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THE STORY OF GLUCOSE AND INSULIN “Let us all be thankful for those, who help us achiev our goals “

glucose metabolism insulin

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THE STORY OFGLUCOSE AND INSULIN

“Let us all be thankful for those, who help us achieve

our goals “

This is gonna help our hero !

. Insulin is a protein hormone

.Secretion by the beta cells of langerhans.Major targets - liver, adipose tissue , and muscle

.INSULIN IS AN IMPORTANT ANABOLIC HORMONE

Crystallization requires Zn Has two peptide chains A and B chains (51 amino acids – 21 A chain and 30 B chain )Plasma level -0.3 to 2 ng/mlMolecular weight – 12000 to 48000

BIOSYNTHESIS OF INSULIN

DIRECT HELPWhen insulin binds to the receptors sites :1.A confirmation change of the receptor2.The receptor cross links and forms microaggregates3.The receptor complex is internalized4.One or more signal is generated

Various mechanisms proposed 1. Role of cyclic AMP2. Role of cyclic GMP3. Role of protein phosphatases4. Action through tyrosine kinase activity5. Role in m- RNA translation6. Role in gene expression

MECHANISM OF ACTION

Role of protein phosphatases (by protein phosphatase 1)1.activate: glycogen synthase-dephosphorylation activates it. pyruvate dehydrogenase complex2.Inactivation : phosphorylase enzyme triacyglycerol kinase

Role in m RNA translation Insulin is known to affect about 50 different types of protiens in a variety of Tissues and many of these involve covalent modification

Role on gene expression Affects the rate of transcription of specific genes Ex : decreses : phosphoenol pyruvate carboxy kinase (PEPCK) (gluconeogenesis) increases: phosphofructokinase pyruvate kinase (glycolysis)

Metabolic role of insulin

NET EFFECT is 1.Lowering of blood glucose2.Increase glycogen store

Action on carbohydrate metabolism1.Increases glucose uptake by GLUT transporters and synthesis of glucokinase2.Increases glycolysis induces the synthesis of PFK1 and pyruvate kinase3. Increases conversion of pyruvate to acetyl coA dephosphorylation of pyruvate dehydrogenase conversion

4. Stimulates glycogenesis by dephosphorylation of key and rate limiting GLYCOGEN SYNTHASE5.Decreases gluconeogenesis repressing the synthesis of PEPCK inhibits allosterically F1,6 bis phosphatase6.Decreses glycogenolysis dephosphorylating glycogen phosphorylase and also glucose 6 phosphate7.Increasing HMP shunt Hmp stimulation causes more and more NADPH by inducing the synthesis of glucose 6 phosphate dehydrogenase