[내분비학] The Pancreatic Islets

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[내분비학] The Pancreatic Islets에 대한 자료입니다.
목차
1.Morphology of the endocrine pancreas
2.Glucagon
Biosynthesis, Secretion, and Metabolism
Physiological actions of glucagon
Glucose production
Glycogenolysis
Gluconeogenesis
Lipogenesis and Ketogenesis
Ureogenesis
3.Regulation of glucagon secretion
본문내용
Histologically, the islets consist of three major and at least two minor cell types.
Beta cells, which synthesize and secrete insulin, make up about 60% of a typical islet.
Alpha cells are the source of glucagon, 30% of islet tissue.
Delta cell, which are less abundant, produce somatostatin.
F cells, which secrete pancreatic polypeptide.
Fifth cell type that secretes ghrelin.
Fifty cell type and F cells occupy the perimeters of islets, whereas the alpha, beta, and delta cells appear to be randomly interspersed.


Glucagon receptor
The glucagon receptor is a 62 kDa peptide that is activated by glucagon and is a member of the G-protein coupled family of receptors.
Stimulation of the receptor results in activation of adenylate cyclase and increased levels of intracellular cAMP.
Glucagon receptors are mainly expressed in liver and in kidney with lesser amounts found in heart, adipose tissue, spleen, thymus, adrenal glands, pancreas, cerebral cortex, and gastrointestinal tract.

Effects of glucagon appear to be mediated by cyclic AMP
Activation of protein kinase A by cyclic AMP.
Phosphorylation of enzyme(activity increase or decrease) or phosphorylation of the transcription factor CREB.
Glucagon increases intracellular concentrations of calcium by a mechanism that depends upon activation of protein kinase A.
Increased intracellular calcium reinforce some cyclic AMP mediated actions of glucagon, particularly on glycogenolysis.


Ketogenesis
Ketogenesis is the process by which ketone bodies are produced as a result of fatty acid breakdown.
Glucagon control the ketogenesis
The same reaction that inhibits fatty acid synthesis promotes fatty acid oxidation and consequently ketogenesis.
Long-chain fatty acid molecules that reach the liver can be either oxidized or esterified and exported to adipose tissue as the triglyceride.
To be esterified, fatty acids must remain in the cytosol, and to be oxidized they must enter the mitochondria.