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FOOD. sugars. fats. proteins. simple sugars (glucose). fatty acids. amino acids. lipids. glycogen. proteins. glucose. glucose. muscle. liver. fat. glucose. glucose. glucose. Metabolism. Gall bladder. liver. Bile Duct. Pancreas. Pancreatic duct. duodenum.

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PowerPoint Slideshow about ' Metabolism' - william-kennedy


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metabolism

FOOD

sugars

fats

proteins

simple sugars

(glucose)

fatty acids

amino acids

lipids

glycogen

proteins

glucose

glucose

muscle

liver

fat

glucose

glucose

glucose

Metabolism
mammalian pancreas

Gall bladder

liver

Bile Duct

Pancreas

Pancreatic duct

duodenum

Mammalian Pancreas

-Exocrine Pancreas: secretes digestive enzymes, alkaline pancreatic fluid

-Endocrine Pancreas: secretes hormones that regulate carbohydrate, lipid, and protein metabolism

endocrine pancreas

Islets of Langerhans

Exocrine cells

capillaries

Endocrine Pancreas
  • Islets of Langerhans: 4 cell types
    •  cells: secrete glucagon
    •  cells: secrete insulin
    •  cells: secrete somatostatin
    • F cells: secrete pancreatic polypeptide
pancreatic hormones
Pancreatic Hormones
  • Insulin
  • Glucagon
  • Somatostatin
insulin
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
insulin1
INSULIN
  • Action at Target Tissues
    • Activation of insulin receptor:
      • Increases transport of glucose, amino acids, and fatty acids into cells

Glucose transporter:

insulin2
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)
pancreatic hormones1
Pancreatic Hormones
  • Insulin
    • Hypoglycemic, glycogenic, lipogenic, anabolic
  • Glucagon
  • Somatostatin
glucagon
Glucagon
  • Hyperglycemic (increases plasma glucose)
    • (one of many in the body)
  • Actions at target cells
    • Liver
      • Promotes glycogenolysis
      • Promotes gluconeogenesis
    • Fat Tissue
      • Promotes lipolysis
pancreatic hormones2
Pancreatic Hormones
  • Insulin
    • Hypoglycemic, glycogenic, lipogenic, anabolic
  • Glucagon
    • Hyperglycemic, lipolytic
  • Somatostatin
    • Paracrine agent
    • Believed to inhibit insulin and glucagon release
    • Inhibits digestion through several pathways
glucose regulation

Insulin: decreases blood glucose levels

Glucagon: increases blood glucose levels

Somatostatin: inhibits insulin and glucagon levels (paracrine) and digestive processes

Glucose Regulation
diabetes mellitus
DIABETES MELLITUS
  • Type 1—juvenile onset—insulin dependent
    • IDDM
    • Underproduction of insulin
  • Type 2—adult onset—non-insulin dependent
    • NIDDM
    • Insulin receptor resistance
    • Post-receptor mechanism problem
type 1 diabetes insulin dependent iddm
Type 1 DiabetesInsulin Dependent: IDDM
  • Likely results from autoimmune reaction
    • The body’s immune system attacks the  cells
  • Pancreatic  markedly reduced
    • Symptoms only appear after ~80% loss of cells
  • No insulin……physiological repercussions?
  • Treatment
    • Insulin injections or insulin pump
    • Recent methods
islet transplantation

Separate islets from exocrine pancreas

Encapsulate islets (immune protection)

Inside the patient

Inject into liver portal vein

Islet Transplantation

http://diabetes.niddk.nih.gov/dm/pubs/pancreaticislet/

type 2 diabetes non insulin dependent niddm
Type 2 Diabetes:Non-Insulin Dependent: NIDDM
  • Accounts for 90-95% of all Diabetes cases
  • Usually occurs in overweight individuals over 40 years of age
    • But ages are getting younger and younger
    • 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
diabetes prevelence in us
Diabetes Prevelence in US

%

Incidence of diagnosed diabetes

1980

1990

2000

2007

slide17

2004

% of adults >20

2007

type 2 risks 2006
Type 2 Risks 2006
  • 7th leading cause of death
  • With Type 2 diabetes
    • 2 to 4-fold increase in heart disease related death
    • 2-fold risk of death
  • Type 2 associated complications
    • 2-4 fold risk of stroke
    • 75% of adults with Type 2 have high blood pressure
    • leading cause of blindness in adults aged 20-74
    • Leading cause of kidney failure
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