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fat metabolisim
Mind map of lipid metabolism. There are many types of lipids and complex structures, which determine the diversity and complexity of their functions in the living body. Lipids are a wide variety of macromolecular substances with complex structures.
Edited at 2023-10-26 21:56:19
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fat metabolisim
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fat metabolisim
The composition, function and analysis of lipids
There are many types of lipids and complex structures, which determine the diversity and complexity of their functions in living bodies.
Lipid molecules are not encoded by genes and are independent of the genetic information system from genes to proteins. Not easily soluble in water is its most basic characteristic. This determines the particularity of lipids in a living body that has proteins as the genetic information system and water as the basic environment. It also determines its special importance in life activities or the occurrence and development of diseases.
Lipids are a wide variety of macromolecular substances with complex structures
Lipid is a general term for fats and lipids
Fats and Triglycerides
Esters include sterols and their lipids, phospholipids and glycolipids, etc.
Triglycerides are fatty acid esters of glycerol
Triglyceride is a lipid formed by lipidizing the three hydroxyl groups of glycerol with the same or different fatty acids.
Structure: Its fatty acyl chain has a complex composition with various lengths and degrees of saturation.
The type of fatty acid composition determines the melting point of triglycerides, which increases with the increase in the chain length and number of saturated fatty acids.
Fatty acids are carboxylic acids of aliphatic hydrocarbons
The general structural formula of fatty acids is CH3(CH2)nCOOH
Fatty acids containing one double bond are called monounsaturated fatty acids
Fatty acids with two or more double bonds are called polyunsaturated fatty acids
Phospholipid molecules contain phosphoric acid
Phospholipids containing glycerol are called glycerophospholipids (most abundant in the body)
Structure: Contains a polar head and two hydrophobic tails, forming the phospholipid bilayer of biological membranes
Cholesterol has cyclopentane polyhydrophenanthrene as its basic structure
Cyclopentane polyhydrophenanthrene is a common structure of sterols
The most abundant steroid compound in animals is cholesterol. Plants do not contain cholesterol but contain plant sterols.
Lipids have a variety of complex biological functions
Triglycerides are important energy substances for the body
Fatty acids have many important physiological functions
Provides essential fatty acids
The human body cannot synthesize fatty acids that must be provided by plants, called essential fatty acids
Synthetic unsaturated fatty acid derivatives
Prostaglandins, TX and leukotrienes have strong biological activity
PGE2 can induce inflammation, promote local blood vessel dilation, increase capillary permeability, and cause redness and swelling. Symptoms such as pain and heat
Phospholipids are important structural components and signaling molecules
Phospholipids are important components of biological membranes
Cardiolipin is the main lipid that builds body membranes
Phosphatidylinositol is the precursor of the second messenger
Cholesterol is an important component of biological membranes and the precursor of sterols with important biological functions.
Cholesterol is a basic structural component of cell membranes
Cholesterol can be converted into some sterol compounds with important biological functions
Cholesterol can be converted into bile acids in the liver, Converts to vitamin D3 in skin
The complexity of lipid components determines the complexity of lipid analysis technology
Extraction of lipids using organic solvents
Neutral lipids use less polar organic solvents such as ether, chloroform, and benzene.
Membrane lipids use relatively polar organic solvents such as ethanol and methanol.
Separation of lipids by chromatography
Chromatography, also called chromatography, is the most commonly used and basic method for lipid separation. There are two forms of column chromatography and thin layer chromatography
Silica gel is usually used as the stationary phase, and organic solvents such as chloroform are used as the mobile phase.
Select analytical methods based on analytical purpose and lipid properties
After chromatography, use dyes such as basic rhodamine, rhodamine or iodine to develop color.
Complex paper analysis requires special processing
Digestion and absorption of lipids
Bile salts assist digestive enzymes in digesting lipids
Lipids are insoluble in water and cannot fully come into contact with digestive enzymes. (The upper part of the small intestine is the main place for lipid digestion)
Bile salts have a strong emulsifying effect: they can reduce interfacial tension and convert large substances into small micelles, increase the contact area between digestive enzymes and lipids, and promote lipid digestion. Disadvantages: It can easily inactivate digestive enzymes
Conditions: 1. Emulsifying effect of emulsifier
2 The catalytic effect of enzymes
Colipase prevents pancreatic esterase from denaturing and inactivating at the lipid-water interface
The absorbed lipids are resynthesized and enter the blood circulation
Lipids and their digestion products are mainly found in the lower duodenum and upper jejunum
1Triglycerides are taken up by intestinal mucosal cells after being emulsified by bile salts. It is hydrolyzed into fatty acids and glycerol under the action of intracellular lipase, and enters the blood circulation through the portal vein.
