Metabolism

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Metabolism
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Mammalian Pancreas
-Exocrine Pancreas secretes digestive enzymes,
alkaline pancreatic fluid -Endocrine Pancreas
secretes hormones that regulate carbohydrate,
lipid, and protein metabolism
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Endocrine Pancreas

• Islets of Langerhans 4 cell types
• ? cells secrete glucagon
• ? cells secrete insulin
• ? cells secrete somatostatin
• F cells secrete pancreatic polypeptide

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Pancreatic Hormones

• Insulin
• Glucagon
• Somatostatin

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INSULIN

• Regulation of Secretion
• Hyperglycemia stimulates release
• Glucose sensors in ? cells
• Gastric Inhibitory Peptide
• Released from cells of the small intestine
• Potent stimulator of insulin secretion
• Somatostatin inhibits insulin release
  (paracrine)
• Autonomic nervous system
• Parasympathetic activation increases insulin
  release
• Sympathetic activation blocks insulin release
• Epinephrine (from adrenal) blocks insulin release

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INSULIN

• Action at Target Tissues
• Activation of insulin receptor
• Increases transport of glucose, amino acids, and
  fatty acids into cells

Glucose transporter
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INSULIN

• Action at Target Tissues
• Activation of insulin receptor
• Increases transport of glucose (glucose
  transporter), amino acids, and fatty acids into
  cells
• Enhancement of anabolic pathways, decrease in
  catabolic pathways
• Increases enzymes that activate
• Glycogen formation (liver)
• Lipogenesis (fat)
• Protein Synthesis (muscle)

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Pancreatic Hormones

• Insulin
• Hypoglycemic, glycogenic, lipogenic, anabolic
• Glucagon
• Somatostatin

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Glucagon

• Hyperglycemic (increases plasma glucose)
• (one of many in the body)
• Actions at target cells
• Liver
• Promotes glycogenolysis
• Promotes gluconeogenesis
• Fat Tissue
• Promotes lipolysis

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Pancreatic Hormones

• Insulin
• Hypoglycemic, glycogenic, lipogenic, anabolic
• Glucagon
• Hyperglycemic, lipolytic

• Somatostatin
• Paracrine agent
• Believed to inhibit insulin and glucagon release
• May regulate uptake of nutrients from the gut

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Glucose Regulation
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DIABETES MELLITUS

• Type Ijuvenile onsetinsulin dependent
• IDDM
• Underproduction of insulin
• Type IIadult onsetnon-insulin dependent
• NIDDM
• Insulin receptor resistance
• Post-receptor mechanism problem

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Insulin Dependent IDDM

• Possibly results from autoimmune reaction
• The bodys immune system attacks the ? cells
• Pancreatic ? markedly reduced
• Symptoms only appear after 80 loss of cells
• No insulinphysiological repercussions?
• Treatment
• Insulin injections
• Recent methods

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Islet Transplantation
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Non-Insulin Dependent NIDDM

• Usually occurs in overweight individuals over 40
  years of age
• Associated with abdominal fat in women
• Target cells become resistant to insulin
• insulin receptor
• Fewer receptors
• Receptors have lower affinity
• Receptor blocked (possibly by antibody)
• Post-receptor mechanisms

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Diabetes Prevelence in US

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