carbohydrate metabolism in fed state

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Carbohydrate metabolism In Fed State By zameera I yr mbbs

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What is Fed / Absorptive State ? Ingested food – digested & absorbed Then either --- oxidised – immediate energy needs --- stored -- later utilized Determined by 2 hormones --- INSULIN ---- GLUCAGON PERIOD FROM START OF ABSORPTION UNTIL A BSORPTION COMPLETE ---- Fed state

Fates of Glucose: 

Fates of Glucose Dietary Carbohydrates Monosaccharides (Glucose) oxidised G-3-P + FA Enter biological Stored TAG (Liver) Pathways as Glycogen VLDL (Blood) Energy Liver & muscle Adipose Energy Tissue

Digestion & Absorption: 

Digestion & Absorption Dietary Monosaccharide Carbohydrates Dietary Polysaccharides Salivary-alpha-amylase Starch Di-,Tri-, Oligosacchd Pancreatic-alpha-amylase Digestive enzymes Di-,Tri-,Oligosaccharides Glucose

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Dietary Disaccharides -- digested by enzymes in brush-border Sucrase Sucrose Glucose + Fructose Lactase Lactose Glucose + Galactose Dietary Monosaccharides Remains same

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Monosaccharide Dietary (from digestion) Monosaccharides Hepatic Portal Vein LIVER – Central organ of distribution of nutrients

Metabolism Of Carbohydrate: 

Metabolism Of Carbohydrate Glucose – Immediate energy needs Glucose Glycogen When more than glycogen storage capacity of liver, Glucose – phosphorylated – to G6P by Glucokinase Other dietary monosacc ( fruct,galact ) – phosphorylated – rearrangd to G6P Metabolism in Liver

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VLDL

Metabolism in Liver: 

Metabolism in Liver Most liver glycogen – synthesised indirectly from GLUCONEOGENIC PRECURSORS ( Pyruvate,Alanine,Lactate ) – returning liver from peripheral tissues Rather than directly from glucose entering liver via portal circulation BECAUSE, Of low phosphorylating activity of liver at physiological concent ’ of glucose

Metabolism in Peripheral Tissues: 

Metabolism in Peripheral Tissues In RBC : lacks mitochondria – so burn glucose ANAEROBICALLY --converts glucose – to lactate – via Glycolysis – small amount of energy --Glucose – source of NADPH – through HMP shunt

In Adipose Tissue:: 

In Adipose Tissue: If energy intake greater than energy expenditure – Conversion of Glucose Fatty acids Fat + VLDL + Chylomicrons (FRM AchoA liver intestine) TAG - stored in adipose tissue Ready source of fuel for most body tissues during postabsorptive & fasting state

In CNS:: 

In CNS: No metabolic mechanism to convert Glucose to Energy Stores ( Glycogen,TAG ) Glucose – available immediately oxidised to produce energy Since brain completely depends on glucose for its energy needs – in hypoglycemia – leads to coma and death A clinnical case- excessv insulin dose- hyperactvty f sns - neuroglycopenia -death-reason.

In Muscle:: 

In Muscle: Glucose stored as glycogen in muscle fibre Immediate energy needs- glucose undergoes AEROBIC – pyruvate ANAEROBIC – lactic acid Too much of lactic acid- causes muscle cramps

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Overa ll – summing up:

Regulation of Carbohydrate Metabolism: 

Regulation of Carbohydrate Metabolism Changes in metabolism of glucose – dat occur during switch frm fed to fasting state – regulated by INSULIN & GLUCAGON. Insulin – elevated in FED state & gluc constant Glucagon – elevated in Fasting state Insulin – stimulates glucose UPTAKE Glucagon – stimulates glucose RELEASE Balance between thes 2 hormones – stable MILLIEU INTERIEUR

Effects of insulin:: 

Effects of insulin: Anabolic hormone Secreted by beta cells of pancreas- responds to high blood glucose level Promotes glucose storage In Liver & Muscle – insulin increases GLYCOGENESIS In Muscle & Adipose – insulin increases GLUCOSE UPTAKE by increasing no.of GLUT-2 in cell memb

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Intravenous administration of insulin – immediate decrease in blood glucose In liver – insulin DECREASES production of glucose through GLYCOGENOLYSIS & GLUCONEOGENESIS

Effects of Glucagon:: 

Effects of Glucagon: Intravenous administration – immediate RISE in blood glucose Activate Hepatic glycogenolysis & gluconeogenesis Inhibits glycolysis & glycogenesis

Diabetes Mellitus:: 

Diabetes Mellitus: Metabolic disease due to absolute / relative INSULIN DEFICIENCY In 10% populatn – 1/5 th persons above 50 – suffer from this disease Insulin def – elevated blood glucose level Inspite,entry of glucose into cells – insufficient Hence all cells starve of GLUCOSE

Type I diabetes: 

Type I diabetes Fatal disease – insulin secretion totally fails – auto immune attack on pancreatic beta cells Increased rate of lipolysis in adipose tissue – KETOACIDOSIS Activation of gluconeogenesis inspite of high blood glucose levels – HYPERGLYCEMIA

Type II diabetes: 

Type II diabetes Insulin resistance – due to obesity, alcoholism etc Hypothalamic insulin resistance Loss of control over hepatic gluconeogenesis Most persons suffer from this type People survive for many years with the disease

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Insulin stimulated opening of hypothalamic K channels results in vagal nerve signaling to the liver and inhibition of gluconeogenesis .  This is part of the normal response to meals and following insulin release from the pancreatic ß-cells.

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