2 Long-chain fatty acids are first converted into fatty acyl-CoA in small intestinal mucosal cells, and then catalyzed by smooth endoplasmic reticulum CoA transferase and powered by ATP, triglycerides are re-synthesized and combined with lipids synthesized in rough endoplasmic reticulum. Proteins, phospholipids, and cholesterol are assembled into chylomicrons, which are secreted by intestinal mucosal cells and enter the blood circulation through the lymphatic system.
Lipid digestion and absorption play an important role in maintaining the body's lipid balance
The small intestine has a selective barrier, and its ability to digest and absorb lipids has great plasticity.
Function: 1. Promote the digestion and absorption of lipids when intake increases, ensure the supply of energy in the body, essential fatty acids, and fat-soluble vitamins.
2 Enhance the body’s ability to adapt to food-deficient environments
triglyceride metabolism
Oxidative decomposition of triglycerides produces large amounts of ATP
Triglyceride catabolism begins with fat mobilization
Fat mobilization definition: The process in which fat stored in white adipocytes is gradually hydrolyzed under the action of lipase (hormone-sensitive triglyceride lipase) to release free fatty acids and glycerol for oxidation and utilization by other tissue cells.
Lipolytic hormones: (can initiate fat mobilization and promote fat hydrolysis into free fatty acids and glycerol) epinephrine, norepinephrine, glucagon, etc.
Anti-lipolytic hormones: insulin, prostaglandin E2, niacin
Glycerol is converted into glycerol 3-phosphate and used
Glycerol can be directly transported through the blood to the liver, kidney, intestine and other tissues for utilization. It is catalyzed by glycerol kinase. The glycerol produced by fat mobilization is mainly taken up and utilized by the liver.
Beta-oxidation is the core process of fatty acid breakdown
Fatty acids can be activated by fatty acids, transferred to mitochondria, and β-oxidized to generate acetyl CoA and acetyl CoA, which enter the tricarboxylic acid cycle.
Activation of fatty acids into fatty acyl-CoA
Catalyzed by fatty acyl-CoA synthetase on the endoplasmic reticulum and outer mitochondrial membrane
Fatty acyl-CoA contains high-energy sulfide bonds, which not only improves reaction activity, but also increases the water solubility of fatty acids. Activation of one molecule of fatty acid actually consumes two high-energy phosphate bonds
Fatty acyl-CoA enters mitochondria
The key enzyme is carnitine acyltransferase I
The entry of fatty acyl-CoA into mitochondria is the rate-limiting step in fatty acid β-oxidation
Fatty acyl-CoA breaks down to produce acetyl-CoA, FADH2 and NADH
It undergoes four processes: dehydrogenation, water addition, dehydrogenation, and thiolysis.
Fatty acid oxidation is an important source of ATP in the body
Taking soft fatty acids as an example, complete oxidation of one molecule of soft fatty acids requires 7 β-oxidations to generate 7 molecules of FADH2, 7 molecules of NADH, and 8 molecules of acetyl CoA. A total of 108 molecules of ATP are generated, with a net generation of 106 molecules of ATP.
Different fatty acids contain different oxidation methods
β-oxidation of unsaturated fatty acids requires a configuration change
Unsaturated fatty acids also undergo beta-oxidation in mitochondria
Very long carbon chain fatty acids need to be oxidized into shorter carbon chain fatty acids in peroxisomes.
Propionyl CoA is converted to succinyl CoA for oxidation
Fatty acid oxidation can also proceed from the distal methyl end
Fatty acids are broken down in the liver to produce ketone bodies
Ketone bodies include acetoacetate, beta-hydroxybutyrate, and acetone
Features: Intrahepatic production, external use
Reason: Tissue distribution specificity of enzyme
The key enzyme is hydroxymethylglutarate-CoA synthase
Acetoacetate is utilized in heart, kidney, brain and skeletal muscle mitochondria, and is catalyzed by succinyl-CoA transsulfurase. 2 In heart, kidney and brain mitochondria catalyzed by acetoacetate thiokinase
Ketone bodies are small molecules, soluble in water, and can be transported in the blood. They can also pass through the blood-brain barrier and be transported to extrahepatic tissues for use through the capillary walls of muscle tissue.
Helps maintain constant blood sugar levels and save protein consumption
Under normal circumstances, blood only contains a small amount of ketone bodies, ranging from 0.03 to 0.5mmol/L.
