Lipoprotein lipase lpl is important for fat

 lipoprotein lipase (LPL) is important for fat
metabolism (making and storage of fat from
excess carbohydrates)
 levels increase during high insulin
(storage processes)
 Glucagon
o Summary
 Hyperglycemic
 Glycogenolytic
 Lipolytic
 increases blood glucose levels
o The effect is hyperglycemic (increases plasma
glucose)
 one of many hormones which does this (as
opposed to insulin, which is the only
hypoglycemic hormone)
o Actions at target cells
 Increases enzymes that activate (most of the
effect is in the liver)
 glycogenolysis and gluconeogenesis in
the liver
 ureogenesis in the liver
 ketogenesis in the liver
 lipolysis in the adipose tissue (fat)
 Decreases enzymes that activate
 glycogen formation in the liver
 lipogenesis in the fat
 protein synthesis in the muscle
o Fatty acids and pyruvate make ketones; pyruvate
also makes glucose, which is also derived from
glycogen
 lipoprotein lipase (LPL) is important for fat
metabolism (making and storage of fat from
excess carbohydrates)
 levels decrease during high glucagon
(liberation processes)
 During extreme hypoglycemia (low blood sugar), the adrenal
medulla releases epinephrine
 epinephrine stimulates glucagon secretion, inhibits insulin
secretion, and works with glucagon to increase blood
glucose
 Insulin, however, shifts toward glycogen synthesis from
glucose in hyperglycemia
 Hormonal Control of Metabolism by Tissue Type (see pp. 18)
o Adipose Tissue (fat)
 Insulin
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 INCREASE glucose uptake
 INCREASE fatty acid synthesis
 INCREASE fatty acid esterification
 DECREASE lipolysis
 INCREASE LDL hydrolysis
 Cortisol
 INCREASE lipolysis
 DECREASE fatty acid esterification
 DECREASE glucose utilization
 DECREASE insulin sensitivity
 Triiodothyronine
 INCREASE glucose utilization
 INCREASE lipolysis
 Catecholamines
 INCREASE lipolysis
 INCREASE glycolysis
 Growth Hormone
 DECREASE glucose utilization
 DECREASE insulin sensitivity
 INCREASE lipolysis
 DECREASE fatty acid esterification
o Liver ( carbohydrates )
 Insulin
 DECREASE glucose production
 INCREASE glycogen synthesis
 INCREASE fatty acid synthesis
 INCREASE fatty acid esterification
 DECREASE ketogenesis
 Cortisol
 INCREASE gluconeogenesis
 INCREASE glycogen synthesis
 DECREASE glucose utilization
 DECREASE insulin sensitivity
 Triiodothyronine
 INCREASE glucose utilization
 INCREASE glycogenolysis
 Glucagon ( anti-insulin effects )
 INCREASE glycogenolysis
 INCREASE gluconeogenesis
 INCREASE ketogenesis
 Catecholamines
 INCREASE glycogenolysis
 Growth Hormone
 INCREASE gluconeogenesis
 DECREASE insulin sensitivity
 INCREASE ketogenesis
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 INCREASE IGF production
o Muscle (protein)
 Insulin
 INCREASE glucose uptake
 INCREASE glycogen synthesis
 INCREASE protein synthesis
 DECREASE protein degradation
 Cortisol
 INCREASE protein degradation
 DECREASE protein synthesis
 DECREASE glucose utilization
 DECREASE insulin sensitivity
 INCREASE fat utilization
 Triiodothyronine
 INCREASE glucose utilization
 INCREASE fat utilization
 Catecholamines
 INCREASE glycogenolysis
 INCREASE glycolysis
 Growth Hormone
 DECREASE glucose utilization
 DECREASE insulin sensitivity
 INCREASE protein synthesis
 INCREASE fat utilization
 Hormonal control of energy balance in the fasting vs. well-fed state
o Fasting state – glucagon predominates
 Glucagon released from pancreas
 Glycogen, glycerol, and amino acids converted into glucose in the
liver via gluconeogenesis
 Liberated glucose and ketone bodies (KBs) power brain