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