Production regulatory factors: Meal status affects ketone body production Glucose metabolism affects ketone body production Malonyl-CoA inhibits ketone body production
Fatty acids from different sources synthesize triglycerides in different organs through different pathways.
Liver, adipose tissue and small intestine are the main sites for triglyceride synthesis
Fat cells can store large amounts of triglycerides and are the body's "lipid depot" for storing triglycerides.
Glycerol and fatty acids are the basic raw materials for the synthesis of triglycerides
Small intestinal mucosal cells primarily use ingested triglyceride digestion products to resynthesize triglycerides in the form of chylomicrons
There are two pathways for triglyceride synthesis: monoglyceride and diglyceride.
Fatty acid activation into fatty acylCOA
Small intestinal mucosal cells synthesize triglycerides via the monoglyceride pathway
Liver and adipose tissue cells synthesize triglycerides via the diacylglycerol pathway
The synthesis of endogenous fatty acids requires the synthesis of palmitic acid first
Palmitic acid is synthesized from acetyl CoA catalyzed by fatty acids and enzyme complexes
Palmitic acid is synthesized in the cytoplasm
Fatty acid synthase complex exists in the cytoplasm of various tissues such as liver, kidney, brain, lung, breast and fat.
The fatty acid synthase complex in the liver has the highest activity and is the main place where the body synthesizes fatty acids.
The sources of fatty acids in adipose tissue are mainly exogenous fatty acids digested and absorbed by the small intestine and endogenous fat synthesized by the liver.
Acetyl CoA is the basic raw material for the synthesis of palmitic acid
Requires citric acid-pyruvate cycle
The synthesis of palmitic acid also requires raw materials such as ATP, NADPH, HCO3- and manganese ions.
Source of NADPH: 1. Pentose phosphate pathway, 2. Malic enzyme catalyzes the oxidative decondensation of malic acid.
One molecule of palmitic acid is formed by the condensation of one molecule of acetyl CoA and 7 molecules of malonyl COA.
The conversion of acetyl-COA into malonyl-CoA is the first step in the synthesis of palmitic acid and is catalyzed by acetyl-CoA condensate (a key enzyme in fatty acid synthesis).
Using manganese ions as activator and containing biological prosthetic groups
Acetyl-CoA carboxylase activity is regulated by chemical modifications with allosteric modulators
Allosteric adjustment: citric acid and isocitrate can allosterically activate. Allosteric inhibition of palmityl-CoA and other long-chain fatty acyl-COA
Chemical modification: Inactivate AMP kinase Glucagon can inhibit enzyme activity, insulin can restore enzyme activity, and high-sugar meals can increase enzyme activity.
Palmitic acid is synthesized through seven basic reaction cycles of condensation, reduction, dehydration, and further reduction.
The core of the E. coli fatty acid synthase complex consists of 7 independent enzymes
Palmitate elongation occurs in the endoplasmic reticulum and mitochondria
The endoplasmic reticulum fatty acid elongation pathway uses malonylCOA as a two-carbon unit complex
This pathway is catalyzed by the fatty acid elongase system, and NADPH co-hydrogenates
The mitochondrial fatty acid elongation pathway uses acetyl CoA as a two-carbon unit donor
Catalyzed by fatty acid elongase system
The synthesis of unsaturated fatty acids requires the catalysis of multiple desaturases
Fatty acid synthesis is regulated by metabolites and hormones
Metabolites regulate fatty acid synthesis by altering feedstock supply and acetyl-CoA carboxylase activity
ATP, NADPH and acetyl COA are raw materials for fatty acid synthesis
Fatty acylCOA is an allosteric inhibitor of acetyl COA carboxylase
Insulin is the primary hormone regulating fatty acid synthesis
Glucagon can increase protein kinase activity and inhibit acetyl COA carboxylase activity
Epinephrine and growth hormone can inhibit acetyl-CoA carboxylase and regulate fatty acid synthesis.
Fatty acid synthase as a target for drug therapy
Fatty acid synthase inhibitors can significantly slow down tumor growth and reduce weight, and are promising anti-tumor and anti-obesity drug candidates.
Plasma lipoproteins and their metabolism
Blood lipids are the collective name for the lipids contained in plasma
Plasma lipids include triglycerides, phospholipids, cholesterol and its lipids, and free fatty acids, etc.
Phospholipids mainly include lecithin, sphingomyelin and cephalin
Exogenous lipids are absorbed into the blood from food, while endogenous lipids are synthesized by liver cells, adipocytes and other tissue cells and then released into the blood.
Blood lipids are not as constant as blood sugar and are affected by diet, age, gender, occupation, metabolism, etc.
