{[ promptMessage ]}

Bookmark it

{[ promptMessage ]}

Lecture 18 _ Control Endocrine Pancreas

Lecture 18 _ Control Endocrine Pancreas - Lecture 18...

Info iconThis preview shows pages 1–2. Sign up to view the full content.

View Full Document Right Arrow Icon
Lecture 18 – Control Endocrine Pancreas Glucose Homeostasis in the Fed and Fasted States - Counter regulatory hormone (function counter the actions of insulin) - Ghrelin/GH are separate hormones Islets of Langerhans (Pancreas) - A cells make glucagon - B cells make insulin - D cells make somatostatin The blood flow from center of islet to periphery - A(alpha) and D (delta) cells directly exposed to insulin secreted by B cells o Alpha produced glucagon doesn’t get to act on the beta cells until it returns to through circulation o Beta cells produced insulin can work on these alpha cells without re-entry through circulations - B (Beta) cells not direcly exposed to secreted glucagon or STT Insulin - Primary role: regulation of blood glucose - Highly conserved across species - Synthesized as pre-pro-insulin by beta cells of the pancreas o Pre-protein with peptide get it into a secretory pathway - the pro-insulin processed to insulin in terminal secretory pathway; insulin and C (connecting peptide) co-secreted o insulin is activated by proteases in beta cells at the terminal end o when insulin is secreted c-peptide (which is kept in the granules) is secreted o used clinically to see how much beta cells reserve a person may have - short term regulation in response to glucose (minutes) at level of secretion , transcription contributes to longer term secretory capacity Mechanism of Glucose-stimulated insulin secretion - When glucose gets above 80-110 mg/dl enter beta cell via GLUT2 transporters - Glucose enters b cell via GLUT-2 transporters - Glucose metabolized by mitochondria to yield ATP - Increased ATP/ADP ratio closes ATP-dependent potassium channel - Resulting membrane depolarization opens voltage- dependent Calcium channels - Increased intracellular Calcium induces fusion of a subset of insulin-containing secretory vesicles to plasma membrane and insulin release Physiologic Secretion/Extraction of Endogenous Insulin - first organ that sees insulin is liver (through portal vein; liver extract about 50% of the insulin) o high extraction is important from the normal action of insulin (suppression of gluconeogenesis and increasing glycogen) - liver needs to see the higher level of insulin o remember that when treating diabetes you need enough insulin to have affect in muscle NOT liver (that would be too much for liver) EXPERIMENTS: Portal Peripheral vein insulin concentrations following oral gluco administration - You can see that portal vein levels are higher Effects of insulin infusion of glucose disposal rate (GDR—how m insulin is taken up by peripheral tissues) and hepatic glucose production (HGP) - With insulin infusion insulin goes up in arterial, portal and lymph the glucose turnover goes up (GDR) and the glucose turnover goes down (HGP) Insulin secretion is also stimulated by AA - If you eat a meal that contain protein protein is digest into AA stimulate insulin secretion - Three ( alanine, lysine, arginine infusion) o Glucose doesn’t change that much but insulin raises significantly o
Background image of page 1

Info iconThis preview has intentionally blurred sections. Sign up to view the full version.

View Full Document Right Arrow Icon
Image of page 2
This is the end of the preview. Sign up to access the rest of the document.

{[ snackBarMessage ]}