Exam
Glucose Metabolism
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Glucose Metabolism
Physiology
Blood Glucose
Released from hepatic stores between meals
Derived from ingested carbohydrates
Postprandial
Glucose
>20 fold over hepatic release
Insulin
Gene
ral
Insulin
produced by pancreatic beta cells
Insulin
release stimulated by
Blood Glucose
Insulin
response to
Glucose
is linear
Insulin
response is based on
Glucose
sensitivity
Glucose
sensitivity depends on
Ambien
t
Glucose
Normal: Rapid
Insulin
release with a meal
Fastin
g: Steeper rate of
Insulin
release
Prolonged
Hyperglycemia
: Flattened response
Phase 1
Insulin
Release
Duration: 10 minutes
Suppresses hepatic
Glucose
release
Phase 2
Insulin
Release
Duration: 2 hours
Controls mealtime carbohydrates
Basal
Insulin
Release
Low continuous
Insulin
level
Covers metabolic needs between meals
Pathophysiology
Type II Diabetes Mellitus
Loss of
Glucose
sensitivity (see above)
Loss of phase 1
Insulin
response
Insufficient phase 2
Insulin
response
Insulin
production by beta cell
First:
Insulin
increases to overcome
Glucose
toxicity
Results in beta-cell exhaustion (
Glucose
Toxicity)
Initially reversible beta cell exhaustion
Permanent later as amyloid replaces beta cells
Insulin
levels decrease as beta cells fail
Beta-cell function reduced to <50% by DM diagnosis
Impaired incretin action
Incretins manage postprandial
Glucose
levels
Incretin released from GI tract following meals
Endogenous Incretin effects
Increases
Glucose
dependent
Insulin
secretion
Delays gastric emptying
Decreases food intake (improves satiety)
Progressive incretin reduced activity
Glucagon-Like Peptide 1
(
GLP-1
) activity decreases
Medications
Increase
Insulin
sensitivity
Metformin
Thiazolidinedione
s
Stimulate
Insulin
release from beta cells
Meglitinide
s (act on phase 1 release)
Sulfonylurea
s (act on phase 2 release)
Replace
Insulin
See
Insulin
Increase incretin levels (
GLP-1
)
Exenatide
(
Byetta
)
Sitagliptin
(
Januvia
)
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