• Plants and animals material contain a group of substances insoluble inwater but soluble in ether, chloroform and benzene, which are commonly calledas lipids.
• Like carbohydrates the fats contain carbon, hydrogen, oxygen but in thefirst two elements (C and H) are present more in fats.• Primary sources of fatty acids foroxidationDietary • Mobilization from cellular stores • LIPID DIGESTIONThere is no enzyme in the saliva capable of attackingfats. • In the case of ruminants, microbial lipase break down fats intofatty acids which are subsequently hydrogenated (converted from unsaturatedfatty acid to saturated fatty acids)• Whereas in the case of monogastrics, warming, softening, dispersionand mechanical separation of lipids from the other nutrients occurs in thestomach.
• The small size of fat particles allow for greater surface exposure topancreatic and intestinal lipases, which absorb on the particle surface andattack fatty acids resulting inhydrolysis of triglycerides to b-monoglycerides and free fatty acids(FFA). • Free fatty acids then combine with salt-phospholipids – cholesterolmicelles to from mixed micelles for efficient absorption. • Digestibility of fatty acid decreases when the length of carbon chainincreases. • A coarse fat emulsion enters the duodenum, which is the site of themajor process of fat digestion and absorption. • Emulsification of fat occurs in the small intestine after contact withbile salts – sodium glycocholate and sodium taurocholate.
This process reduces the lipid particle sizeto 500-1000 Ao (500-1000mm diameters).• The bile salts form aggregates called micelles where the polar or watersoluble portion is towards the periphery and the inner core comprises of theapolar or water insoluble fraction. • METABOLISMFatty acids must be activated in the cytoplasm beforebeing oxidized in the mitochondria. • Activation is catalyzed by fatty acyl-CoAsynthase • The net result of this activation process is theconsumption of ATP. • Fatty acid + ATP + CoA ——-> Acyl- CoA +PPi + AMP • Oxidation of fatty acids occurs in themitochondria. The transport of fatty acyl-CoA into the mitochondria isaccomplished via an acyl-carnitine intermediateThe process of fatty acidoxidation is termed b-oxidation since it occurs through the sequential removalof 2-carbon units by oxidation at the b-carbon position of the fatty acyl-CoAmolecule.
• Each round of b-oxidation produces one mole ofNADH, one mole of FADH2 and one mole of acetyl-CoA. • The acetyl-CoA— the end product of each roundof b-oxidation— then enters the TCA cycle, where it is further oxidized toCO2 with the concomitant generation of three moles of NADH, one mole of FADH2and one mole of ATP. • The NADH and FADH2 generated during the fatoxidation and acetyl-CoA oxidation in the TCA cycle then can enter therespiratory pathway for the production of ATP. • During high rates of fatty acid oxidation,primarily in the liver, large amounts of acetyl-CoA are generated. • These exceed the capacity of the TCA cycle, andresult is the synthesis of ketone bodies, or ketogenesis. • The ketone bodies are • acetoacetate,• b-hydroxybutyrate, • acetone Mobilization of Adipose Fatty Acids• During fasting or starvation, stored fuel needs to beutilized.
• the body secretes hormones such as epinephrine andglucagon.• These hormones release the second messenger cAMP which activatehormone-sensitive lipase.• HSL hydrolyzes stored TG to release FA.• The mobilized fatty acids are released into thebloodstream where they associate with albumin and cirulate to various tissuesin need of fuel.KETOSIS• Ketotic cows often have low blood glucose (blood sugar) concentrations. • When large amounts of body fat are utilized as an energy source tosupport milk production, fat is sometimes mobilized faster than the liver canproperly metabolize it.
• If this situation occurs, ketone production exceeds ketone utilizationby the cow, and ketosis results. • Dairy cattle normally produce ketones at low levels for use as energysubstrates. • It is only when ketone production exceeds demand that problems arise andketosis occurs. • Ketosis is important because it decreases feed intake in affected cowsand greatly increases the risk of other diseases. • Prevention is by feeding niacin in ration of cows prior to calving atthe rate of 6-10 grams/head/day. • Feed glucose precursors. Glucose precursors should increase glucoseproduction by the liver, thereby reducing the need to mobilize body fat to meetenergy demands.
• The two commonly available glucose precursors are propionate, in theform of Ca+ propionate and propylene glycolOTHERABNORMALITIES• Fatty liver in cattle.v Increase in triacylglcerol in hepatocytes Hyperlipidemia