BIOCHEM-LEC-LESSON-2_finals (1) PDF Carbohydrates Metabolism Lecture Notes

Carbohydrates Metabolism Digestion of Carbohydrates − Glucose absorption occurs in the small intestine via the SGLT-1 transporter − Dietary CHO (sodium glucose...

Carbohydrates Metabolism Digestion of Carbohydrates − Glucose absorption occurs in the small intestine via the SGLT-1 transporter − Dietary CHO (sodium glucose cotransporter) usually consists of starch; initially − The transporter is more prevalent in the hydrolyzed in the oral cavity by duodenum and jejunum. AMYLASE secreted by the salivary − Glucose transport is driven by a sodium and parotid glands gradient across the apical cell membrane − Amylase converts starch into Maltodextrins generated by the Na+, K+ -ATPase pump and Maltose located in the basolateral membrane of the − Amylase’s activity is inhibited in the enterocyte stomach by gastric activity − Two Na+ ions bind to the outer face of the − Completion of CHO digestion occurs in the SGLT-1 transporter which results in a small intestine by Pancreatic Amylase conformational change permitting − Starch is digested in the small intestine to subsequent glucose binding simple components derived from branched − The two Na+ ions and the glucose amylopectin (maltose, maltotriose and α- molecule are then transferred to the limit dextrin). Oligosaccharides and cytoplasmic side of the membrane disaccharides are digested by specific following another conformational change enzymes in the microvillus membrane that involves rotation of the receptor (brush border) − The Na+ ion is subsequently expelled by − Disaccharidases are protected from Na+, K+ -ATPase pump to maintain the proteolysis by glycosylation and are found gradient. in higher concentration in villus − The SGLT-1 transporter undergoes enterocytes of the proximal small bowel. another conformational change resulting in (Maltase, sucrase, trehalase, lactase & the binding sites again being exposed at isomaltase) the apical surface − Sucrose uptake is regulated after − Sodium ions and accompanying anions hydrolysis by the apical membrane uptake and water follow the glucose, maintaining rate of fructose and glucose, whereas iso-osmolarity. lactose absorption is limited by the rate of − A small portion of the glucose is utilized by hydrolysis. the cell. − Carbohydrates not digested in the small intestine pass into the large intestine Metabolism of Carbohydrates where they are digested by colonic bacteria. − Following absorption into the portal vein, − Different monosaccharides are absorbed Hexoses are transported into the liver completely by the intestinal mucosa − Processes involved in CHO metabolism: Hexoses (glucose & fructose) GLYCOLYSIS actively transported. GLYCOGENESIS Pentoses passively absorbed via GLYCOGENOLYSIS diffusion. GLUCONEOGENESIS LIPOGENESIS Absorption Glycolysis J.C.D  Carbohydrates Metabolism − Metabolic utilization or oxidation of (PROTEINS), glycerol (LIPIDS) and lactic GLUCOSE to lactate and/or pyruvate via acid the Embden Meyerhoff pathway − Proteins/Lipids → Glucose → Energy − GLUCOSE is used as a source of energy Steps in Gluconeogenesis − Glucose → Energy 1. The conversion of pyruvate to − Glycolysis takes place in the cytosol of a phosphoenolpyruvic acid (PEP). cell, and it can be broken down into two Enzymes: Pyruvate main phases: carboxylase, PEP − energy-requiring phase - In this phase, the carboxykinase and malate starting molecule of glucose gets dehydrogenase rearranged, and two phosphate groups are 2. The conversion of fructose-1,6-bP to attached to it. fructose-6-P with the use of the − energy-releasing phase- In this phase, enzyme fructose-1,6- phosphatase. each three-carbon sugar is converted into 3. The conversion of glucose-6-P to another three-carbon molecule, pyruvate, glucose with the enzyme glucose-6- through a series of reactions phosphatase. − The most important enzyme for regulation Regulation: of glycolysis is phosphofructokinase, 1. The conversion of pyruvate to PEP is which catalyzes formation of the unstable, regulated by acetyl-CoA. two-phosphate sugar molecule, fructose- 2. The conversion of fructose-1,6-bP to 1,6-bisphosphate fructose-6-P with the use of fructose- − Overall, glycolysis converts one six-carbon 1,6-phosphatase is negatively molecule of glucose into two three-carbon regulated and inhibited by the molecules of