Plasma lipoproteins are the transport and metabolic forms of blood lipids
Plasma lipoproteins can be classified by electrophoresis and ultracentrifugation
Different lipoproteins contain different lipids and proteins and have different physical and chemical properties, such as density, particle size, surface charge, electrophoretic behavior, immunological properties and physiological functions.
Electrophoresis method classifies plasma lipoproteins according to their mobility in an electric field: CM, pre-β-lipoprotein, β-lipoprotein and α-lipoprotein
Classification of plasma lipoproteins by density by ultracentrifugation: chylomicrons, very low density lipoproteins, low density lipoproteins, high density lipoproteins
Related to atherosclerosis are very low density lipoproteins, low density lipoproteins, high density lipoproteins
Plasma lipoproteins are complexes of lipids and proteins
The proteins in plasma lipoproteins are called apolipoproteins
There are more than 20 kinds of apolipoproteins, mainly: apoA, B, C, D and E
Function: 1 Bind and transport lipids, stabilize the structure of lipoproteins 2Apolipoproteins can participate in the recognition of lipoprotein receptors 3Apolipoproteins can regulate the activity of key enzymes in lipoprotein metabolism
Different lipoproteins have similar basic structures
Lipoproteins from different sources have different functions and metabolic pathways
Chylomicrons mainly transport exogenous triglycerides and cholesterol
Chylomicron metabolic pathway is also called exogenous lipid transport pathway or exogenous lipid metabolism pathway
CM physiological function: transport exogenous TG and cholesterol esters
Source: TG synthesized in the small intestine and phospholipids synthesized and absorbed, cholesterol
Very low-density lipoprotein primarily transports endogenous triglycerides
Source: Mainly liver, small intestine and small amounts can be synthesized
Very low-density lipoprotein is the main form of transporting endogenous TG, and its plasma metabolite low-density lipoprotein is the main form of transporting endogenous cholesterol.
VLDL physiological function: transport endogenous TG
Low-density lipoprotein mainly transports endogenous cholesterol
LDL physiological function: transports endogenous cholesterol synthesized by the liver
LDL receptors are widely distributed throughout the body, especially on the cell membrane surfaces of tissues such as liver, adrenal cortex, ovaries, testicles, and arterial walls.
HDL mainly reverse transports cholesterol
New high-density lipoprotein is mainly synthesized by the liver, and some can be synthesized by the small intestine.
The body cannot completely decompose cholesterol and can only convert it into bile acids in the liver and excrete it or directly excrete it through the bile in the form of FC.
Disturbance of plasma lipoprotein metabolism leading to dyslipoproteinemia
Abnormal changes in different lipoproteins cause different types of hyperlipidemia
Abnormally elevated plasma lipid levels beyond the upper limit of the normal range are called hyperlipidemia
In hyperlipidemic plasma, the lipid content of some lipoproteins is increased, while the lipid content of others may be decreased.
Normal values: For adults, triglycerides exceed 2.26mmol/L and cholesterol exceeds 6.21mmol/L after fasting for 12 to 14 hours. Children: Cholesterol exceeds 4.14mmol/L
Inherited defects in genes related to plasma lipoprotein metabolism cause dyslipoproteinemia
cholesterol metabolism
Cholesterol in the body comes from food and endogenous synthesis
The main place where cholesterol is synthesized in the body is the liver
Except for the brain tissue and mature red blood cells of adult animals, almost every tissue in the body can synthesize cholesterol. The liver is the main synthetic organ, followed by the small intestine.
Cholesterol synthase is present in the cytoplasm and smooth endoplasmic reticulum membrane
Acetyl CoA and NADPH are the basic raw materials for cholesterol synthesis
For each molecule of acetyl-CoA transported, 1 molecule of ATP is consumed when cleaving citric acid into acetyl-CoA. The synthesis of cholesterol also requires NADPH for hydrogen and ATP for energy. The synthesis of 1 molecule of cholesterol requires 18 molecules of acetyl-CoA, 36 molecules of ATP and 16 molecules of NADPH.
Cholesterol synthesis is completed by a series of enzymatic reactions with HMG-CoA reductase as the key enzyme.
