leptin suppresses appetite when enough body fat is present.
PYY—suppresses appetite after eating (counters ghrelin)
Mutations in the gene for leptin or the leptin receptor have been found to cause obesity in mice.
The mouse on the right lacks a normal leptin receptor.