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Animal Physiology - Coggle Diagram
Animal Physiology
Animal Nutrition
Food Processing Stages
Ingestion
Prehension strategies (teeth, beaks, tongues, proboscises) determine particle size and feeding rate; particle size influences the surface area available for digestion
Cephalic-phase responses: sensory cues (sight, smell, taste) trigger anticipatory secretion (saliva, gastric acid, insulin) that primes digestive tract and reduces postprandial lag.
Digestion
Mechanical digestion: Mastication and stomach churning increase surface area and expose substrates to enzymes; segmentation in intestine enhances mixing.
Chemical digestion
Proteolysis: Begins with pepsin (stomach) and continues with trypsin/chymotrypsin in small intestine; zymogens are activated in lumen to avoid autodigestion.
Carbohydrate digestion: Salivary and pancreatic amylases break polysaccharides to disaccharides and monosaccharides; brush‑border enzymes (maltase, sucrase) finish hydrolysis.
Lipid digestion: Bile salts emulsify lipids into micelles; pancreatic lipase hydrolyzes triglycerides into monoglycerides and free fatty acids for absorption.
pH gradients and enzyme localization: Low gastric pH activates gastric enzymes and sterilizes food; bicarbonate from pancreas neutralizes chyme to optimize pancreatic enzyme activity.
Absorption
Monosaccharides and amino acids: Enter enterocytes via specific transporters (SGLT1 for glucose/Na⁺ cotransport; GLUT transporters basolaterally), then pass to capillaries and hepatic portal circulation.
Lipids: Form micelles, diffuse into enterocytes, reassembled into triglycerides, packaged into chylomicrons with apolipoproteins, and enter lacteals (lymphatics) to bypass first‑pass hepatic uptake initially.
Water, electrolytes, vitamins: Water follows osmotic gradients; vitamins vary (fat‑soluble absorbed with lipids; water‑soluble via transporters); B12 requires intrinsic factor and ileal receptors.
Enterocyte turnover and barrier: Rapid epithelial renewal maintains absorptive function; tight junction regulation controls paracellular permeability; immune surveillance in gut‑associated lymphoid tissue prevents pathogen translocation.
Elimination
Large intestine functions: Absorbs water/electrolytes, compacts feces; bacterial fermentation of residual carbs produces short‑chain fatty acids (SCFAs) absorbed as additional energy sources.
Microbiome role in elimination: Microbes synthesize vitamins (K, some B), metabolize bile salts, and contribute to fecal bulk; dysbiosis can alter stool consistency and systemic physiology.
Defecation reflexes: Coordinated by enteric and central nervous systems (rectal stretch → parasympathetic reflex → relaxation of internal anal sphincter; voluntary control over external sphincter).
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Diet neccesities
Chemical energy
Macronutrients supply calories converted to ATP via cellular respiration: glycolysis → pyruvate oxidation → Krebs cycle → oxidative phosphorylation; net ATP yield differs by substrate
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Carbohydrates: Rapidly metabolized; maintain blood glucose; fuel high-intensity work and central nervous system.
Fats: Dense long-term energy storage (triacylglycerols in adipocytes); fatty acids broken into acetyl‑CoA for high ATP yield; provide insulation and membrane lipids.
Proteins: Primarily structural/enzymatic; amino acids can be deaminated and fed into Krebs for energy during starvation or high-protein diets; nitrogen disposal via urea cycle in liver.
Amino acids: Provide carbon and nitrogen for protein synthesis, neurotransmitters, purines/pyrimidines; some are glucogenic or ketogenic depending on metabolic fate.
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Fatty acids and cholesterol: Build phospholipid bilayers, produce steroid hormones and signaling lipids (eicosanoids); membrane lipid composition affects fluidity and cell signaling.
(omega‑3/omega‑6): Precursors for inflammatory mediators and maintain membrane properties; deficiency affects growth, immunity, neural development.
Simple sugars and intermediates: Supply carbon skeletons for nucleotide synthesis and glycogen stores; central metabolites (e.g., acetyl‑CoA, citrate) link energy and biosynthesis.
Vitamins
Fat‑soluble (A, D, E, K): Stored in tissues; A for vision and epithelial maintenance; D for Ca²⁺ homeostasis; K for clotting.
Water‑soluble (B complex, C): Coenzymes (NAD+, FAD, coA, folate) and antioxidant role (C); deficiencies cause defined syndromes (scurvy, beriberi, pellagra).
Minerals
Electrolytes (Na⁺, K⁺) for membrane potentials
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I⁻ for thyroid hormones; trace elements serve catalytic roles (Zn, Cu, Se).
Adaptations
Herbivores
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Foregut (ruminants) or hindgut (horses, rabbits) chambers host fermentative bacteria/archaea/protists that hydrolyze cellulose into SCFAs absorbed by host.
Enlarged cecum or multi‑chambered stomachs, elongated intestines to increase retention time and exposure to microbes.
Coprophagy in some hindgut fermenters to recover microbial protein and vitamins; selective foraging to balance fiber and nutrient intake.
Carnivores
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apid digestion and pathogen suppression; high pepsin and low pH optimize protein breakdown and reduce reliance on microbial fermentation.
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Omnivores
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Intermediate gut length, mixed dentition for both tearing and grinding, broad enzymatic repertoire (amylases, proteases, lipases) to exploit variable diets.
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Microbiome evolution
Microbes assist in complex carbohydrate breakdown, vitamin biosynthesis, bile modification, and training the immune system; host diet strongly shapes microbial composition.
Vertical and horizontal transmission, rapid microbial adaptation to diet, and host genetic factors produce co adapted host microbe relationships with fitness consequences.
Regulation and Feedback
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Cholecystokinin
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Action: CCK stimulates pancreatic enzyme secretion and gallbladder contraction; slows gastric emptying to prolong intestinal digestion and absorption.
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Insulin and glucagon
Insulin (fed state): Stimulates glucose uptake (GLUT4 translocation in muscle/adipose), glycogen synthesis (liver/muscle), lipogenesis, and inhibits lipolysis; central to storing excess energy.
Glucagon (fasted state): Stimulates hepatic glycogenolysis and gluconeogenesis, mobilizing glucose; promotes lipolysis in adipose to supply energy substrates.
Appetite regulation
Short‑term
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PYY and GLP‑1: Released postprandially from intestine to promote satiety and slow gastric emptying; GLP‑1 also enhances insulin secretion (incretin effect).
Long‑term
Leptin: Proportional to adipose mass; signals energy sufficiency to hypothalamus, reducing food intake and increasing energy expenditure via melanocortin pathways.
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