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regulation of metabolism
chapter 19, Human Physiology, Fox
Undergraduate 3

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absorptive state

post absorptive state



rate of deposit, withdrawal in and from and conversion of one type to another regulated by hormones

Balance of anabolic and catabolic determined by insulin vs glucogen, GH, T4 etc

Energy regulation by pancreatic Islets

increased BS = increased insulin = promotes synthesis of glycogen and fat


degreased BS = increased glucagon and increased glycogenesis in liver


beta cells secete insulin the major hormone that maintains he=omeostsis in BS


alpha cells secrete glucagon


delta produce somatosttin ( same as produced in hypothalmus and intestine)


Brain uses 60% of glucose

Can keep BS by pancreatic regulation of liver (glucose from glycogen and non carb molecules)

only in the liver can glucose be made from glycogen




Insulin stimulates insertion of GLUT 4 carrier proteins in plasma membrane of target cells=heart, muscle, adipose and liver


permits entry of glucose into target cells by facilitated diffusion


Insulin promotes the productin of energy storing molecules of glycogen and fat and decreased BS.  Insulin inhibits breakdown of fat

induces fat forming enzymes

inhigits breakdown of muscle protein

promotes anabolism


Prevents BS from going above 170 mg per 100 ml after a meal

or below 50 per 100 molecules between meals


If BS goes too low it can damage brain

weak, dizzy, act odd, coma and death.


fasting BS 65- 105 mg/dl     eat   140 - 150 mg/dl


beta cells of islets acted on  leads to closing of K+ channels

Produces depolarization that opens voltage gated Ca++ channels

the rise in cytoplasm Ca++ stimulates exocytosis of vsicules containing insulin


Inhibits secretion of glucogen from alpha



changes in insulin and glucogon maintain homeostasis


Type 1 diabetes mellitus


glucose cannot enter adipose cells

breakdown of fat and free fatty acids are released from adipose tissue and converted to ketone bodies in liver

ketosis-and if buffer reserves of bicarbonate is neutralized get detoacidosis

glucose and detone act as osmotic diuretics

severe dehydration and ketoacidosis and electrolyte imbalance can lead to coma and death


Plus type 1 diabetic have a high secretion of glucagon from alpha cells


glucagon stimulates glycogneolysis in liver and increases BS


glucagon stimulates production in liver that converts fatty acids to ketone bodies



Type 2 diabetes mellitus

effects of hormones depend on concentration in blood and sensitivity of trget organs to given amount of hormone.


Type 2 have low tissue sensitivity  

insulin resistance


In insulin resistance increased glucagon secretion gives much increase of BS aby stimulating liver glycogenolysis and gluconeogenesis


pre diabetic  glucosde tolerance test 140 -200

over 200 = diaabetes


exercise increases GLUT 4 carriers and helps


type 2 usually do not develope ketoacidosis


increased insulin level = increased triglycerides, decreased HDL cholesterol, metabolic changed that increase CV disease, increase BP, CVA ett

this is metabolic syndrome

Adrenal hormones, Thyroxine and GH metabolic regulation by

epinephrine, cortisol, thyroxine, GH stimulate catabolism of carbs and lipids


GH has both anabolic and catobolic effects

it promotes protein synthesis   anabolism

and stimulates catabolism of fat and release of fatty acids from adipose in fasting

decreases glucose use by cells

GH increases blood sugar so has a diabetogenic effect


Thyroxine and GH stimulate protein synthesis, body growth and development of CNS

metabolic effects of catecholamines

similar to that of glucagon

stimulate glycogenolysis andd release of glucose from liver and lypolysis and release of fatty acids from adipose tissue


glucagon and epinephrine have similar mechanisms of actin where both are mediated by cAMP


brown fat an have a high rate of energy expendituure that is stimulated by spinephrin (unchecked by negative feedback from ATP)

Effects of GH on body growth

skeleton increases epithysial growth plates in cartilage in long bones mediated by IGF-1 and IGF-2


in adults too much causes acromegaly


promotes lipolysis and ketogenesis and stimulates making of liver enzymes that increase glyconeogenesis


and glucagon



from hypothalmus

inhibits GH

regulation of GH


GHRH stimulates growth hormone secretion

unique in that its secretion is controlled by releasing and inhibiting hormone from hypothalmus


anterior pituitary gland, adenohypophysis, secretes the growth hormone. the secretion is under control of growth hormone releasing factor and growth ...

Insulin-like growth factors   IGF's

polypeptides from many tissues

similar to pro-insulin structure

it effects (somatomedian) and mediates some fo GH actions


liver makes and secretes IGF-1 in response to GH stimulation

IGF-1 then acts as a hormone itself and goes to targets

cartilage is a major target of IGF-1= stimulates growth


It also functions as an autocrine regulator because cartidedge also produce IGF-1 in response to GH stimulation

Growth promoting IGF-1 acts as a hormone and an autocrine regulator and is a jajor regulator of bone growth



these actions are supported by IGF-2 which has a more insulin like actin. 

GH stimulates lipolysis in adipose tissue  but glucose use is not mediated by somatomedians IGF-1  or IGF-2

regulation of Ca++ and phosphorus

necessary for contaction of muscles and up keep of membrane permeability


low plasma Ca+=

increases PTH=

robs bone of Ca++

decreases excretion of Ca++ from kidney

no effect on intestines

1,25 dihydroxyvitamine D3 increases uptake of Ca++ in intestines


disease=hypercalcemia adn osteofibrosa



high Ca++ in blood

calcitonin secreted=

put Ca++ in bones

excretes Ca++ by kidney

nothing in intestines

no disease known



vitamin D

puts Ca++ in bone

kidney keeps Ca++

intestines absorb Ca++


diseases osteomalasis

rickets in kids


osteoblasts = bone forming


osteoclast = bone breaking = puts Ca++ in blood




is used for clotting

cell signaling

second messenger for hormone actions

stimulus for muscle contraction

for cell membrane permeability


decreased Ca++ = increased permeability of cell membrane to Na+ and other ions


high Ca++ = reduces exitability of muscles


Low Ca++ = muscle contraction becomes abnormal and the nervous system more excitable




Parathyroid hormone PTH

and calcitonin


if plasma levels of Ca++ decrease

PTH increases


if no parathyroid = hypocalcemia'

decreased PTH

decreased D#

decreased Mg


hypocalcemia= muscle twitching, spasm, tetany


hypercalcemia = muscles become less excitable


1st in skin from 7 dehydrocholesterol + sun

enzymes  and convert to active form


Primary action of D is to increase intestinal absorption of Calcium


a kidney enzyme stimulated by PTH also does something to increase absorption from intestines

put Ca++ in bones but must have enough Ca++

if calcium intake is too low then D causes demineralization of bones

kidneys resorb Ca++


D3 is also and autocrine / paracrin regulator by skin, breasts, colon, prostrate and some immune cells.  they convert inactive form from liver to active regulator and it remain in tissue of organ that makes it


D is an autocrine or paracrine regulator in tissues and organs

it promotes cell differentiation and inhibits cell proliferation and helps immune system fight infection


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