[내분비학] The Pancreatic Islets

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2011.05.25 / 2019.12.24
68페이지 / ppt (파워포인트 2003)
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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.

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the neuromuscular junction and adjacent structures.The anatomy of the motor end plate, shown at the left, and the sequence of events from liberation of acetylcholine (ACh) by the nerve action potential (AP) to contraction of the muscle fiber, indicated by the middle column. The modification of these processes by various agents is shown on the right; an arrow marked with an X indicates inhibition or block; an unmarked arrow indicates enhancement or activation. The insets are enlargements of the indicated structures. The highest magnification depicts the receptor in the bilayer of the postsyna

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PancreaticEntericCrohns diseaseGastrointestinal bleedingPortal hypertensive gastropathyEsophageal and gastric varices▦ Endocrine Tumors of the GI Tract & Pan-creas* Biologic ConsiderationAPUDomaSlow growingSx due to hormonal effect, not due to tissue invasionMaintain normal endocrine cell function (but, hypersecretion)DistributionGI tract - carcinoid tumorPancreas - Islet cell carcinomaCNS - ganglioneuroblastoma, neuroblastoma, chemodactoma, paraganglionomaThyroid - medullary carcinomaSkin - melanomaAdrenal medulla - pheochromocytomaLung - carcinoid tumor, small cell ca

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TYPE I DIABETES MELLITUS(Insulin-Dependent Diabetes Mellitus IDDM; Juvenile-Onset Diabetes)ETIOLOGY AND PATHOGENESIS. the sharply diminished secretion of insulin. The mechanisms : autoimmune destruction of pancreatic islets in predisposed individuals. increased prevalence among persons with such disorders as Addison disease, Hashimoto thyroiditis, and pernicious anemia. increased frequency of certain HLAs, : HLA-B8, -DR3, -B15, and -DR4.Inheritance of HLA-D3 or -D4 antigens : two- to threefold increased risk Inheritance of both D3 and D4 : sevenfold to 10-fold.A genetic type of prop

TYPE I DIABETES MELLITUS

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