Synthesis of mevalonate from acetyl CoA
In mitochondria, HMC-CoA is cleaved to generate ketone bodies, The HMG-CoA produced in the cytoplasm is reduced to mevalonate by donating hydrogen from NADPH under the action of the endoplasmic reticulum HMC.CoA reductase (HMG-CoA reductase). HMG-CoA reductase is the key enzyme for cholesterol synthesis
Mevalonic acid is converted into a 30-carbon squalene via a 15-carbon compound
Squalene is cyclized to lanosterol and then converted to cholesterol
Cholesterol synthesis is regulated by HMG-CoA reductase
HMG-CoA reductase activity has the same circadian rhythm as cholesterol synthesis
Midnight, highest, lowest
HMG-CoA reductase activity is regulated by allosteric, chemical modification and enzyme content
Cytoplasmic cAMP inactivates this reductase Phosphoprotein phosphatase can restore the activity of this enzyme
Cellular cholesterol content is one of the main factors affecting cholesterol synthesis
Meal status affects cholesterol synthesis
Cholesterol synthesis is regulated by hormones
Insulin and thyroxine can induce the synthesis of HMG-CoA reductase in liver cells and increase cholesterol synthesis.
Thyroxine can also promote the conversion of cholesterol into bile acids in the liver, so serum cholesterol levels in patients with hyperthyroidism are reduced.
Glucagon can inactivate the phosphorylation of HMG-CoA reductase through chemical modification and inhibit cholesterol synthesis.
Cortisol can inhibit HMG-CoA reductase activity and reduce cholesterol synthesis
Cholesterol comes in two forms: free cholesterol and cholesterol lipids, which are widely distributed in various tissues. About 1/4 is distributed in the brain and nervous tissue, adrenal glands, ovaries and other steroid hormone-secreting glands.
The main route of cholesterol is to convert into bile acids
The mother core of cholesterol - cyclopentane polyhydrophenanthrene cannot be degraded in the body. However, its side chain can be oxidized, reduced or degraded and transformed into other products with a cyclopentane polyhydrophenanthrene core, or participate in metabolic regulation or be excreted from the body. Achieve cholesterol conversion.
It is converted into bile acids in the liver, which is the main route for cholesterol metabolism in the body.
Cholesterol can be oxidized into 7-dehydrocholesterol in the skin and converted into vitamin D 3 by ultraviolet irradiation
Phospholipid metabolism
Phosphatidic acid is an important intermediate product in the synthesis of glycerophospholipids
The raw materials for glycerophospholipid synthesis come from sugar, lipid and amino acid metabolism.
The endoplasmic reticulum of cells in various tissues of the human body contains glycerophospholipid synthase enzymes, with the highest activity in the liver, kidneys and intestines.
Ingredients: Glycerin, fatty acids, phosphates, choline, serine, inositol, ATP, CTP
CTP participates in the activation of ethanolamine, choline, and diglyceride to form activation intermediates such as CDP-ethanolamine, CDP-choline, and CDP-diglyceride.
There are two pathways for glycerophospholipid synthesis.
Phosphatidylcholine and phosphatidylethanolamine are synthesized via the diglyceride pathway
Products: phosphatidylcholine (PC), phosphatidylethanolamine (accounting for more than 75% of tissue and blood lipids)
PC is the most abundant phospholipid in eukaryotic cell membranes. It plays an important role in cell proliferation and differentiation and is of great significance in maintaining normal cell cycle.
Some diseases such as cancer, Alzheimer's disease. The occurrence of stroke and other diseases are closely related to abnormal PC metabolism.
PC content is one of the main determinants of the bending elastic tension of membrane bimolecules.
Phosphatidylserine can also be produced by carboxylation of phosphatidylethanolamine or the exchange of ethanolamine and serine.
Inositol phospholipids, serine phospholipids and cardiolipin are synthesized through the CDP-diglycerol pathway
Inositol and serine do not require activation
Production: inositol phospholipid, serine phospholipid, cardiolipin
Phospholipid exchange proteins: A class of proteins that facilitate the exchange of phospholipids between intracellular membranes
Glycerophospholipid synthesis occurs on the outside of the endoplasmic reticulum membrane
Glycerophospholipids are degraded by phospholipases
Lysophospholipid 1 has strong surface activity and can damage red blood cell membranes or other cell membranes, causing hemolysis or cell necrosis.
Sphingomyelin is an important intermediate product in the synthesis of sphingomyelin
Sphingomyelin is the most abundant phospholipid in the human body and is composed of sphingosine, fatty acids and phosphocholine
The basic raw materials for the synthesis of sphingosine are coenzyme CoA, serine and choline, and also require the participation of coenzymes such as pyridoxal phosphate, NADPH and FAD.
Sphingomyelin is degraded by sphingomyelinase
Sphingomyelinase exists in the lysosomes of brain, liver, spleen, kidney and other tissue cells and belongs to the phospholipase C class. It can hydrolyze phosphate bonds to produce phosphocholine and N-esteryl sphingosine.