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metabolism, regulation of
human physiology, Fox edition 12
Undergraduate 3

Additional Physiology Flashcards





Energy regulation of the pancrease

The cell types in the Islets of Langerhans and what they secrete


alpha cells secrete    glucacon    that ^ BS

beta cells secrete    insulin       that v BS

delta cells  secrete somatostatin


these are NOT regulated by the pituitary or hypothalmus


Normal fasting blood sugar
65 - 105
Describe the regulation of Insulin and Glucagon

regulated mainly by glood glucose

-----lesser effect from amino acids


regulated by negative feedback


**glucose enters the brain by facilitated diffusion**


normal fasting BS is 65 - 105 mg / dl.



High blood glucose (increases)  = then glucose binds to GLUT 2  receptor protein in beta cells

stimulating production and release of insulin

glucose binds to GLUT 2 when blood sugar rises


and insulin stimulates skeletal muscle cells and adipocytes to incorporate

GLUT 4 (glucose facilated diffusion carrier)

into the plasma membrane


insulin promotes anabolism







 insulin stimulates skeletal muscle cells and adipocytes to incorporate

GLUT 4 (glucose facilated diffusion carrier)

into the plasma membrane


insulin promotes anabolism

Effects of intestinal hormones

intestinal hormones stimulate insulin activity


insulin is released when you eat


All three hormones GIP, GLP-1, and CCK stimulate insulin in anticipation of increased blood glucose


Effects of autonomic nerves

on insulin and glucagon secretion


Parasympathetic nervous system (calm)

stimulates insulin secretion


Sympathetic nervous system (excited)

stimulates glucagon secretion

In the absorptive state what happens

Insulin is the major hormone that promotes anabolism in the body ***


When blood insulin increases these things happen:

promotes cellular uptake of glucose

(facilitative diffusion)

1. Stimulates glycogen storage in the liver and muscles

2. Stimulates triglyceride storage in adipose cells (lypogenesis)

3. Promotes cellular uptake of amino acids and synthesis of protein

In the postabsorptive state what goes on?

Glucogen between meals by glyconeogenesis


Maintains blood glucose concentrations


When blood glucagon*** is increased:

1. stimulates glycogenolysis (ONLY IN THE LIVER) 

in the liver (glucose-6-phosphatase)-- 

2. Stimulates gluconeogenelysis

3. Skeletal muscles, heart, liver and kidneys use fatty acids as a major souorce of fuel (hormone-sensitive lipase)    

 stimulates lipolysis and ketogenesis  (anabolic and catabolic responses)


Remember only  in the  liver  glycogenolysis







Effects of feeding and fasting on metabolism


feeding increases glucose which

increases insulin and decreases glucagon

the effects are

the formation of glycogen, fat, and proten

^ glycogon, fat and protein

v  blood glucose        goes down

v  blood amino acids   goes down

v   blood fatty acids    goes down

v   ketone bodies      goes down




Fasting decreases blood glucose

decreases insulin and increases glucagon

the effects are

hydrolysis of glycogen, fat and protein

+ gluconeogensis and ketogenesis


v glycogon, fat and protein

^  blood glucose        goes up      

^  blood amino acids   goes up

^   blood fatty acids    goes up

^   ketone bodies      goes up


Oral Glucose Tolerance Test

Measures the ability of beta cells to secrete insulin

the ability of insulin to lower blood glucose

Normal person's rise in blood glucose after drinking solution is reversed to normal in 2 hours

Diabetes Mellitus

chronic high blood glucose


2 forms: 

1.  Type 1:        insulin dependent diabetes (IDDM)

2.  Type 2:  non-insulin dependent diabetes (NIDDM

Compare type 1 diabetes and type 2 diabetes

Type 1 diabetes mellitus =


beta cells of the islets of Langerhans are destroyed by autoimmune attack which may be provoked by environmental agent


Glucose cannot enter the adipose cells with out insulin which causes the rate of fate synthesis to lag behind the rate of lypolysis...and fatty acids convert to ketone bodies producing ketoacidosis


Increased blood glucagon  that stimulates glycogenolysis in the liver



consequences of uncorrected deficiency in type 1 diabetes mullitus:


high liver glycogenolysis  + high liver gluconeogenesis

and so low glucose use and hyperglycemia

and osmotic diuresis H20, Na, K Ca,P

dehydration, volume depletion, hypotension


PUPD  =  drink and urinate  thirst and urinate


high liver ketogenesis    high lipolysis

decreased keton utilization


metabolic acidosis


Type 2 diabetes mellitus

slow to develop

Genetic actors are significant

most often occurs in overweight (even 5 or 10 lbs)

Do not respond to insulin 

Tyrosine kinase not activated

Decreased sensitivity of cells to insulin = insulin resistance---obesity=fat interfers

Do not usually develop ketoacidosis

may have high or normal insulin


PUPD  drink and urinate


Treatment in diabetes

lifestyle change

increase exercise + increases the amount of membrane GLUT-4 carriers in the skeletal muscles

weight reduction

increased fiber in diet

reduced saturated fat


Not Adkins diet = bad for kidneys

Catecholamines, metabolic effect of

adrenal medulla part of sympathetic nervous sisten...

