biokimia sistem pencernaan.ppt
DESCRIPTION
Biokimia Sistem Pencernaan.PPTTRANSCRIPT
-
PENCERNAAN, ABSORPSI DAN METABOLISME KARBOHIDRATDrs. Hendri Busman, M.Biomed
FAKULTAS KEDOKTERANUNIVERSITAS MALAHAYATIBANDAR LAMPUNG
-
FUNGSI KARBOHIDRATSUMBER ENERGI UTAMACADANGAN ENERGI ( GLIKOGEN )BAHAN PEMBENTUK ZAT LAIN : - AS. ASCORBAT ( VITAMIN C ) - AS. GLUCORONAT - PENTOSA * NUKLEOTIDA * AS. NUKLEAT - AS. AMINO - LIPID : TAG, GANGLIOSIDA, GLIKOLIPID4. STRUKTUR BIOLOGIS
-
PENCERNAAN KARBOHIDRAT* MULUT : - MEKANIS - ENZIMATIK AMYLASE * OLIGOSAKARIDA AMILUM * MALTOTRIOSA SALIVA * MALTOSA ION Cl- pH : 7,1
-
* USUS HALUS AMILUM AMYLASE - OLIGOSAKARIDA GLIKOGEN PANCREAS - MALTOTRIOSA pH : 7,1 - MALTOSA SUKRASE SUKROSA GLUKOSA + FRUKTOSA pH : 5 7 MALTASE MALTOSA GLUKOSA pH : 5,8 6,2
-
LACTASE LAKTOSA GLUKOSA + GALAKTOSA pH : 5,4 6
TRIHALASE TRIHALOSA GLUKOSA
GLUKOSIDASE OLIGOSAKARIDA GLUKOSA
INHIBITOR GLUKOSIDASE : OAD
-
ABSORPSI KARBOHIDRAT* ABSORPSI : - HEKSOSA : * GLUKOSA * GALAKTOSA * FRUKTOSA * MANNOSA - PENTOSA : RIBOSA* ABSORPSI : - PASIF : * SIMPLE DIFFUSION * FACILITATED DIFFUSION (GLUT-5) - ACTIF : SGLT-1 (K+)Na+ PUMP)
-
KETERANGANACTIVE TRANSPORTFACILITATED DIFFUSIONSIMPLE DIFFUSION123Gluc.Gluc.
-
* Penghambatan transport aktif - Ouabain ( inhibitor K+ / Na+ pump ) - Phlorizin
-
ASPEK KLINIKLACTOSE INTOLERANCE * DEF. : ENZIM LACTASE * GEJALA : - COLIC USUS - DIARE - FLATULENS a). DEF. LACTASE HEREDITER - JARANG TERJADI - PADA NEONATUS - PEMBERIAN SUSU DIARE - TH : * LLM (LOW LACT MILK) * YOGURT (PENGGANTI SUSU)
-
b). PRIMARY LOW LACTASE ACTIVITY - SERING TERJADI - PADA ORANG DEWASA - PENURUNAN AKTIVITAS LAKTASE SECARA BERANGSUR-ANGSUR c). SECONDARY LOW LACTASE ACTIVITY - SEKUNDER DARI PENYAKIT : * TROPICAL SPRUE * CELIAC DISEASE * KWASHIORKOR * COLITIS * GASTRO ENTERITIS
-
2. SUCRASE DEFICIENCY - HEREDITER - NEONATUS - BERSAMA-SAMA DENGAN ISOMALTASE DEFICIENCY - GEJALA : * DIARE * COLIC USUS * FLATULENS3. DISSACHARIDURIA - DEF. : DISACHARIDASE - > 30 mg DISAKARIDA ( URINE )
-
4. MONOSACHARID MALABSORPSION - CONGENITAL - ABSORPSI GLUK / GAL : LAMBAT - GANGGUAN : GLUT : SGLT-1 - GEJALA : * DIARE * COLIC USUS * FLATULENS
-
TRANSPORT GLUKOSA KE DALAM SEL
-
CARBOHYDRATE METABOLISM GLUCOSE METABOLISM
NONCARBOHYDRATE SUBSTRATE PENTOSE-PHOSPHATE
LACTATE Gluconeogenesis Hexose Monophosphate Shunt Anaerobic condition
PYRUVATE GLUCOSE GLUCORONATE Glycolysis EM Uronic acid Pathway Aerobic (Embden Meyerhof) condition Glycogenesis Glycogenolysis LACTATE PYRUVATEACETYL-CoA (liver)
Glycogenolysis GLYCOGEN GLUCOSE-6-P (Muscle) TCC
CO2 + H2O + E TCC = TRI CARBOXYLIC ACID CYCLE
-
GLYCOLYSIS EMBDEN MEYERHOF* Oxidation of glucose to form pyruvate or lactate* Occur in all of the tissues, in cytosol of the cells* ATP are generated from 1 mol of glucose - In aerobic condition : 8 ATP - In anaerobic condition : 2 ATP* Influenced by several factors Inducer : - AMP - ADP - C.H. Meal Supresor : - ATP - Yodo acetate - Citrate - Fluoride - Glucose-6P - Fast condtion - NADH
-
GLIKOLISIS EMBDEN MEYERHOF
-
Three possible catabolic fates of the pyruvate formed in the pay off phase of glycolysisGLUCOSE Glycolysis (10 successive reactions)2 PYRUVATE Anaerobic conditions anaerobic conditions
2 ETHANOL + 2 CO2 LACTATE
2 ACETYL-CoA
4 CO2 + 4H2OO2 aerobic conditions
2C02Fermentation to lactate in vigorouslyContracting muscle, in erythrocytes, andis some microorganismeAlcohol fermentaion in yeastCitricAcidcycleAnimal, plant, and many microbialCells under aerobic conditions