pyruvate. The net products of molecules AMP and fructose-2,6-bP. this process are two molecules of ATP and 3. The conversion of glucose-6-P to two molecules of NADH. glucose with use of glucose-6- phosphatase is controlled by substrate Glycogenesis level regulation − Synthesis of GLYCOGEN from glucose and other sugars whenever there is an excess of blood glucose levels Lipogenesis − GLYCOGEN is stored in the liver − Synthesis of LIPIDS from GLUCOSE − Glucose → Glycogen − Glucose → Fatty Acids Glycogenolysis Hormones that regulate Glucose − Breakdown of GLYCOGEN back to metabolism GLUCOSE when supply is depleted Hormone − Organ − Glycogen → Glucose → Energy Insulin − Pancreas (β- Gluconeogenesis cells of Islets of Langerhans) − Synthesis of GLUCOSE from non- carbohydrate sources such as amino acids J.C.D  Carbohydrates Metabolism Glucagon − Pancreas (α- Growth Hormone cells of Islets of − Inhibits glucose uptake by tissues Langerhans) − Increases hepatic glucose availability Epinephrine − Adrenal − Inhibits LIPOGENESIS medulla − Antagonistic to INSULIN Growth hormone − Anterior pituitary gland Adrenocorticotropic Hormone ACTH − Anterior − Promotes protein catabolism and Cortisol pituitary gland deamination of amino acids − Adrenal cortex − Promotes GLUCONEOGENESIS from Thyroid Hormone − Thyroid gland amino acids (T3, T4) − Inhibits glucose metabolism in peripheral tissues − Antagonistic to INSULIN Insulin Hydrocortisone − promotes GLYCOGENESIS − Promotes GLUCONEOGENESIS − promotes LIPOGENESIS − Similar actions to ACTH − Increases permeability of cells to glucose Carbohydrates Metabolic Disorders Lack of Insulin: − Hyperglycemia – increase in blood − Increase blood sugar level (FBS) glucose level. − Less ability of the body to metabolize − Hypoglycemia – decrease in blood CHO glucose level. Glucagon − Increases blood glucose by stimulating Diabetes Mellitus (Dm) Hepatic GLYCOGENOLYSIS − Inability to metabolize CHO − promotes hepatic − Characterized by HYPERGLYCEMIA – GLUCONEOGENESIS high blood glucose level − promotes hepatic LIPOLYSIS − Caused by problems in insulin Thyroxine & Triiodothyronine (primary) and other hormones − Increases absorption of glucose from (secondary) gastrointestinal tract − FBS level: >126mg/dl − Accelerates degradation of insulin Characteristics of DM Epinephrine − Polyphagia − Also known as ADRENALINE excessive eating Due to failure − Stimulates GLYCOGENOLYSIS thus of glucose to enter cells elevates blood sugar levels − Polyuria − Decreases insulin release from excessive urine output Since pancreas glucose is an osmotic diuretic − Breakdown of triglycerides in fat Occurs when blood sugar is tissues 170-180 mg/dL − Polydypsia excessive drinking J.C.D  Carbohydrates Metabolism Response to polyuria Respiratory distress syndrome − Hyperventilation Low calcium level − Weight loss or weight gain High bilirubin level to fetus − Mental confusion Diabetes Insipidus − Loss of consciousness − Not related to carbohydrate − GLUCOSURIA – glucose in urine metabolism − Yeast cells in urine – due to glucose − Water diabetes Complications of DM − Rare metabolic disorder where there is − Neuropathy – malfunction of the brain large quantities of urine output and − Nephropathy – malfunction of the constant thirst kidney Blood Glucose Tests − Retinopathy – malfunction of the eyes − Fasting Blood Sugar Type I DM screening test for DM from 6-8 − Insulin-dependent DM – total lack of hours fasting insulin production − Random Blood Sugar − Juvenile onset DM – occurs at age determination of glucose on below 30 sample randomly collected − Frequently in thin individuals − 2 hours Post Prandial − Severe form of diabetes glucose determination two hours after meal − Autoimmune disease – against β cells − Oral Glucose Tolerance Test serial measurement of glucose − KETOSIS is prominent, predisposed to before and after (1,2,3 hrs) a KETOACIDOSIS specific amount of glucose Type II DM (50,75,100 g) is given orally − Non-insulin-dependent DM − Maturity onset DM –occurs at age above 30 years − Hereditary − High insulin – requires drugs that would potentiate insulin release − Usually in obese individuals − Caused by Insulin resistance Gestational Diabetes − Pregnant women who have hyperglycemia − Due to extra metabolic demand of fetus − Hormonal imbalance in pregnancy − Usually blood sugar returns to normal postpartum − Will cause: J.C.D