similar effects to glucagon


metabolic effects similar to glucagon


stimulates glycogenolysis

---stimulates release of glucose from liver

---stimulates lipolysis and release of fatty acids

Glucocorticoids, metabolic effects of

glucocorticoids are secreted in response to



glucocorticoids support the effects of increased glucagon


Promote lipolysis  and ketogenesis


Promote protein breakdown in the muscles  (increases blood amino acids)


Promote liver gluconeogenesis


mineral = aldosterone

glucocortical = cortison


follicular cells
active form is T3   

increase T3     decreases TSH  like in Graves Disease 


Stimulates cellular respiration by

 production of uncoupling protein


Stimulation of active transport Na+/K+ pump

(lowers ATP by using it up)


Increases metabolic heat


Increases metabolic rate


Contributes to proper growth and development of CNA in children

Lack of prenatally and 6 mo postnatally = creatinism



Aldosterone is a hormone that increases the reabsorption of sodium ions and water

and the release (secretion) of potassium ions

in the cortical collecting ducts and collecting ducts of the kidneys.

This increases blood volume and, therefore, increases blood pressure.


Aldosterone is a yellow steroid hormone

 mineralcorticoid family)

produced by the outer-section (zona glomerulosa) 

of the adrenal cortex,

and acts on the the kidney to cause the conservation of Na+, secretion of K+, increased water retention, and increased BP.

The overall effect

of aldosterone

is to increase reabsorption

of ions and water in the kidney.


aldosterone is reduced in Addison disease

increased in Conn syndrome


Growth Hormone





hypothalmus GhHR


Inhibited by somatostatin

stimulates growth in kids and adolescents

Stimulated by GHRH


causes increase in blood amino acids

decrease in blood glucose

pulsatile, increasing during sleep, decreasing during day



inhibited by IGF 1

IGF 1 is produced in the liver in response to stimulates cell division and growth of cartilage


IGF 2 has more insulin-like actions


liver produces and secretes IFG-1 in response to GH


It  stimulates  cell division  and growth of  cartilage

IGF - 2

More insulin - like actions


promotes anabolism          and catabolism

reduction                hydrolysis


stimulates cellular uptake of amino acids and protein synthesis


Raises blood glucose


Growth Hormone and effects on body growth


gigantism = excess secetion in children

maintain normal body proportions



Excess GH secretion in adults after  epithyseal discs are sealed

no increase in height


Growth of soft tissue

elongation of jaw, deformities in hands, feet and bones of face



Dwarfism = inadequate



¾³Bone deposition and reabsorption

CA++ and phosphate concentrations are affected by:


bone formation and resorption

Intestinal absorption of Ca++  and PO4---

Urinary excretion


Osteoblasts secrete and organic matrix of collagen proteins


Deposit hydroxyapatite crystals



Osteoclasts secrete enzymes to dissolve hydroxyapatite


Formation and resorption of bone occur constantly at rates determined by osteoblasts and osteoclasts



Bone resorption occurs when and osteoclast attaches to the bond matrix and forms ruffled membrane


Osteoclast secretes products that dissolve both Ca++ and PO4³-:  and digest the matix

----Transport of H+ aby H+ ATPase pump in ruffled border

----Cl- channel allows Cl- to flow to H+ to maintain electrical neutrality



Protein matrix digested by cathepsin K releasted by osteoclasts

Parahormone  ( PTH )

THE single most important hormone in control of Ca++

---stimulated by decreased blood Ca++


Stimulates osteoclasts to reabsorb bone


Stimulates kidneys to reabsorb Ca++ from glomerular filtrate, and inhibit reabsorption of PO4³-


Promotes formation of 1, 25 vitamine D3


Works with PTH and 1, 25 vitamin D3 to regulate blood Ca++


Stimulated by increase of plasma Ca++


Inhibited by activity of osteoclasts


Stimulates urinary excretion of Ca++ and PO4³- by inhibiting reabsorption


Physiological significants in adults is questionable


1, 25 Vitamin D3 (1, 25-Dihydroxyvitamine D3)


Pre-vitamine D3 is synthesized in the skin when exposed to mid-ultrviolet waves

---previtamin D3 isomerized to vitamine D3 (cholecalciferol)


Cholecalciferol is hydroxylated in the liver to form 25-hydroxycholecalciferol


In proximal convoluted tubules is hydroxylated to

1, 25- dihydroxycholecalcifer (active vitamin D3)

---Stimulated by PTH


Directly stimulates intestinal absorption of ca++ and PO4³-


When Ca++ intake in inadequate ,  directly stimulates bone reabsorption


Stimulates reabsorption of Ca++ and PO4³- by the kidneys

---simutaneously raising Ca++ and PO4³- results in increased tnedency of these 2 ions to precipitate as hydroxyapatite crystals


Stimulated by PTH

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