Download Free Medical Lipids Metabolism PowerPoint Presentation

Lipids Metabolism PowerPoint Presentation

DOWNLOAD MEDICAL POWERPOINT PRESENTATION

About This Presentation

Description : Check out this medical PowerPoint presentation titled "Lipids Metabolism".

This medical PowerPoint presentation talks about Lipid metabolism which refers to the processes involved in the synthesis, utilization, and breakdown of lipids (fats and oils) in the body. Lipids serve as a source of energy, play a structural role in the cell membrane, and serve as signaling molecules.

The main types of lipids in the body are triglycerides, phospholipids, and cholesterol. Triglycerides are the main form of energy storage in the body, while phospholipids are important components of cell membranes. Cholesterol plays a key role in membrane structure and is a precursor for the synthesis of steroid hormones.

Lipid metabolism is regulated by several hormones, including insulin, glucagon, and epinephrine. Insulin stimulates the storage of triglycerides in adipose tissue, while glucagon and epinephrine stimulate the breakdown of stored triglycerides to release energy.

The process of lipid metabolism involves several steps. First, lipids are broken down into their component parts, including fatty acids and glycerol. Fatty acids are transported to cells throughout the body where they can be utilized for energy production or stored as triglycerides. Glycerol can also be used for energy production or converted to glucose through a process called gluconeogenesis.

In addition to the breakdown and utilization of lipids, lipid metabolism also involves the synthesis of new lipids. This process occurs mainly in the liver and involves the conversion of glucose or amino acids into fatty acids, which are then used to synthesize triglycerides.

Disruptions in lipid metabolism can lead to several diseases, including obesity, diabetes, and heart disease. For example, excess consumption of dietary fats and sugars can lead to the accumulation of triglycerides in adipose tissue, which can contribute to obesity and insulin resistance. Additionally, high levels of cholesterol can contribute to the development of atherosclerosis, which can lead to heart disease.

Tags : Lipids Metabolism, triglycerides, phospholipids, cholesterol, endocrinology, endocrinology PowerPoint presentation

Published on : Apr 18, 2023 | Views : 2433 | Downloads : 8

Shareable Url :

Embed Code :

Comment

Transcript

Slide 1-

Lipids Metabolism
Slide 2-

Definition of Lipids Naturally occurring compounds Dietary essential constituents Known as fats and oils Hydrophobic and soluble in ethanol, alcohol, petroleum and chloroform High energy value(9 kcal/g)
Slide 3-

Classification of Lipids Classified into Fats Waxes Steroids Terpenoides Phospholipids Glycolipids
Slide 4-

Type of Lipids(on the basis of chemical bonding ) Saturated fat Animal fat like meat, milk, butter Vegetable oil like coconut and palm kernel oil
Slide 5-

contd…Type of Lipids(on the basis of chemical bonding ) Monounsaturated fat Plant and animal product like olive oil, canola oil and peanut oil Polyunsaturated fat Plant source like corn, cottonseed, sunflower oil and soybean oil
Slide 6-

Location of Lipids Most tissues including fat depots which occur mostly Under skin In the omentum Around the kidneys The depot fat is mainly neutral fat i.e triglycerides
Slide 7-

contd…Location of Lipids Lipid of other tissues consist of Neutral fat phospholipids cholesterol glycolipids
Slide 8-

Lipids Functions Excellent energy reserves Structure of cell membranes Organ padding Body thermal insulation Essential fatty acids (EFA) Hormone synthesis Fat soluble vitamin absorption
Slide 9-

Explanation Insoluble in water Therefore all lipids in blood plasma occur in the form of complexes They are made water miscible due to their content of electrically charged molecules Phospholipids Specific protein
Slide 10-

Explanation Plasma lipids are carried in two forms Lipoproteins Free Fatty Acids The lipoproteins Chylomicrons LDL HDL The free fatty acids(FFA) also called Non esterified fatty acids (NEFA) Unesterified fatty acids (UFA)
Slide 11-

Lipids Disorder Lipids deficiency (Shortage in Lipids intake) Lipids exceeding (Overtaking in Lipids intake)
Slide 12-

Lipids Exceeding Fat should comprise not more than 30% of total calories to prevent lipids exceeding To prevent overtaking, we should consume fat breakdown (% total calories) <8% from saturated fat 10% from polyunsaturated fat 10-15% from monounsaturated fat
Slide 13-

Health Problems Energy Intake > Energy needed = Lipids overtaking Develop medical problem Cancer Heart disease Diabetes Obesity High blood pressure High blood cholesterol
Slide 14-