-
TOTAL ENERGY ARE GENERATED FROM OXIDATION OF ONE MOL OF GLUCOSE TO FORM CO2 + H2OGLUCOSE
8 ATP
Pyruvate Pyruvate
3 ATP 3 ATP
Acetyl- CoA Acetyl Co-A
TCC TCC 12 ATP 12 ATP
38 ATP
-
EFICIENCY OF GLUCOSE OXIDATIONOne mol of glucose oxidation to form.CO2 + H2O, are generated 38 ATP
38 ATP = 38 x 51,6 KJ (Kilo Joule) = 1961 KJ
One mol of glucose is combusted in a calorimeter (in vitro), approximatelly 2870 KJ are liberated as heat. 1961Eficiency : x 100% = 68% 2870 32% are liberated as heat.
-
GLYCOGENESIS & GLYCOGENOLYSIS* Almost occur in all of the tissues Especially in the liver and muscles
* Biomedical importance : - Liver glycogen is source of blood glucose, because there is glucose-6-phosphatase activity in the liver - Muscle glycogen is not source of blood glucose, because there is not glucose-6-phosphatase activity in muscle. So muscle glycogen is only source of glucose for glycolysis within the muscle itself (anaerobic glycolysis)
-
* Glycogen storage diseases - Inherited - Deficient mobilization of glycogen - Or deposition of abnormal forms of glycogen muscular weakness or even death
* Influenced by several factors - Hormonal : insulin, glucagon etc. - Nutrition : - Carbohydrate meal Gluccogenesis - During fasting glycogenolysis
-
REGULATION OF GLYCOGENESIS & GLYCOGENOLYSISPhosphodiesterase
cAMP
Glycogenesis
GlycogenolysisAdenyl Cyclase
cAMP
Glycogenesis
Glycogenolysis* Insulin* Epinephrin* Glucagon : (only on the liver)++Equilibrium
-
GLUCONEOGENESIS* Biomedical importance : - To maintain blood glucose concentration - To clear the products of the metabolism of other tissues from the blood eg, Lactate & Glycerol* Occur especially in the liver and kidney* Influenced by several factors : - hormonal - Nutrition* Sources of noncarbohydrate substrates : - Lactate- Propionat (Plants) - Glycerol (fat)- Glucogenic Amino Acids
-
Perubahan berbagai macam gula menjadi glukosaD-GlucoseLactoseTrehaloseSucroseGlycogenGlucose-1-PhosphateGlucose-6-PhosphateFructose-6-PhosphateFructose-1,6-BiphosphateFructose-1-phospateLiceralhehide +Glyceraldehid-3-phospateMannose-6-phosphatePhosphomannose isomerasePhosphorylasePhosphoglucose-mutaseUDP-galactoseUDP-glucoseATPATPHexokinaseHexokinaseTriose phosphateisomeraseTriose kinasefruktokinaseSucraseLactasetrehalaseHexokinaseATPATPATPDihydroacetone phospatePiD-GalaktoseD-Mannose
-
BLOOD GLUCOSESources :Carbohydrate (Diet)Liver glycogens (Glycogenolysis)Noncarbohydrate substrates (Gluconeogenesis)
* Concentration : During fasting : 3,3 - 3,9 mmol/l = 60 - 70 mg% After the ingestion of a carbohydrate meal : 6,5 7,2 mmol/l = 120 130 mg% Post absorptive state : 4,5 5,5 mmol/l = 80 100 mg% Normal fasting blood glucose : 3,9 6 mmol/l = 70 110 mg%
-
* Renal threshold : 9,5 10 mmol/l = 170 180 mg% More than 9,5 mmol/l = 170 mg% Glucosuria* Influenced by several factors : - Hormonal : insulin & secretin Epinephrin / nor epinephrin Glucagon Growth Hormon ACTH Glucocorticoids Tyroxin - Nutrition & Drug : Tolbutamid (OAD) Amino acids FFA
-
REGULATION OF BLOOD GLUCOSE
-
GLUCOSE TOLERANCEGlucose tolerance Diabetes mellitus Liver damage Several infection disease Obesity Hyperpituitarism Cortex adrenal hyperfunction Hyperglycemia Glucosuria
-
Glucose tolerance Hypopitutarissm Cortex adrenal hypofunction (Addisons disease) Hyper insulinism Hypoglycemia