Blood levels for Lipids Total Cholesterol: <200 mg/dl = desirable 200-239 mg/dl = borderline hyperlipidemia >240 mg/dl = hyperlipidemia LDL < 130 mg/dl is favorable HDL > 35 mg/dl is favorable
Slide 15-

Prevention of Lipid Disorder Reduce fat Cut down on high fat foods E.g. butter, margarine, oil, mayonnaise
Slide 16-

Prevention of Lipid Disorder Increase intake of vegetables, fruits, and whole grains Loaded with fiber Contain high amounts of vitamins, minerals, and phytonutrients Include low-fat protein-rich food with every meal E.g. beans, eggs, and fish
Slide 17-

Prevention of Lipid Disorder Slow down when eating Too fast eating will exceed calorie needs before realizing we are full
Slide 18-

Lipid Metabolism
Slide 19-

Lipid Metabolism
Slide 20-

Utilization of Depot Fat The depot fat is stored as a source of energy (9 kcal per gram) Lipolysis of the neutral fat of the adipose tissue results into into fatty acid and glycerol Catalyzed by 3 lipase which catalyze 3 successive steps
Slide 21-

Lipid Metabolism
Slide 22-

Utilization of Depot Fat (Adipose Tissues) Triglyceride + Water Diglyceride + Fatty acid Catalyzed by triglyceride lipase
Slide 23-

Utilization of Depot Fat (Adipose Tissues) Diglyceride + Water Monoglyceride + Fatty acid Catalyzed by diglyceride lipase
Slide 24-

Utilization of Depot Fat (Adipose Tissues) Monoglyceride + Water Glycerol + Fatty acid Catalyzed by monoglyceride lipase
Slide 25-

Utilization of Depot Fat STEP 1 is rate limiting one and cAMP is involved in its activation Insulin inhibits lipolysis by stimulating lipogensis Prostaglandins also inhibit lipolysis by decreasing cAMP levels
Slide 26-

Utilization of Depot Fat (Adipose Tissue) Fate of both constituents of fat is different Fate of glycerol Fate of fatty acids
Slide 27-

Fate of Glycerol Adipose tissue lack the enzyme glycerol kinase required for this reaction Glycerol + ATP Glycerol 3-phosphate + ADP Essential for the further utilization of glycerol
Slide 28-

Fate of Glycerol Due to the absence of glycerol kinase, adipocytes (fat cells) cannot utilize the glycerol librated from triglyceride Glycerol is librated into the blood stream and is carried to liver where it is converted into glucose
Slide 29-

Fate of Glycerol Glycerol used for esterification with fatty acids (lipogenesis) in the adipose tissue has to be present as glycerol 3-phosphate which is supplied by glucose metabolism
Slide 30-

Fate of Fatty Acids Fatty acids in plasma (free fatty acids) circulate in combination with plasma albumin Oxidized to supply energy This occurs in mitochondria of many tissues where the citric acid cycle takes place
Slide 31-

Fate of Fatty Acids Oxidative phosphorylation also takes place in mitochondria In the cytosol of a tissue cell, fatty acid undergo 2 different fates depending upon their chain length
Slide 32-

Fate of Fatty Acids Long chain fatty acids (12 carbon or longer) are acted upon by Acyl-CoA synthetase (thiokinase) present in endoplasmic reticulum Long chain fatty acyl-CoA is then transported across the inner mitochondrial membrane by carnitine
Slide 33-

Fate of Fatty Acids Short (2-3 C atoms) and medium chain fatty acids(4-10 C atoms) easily pass through inner mitrochondrial membrane Changed their CoA derivatives by acyl-CoA synthetases in mitrochondrial matrix
Slide 34-

Fatty Acid Oxidation Fatty acids are oxidized by Beta oxidation Omega oxidation Alpha oxidation
Slide 35-

Beta Oxidation of Saturated Fatty Acid CH3-(CH2)14-COOH + 23 O2 16 CO2 + 16 H2O Large amount of energy is produced Palmatic acid (16 carbon) is taken as prototype Palmitic acid first gives rise to 14 C fatty acid along with 2 C fragment
Slide 36-

Beta Oxidation of Saturated Fatty Acid The 14 C fatty acid is successively broken down to 12 C Then to 12 C fatty acid Then to 10 C fatty acid and so on till the last 2 C fragment is left behind in the form of acetyl-CoA
Slide 37-

Beta Oxidation of Saturated Fatty Acid 8 moles of acetyl-CoA are formed of 1 mole of palmitic acid Enzyme catalyzing reactions of beta oxidation occur in mitochondrial matrix
Slide 38-

Over View
Slide 39-

Complete Beta Oxidation of Palmitic Acid 7 Cycles 8 CH3COSCoA + 7 FADH2 + 7 NADH + 7 H+
Slide 40-

Lipid Metabolism
Slide 41-

Fatty Acid Activation Enzyme acyl-CoA snthetase also called fatty acyl thiokinase Reaction occur in cytosol Irreversible as pyrophosphatase (PPi) is hydrolyzed Palmitic acid + CoA + ATP Palmityl-CoA + AMP +PPi
Slide 42-

Beta Oxidation
Slide 43-

Beta Oxidation
Slide 44-

Beta Oxidation
Slide 45-

Beta Oxidation
Slide 46-

Beta Oxidation
Slide 47-

Beta Oxidation
Slide 48-

Energy Output in Fatty Acid Oxidation Beta oxidation of 1 mole of palmitic acid yields 8mole of Acetyl CoA One mole of Acetyl CoA yields 12 ATP So total 96 ATP are formed
Slide 49-

Energy Output in Fatty Acid Oxidation In addition 7NADH+H+ and 7FADH 1NADH+H+ yields 3ATP and total 21 ATP 1FADH2 yields 2ATP and total 14ATP Hence total 96+35=131ATP are formed.
Slide 50-

Energy Output in Fatty Acid Oxidation However in 1st step where Palmitic acid is changed to active form Palmitoyl-CoA one ATP was used. Which shows expenditure of 2 high energy phosphate bond Thus complete oxidation yields 131-2=129ATP.ss
Slide 51-

Oxidation of Odd Chain Fatty Acids In human metabolism, mostly even fatty acids are imp. But some odd carbon no. fatty acids are also there. Oxidation at successive carbon atoms continues, each cycle produce 1Acetyl CoA
Slide 52-

Oxidation of Odd chain fatty acids Finally 3C comp. Propionyl-CoA is formed. It change to Succinyl-CoA Propionyl-CoA+ CO2Biotin dependent Propionyl CoA Carboxylase D-methylmalonyl-CoA epimerase Epimerisation L-Methylmalonyl-CoA Methylmalonyl-CoA mutase 5-deoxyadenosyl cobalamin as cofactor of this enzyme Succinyl-CoA
Slide 53-

Oxidation of Odd Chain Fatty Acids Succinyl-CoA enter citric acid cycle. May form glycogen (gluconeogenesis) For synthesis of porphyrins In utilization of acetoacetic acid
Slide 54-

Oxidation of Unsaturated Fatty Acids Mono and poly unsaturated fatty acids are 50% of human diet. Beta-oxidation occur in trans configuration. For beta-oxidation double bond at carbon no. 2 has to be trans
Slide 55-

Oxidation of Unsaturated Fatty Acids Start from –COOH (Carboxyl) end of fatty acid and 1 Acetyl-CoA formed in each step cycle.
Slide 56-

Measures which body adopt if fatty acid has cis configuration If cis bond is at carbon 3, enzyme enoyl-CoA isomerase convert fatty acyl CoA to double bond at carbon no. 2. and then beta-oxidation occur
Slide 57-

Measures which body adopt if fatty acid has cis configuration If fatty acyl CoA has 2 double bonds i.e. one trans at carbon 2 and one cis at carbon 4 then enzyme 2,4 dienoyl reductase removes one of these 2 double bonds by adding 2H taken from NADH+H+ and one trans bond is formed at carbon no. 3. then enzyme enoyl-CoA isomerase shifts double bond to carbon no. 2 and beta-oxidation occur.
Slide 58-

Omega oxidation of fatty acids Start from terminal omega methyl group and formation of omega hydroxy fatty acid Then –CH2OH oxidized to –COOH. Then beta-oxidation occur Occur in liver
Slide 59-

Alpha oxidation of fatty acids Occur in branched chain fatty acids e,g, Phytanic acid (3,7,11,15 tetramethylhexadecanoic acid) Beta-oxidation not occur because beta carbon is blocked by methyl groups. First oxidation occur at alpha carbon and alpha hydroxy derivativesformed.
Slide 60-

Alpha oxidation of fatty acids Further oxidation removes alpha carbon and then beta-oxidation occur. Propionyl-CoA is formed not the acetyl-CoA. Propionyl-CoA Succinyl-CoA Succinyl-CoA enter citric acid cycle.