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1. The pancreas secretes digestive juices and hormones like insulin and glucagon that regulate blood glucose levels. Insulin promotes glucose uptake and storage, while glucagon has the opposite effect. 2. Insulin and glucagon levels are regulated by blood glucose levels in a feedback loop. High glucose stimulates insulin secretion which lowers blood glucose, while low glucose stimulates glucagon. The hormones work antagonistically to maintain normal blood glucose. 3. Diabetes mellitus occurs when insulin production or sensitivity is impaired, preventing proper blood glucose regulation. This can cause high blood glucose levels and damage to tissues over time.

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100% found this document useful (1 vote)
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1. The pancreas secretes digestive juices and hormones like insulin and glucagon that regulate blood glucose levels. Insulin promotes glucose uptake and storage, while glucagon has the opposite effect. 2. Insulin and glucagon levels are regulated by blood glucose levels in a feedback loop. High glucose stimulates insulin secretion which lowers blood glucose, while low glucose stimulates glucagon. The hormones work antagonistically to maintain normal blood glucose. 3. Diabetes mellitus occurs when insulin production or sensitivity is impaired, preventing proper blood glucose regulation. This can cause high blood glucose levels and damage to tissues over time.

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THE
PANCREAS
TYPES OF TISSUES

1.Acini ± secretes digestive juices

2.Islets of Langerhans- has 3 types of cells namely


a. Alpha cells ± 25% - secrete D 
[.Beta cells ± 60% - secrete  
and 
c. Delta cells ± 10% - secrete   
d. PP cells ± secrete  
  
INSULIN ± Hormone Associated with
Energy A[undance

1.Effect on Car[ohydrate Meta[olism

A. Promotes Muscle Glucose Uptake and Meta[olism


-Storage of Glycogen in Muscle

B. Promotes Liver Uptake, Storage and Use of Glucose


Mechanisms:

 

 
[. causes 


  from the
[lood [y the liver cells ([y  


  


    
C. increases activity of enzyme  
  , that
promote glycogen synthesis

- Glucose is released from the liver [etween meals


Lack of insulin activates   , which
causes splitting of glycogen into glucose phosphate

- Insulin promotes Conversion of Excess Glucose into


fatty Acids and   
D   in the
liver
x Lack of Effect of Insulin on Glucose Uptake and Usage
by the Brain
2. Effect on Fat Meta[olism
A.Insulin promotes Fat Synthesis and Storage
Ñ Storage of Fat n the Adipose Cells
  
  

 

   




 
 
 




 



 
B. Insulin deficiency Causes Increase Meta[olic Use of Fat
causing

a 
    of Storage Fat and Release of Free Fatty
Acids
[. Increase Plasma Cholesterol and Phospholipid
c. Excess Usage of Fats during Insulin Lack Causes
  and   
3. Effect of Insulin on Protein Meta[olism
A. INSULIN PROMOTES PROTEIN Synthesis and Storage

a. stimulates transport of amino acids into the cells


( 
 
  
  

   X
[. increases the translation of messenger RNA,
forming new proteins
c. increases the rate of transcription of DNA genetic
sequences in cell nuclei
d. inhi[its cata[olism of proteins
e. depresses the rate of gluconeogenesis
INSULIN PROMOTES PROTEIN FORMATION AND
PREVENTS DEGRADATION OF PROTEINS

B. Insulin Lack Causes Protein Depletion and Increased


Plasma Amino Acids
Ñ protein wasting is one of the most serious of
all effects of severe dia[etes mellitus

C. Insulin and Growth Hormone Interact Synergistically to


Promote Growth
MExANISMS OF INSULIN
SExRETION
CONTROL OF INSULIN SECRETION

1. Increased Blood Glucose Stimulates Insulin secretion


u Other Factors That Stimulate Insulin Secretion:
a Amino Acid ± most potent are V  and 
- 

V
 

    
       
 

b Gastrointestinal ormones ± V


  
  

V
  
 


c Other ormones-  V   


  

   
  V 

d Autonomic Nervous System
-Stimulation of the parasympathetic nerves to the pancreas can
increase insulin secretion
Role of Insulin in ³Switching´ Between Car[ohydrate
and Lipid Meta[olism

D ! D"#± a hormone secreted [y the  


 
of
the islets of Langerhans when [lood glucose
concentration falls. Its important function is to 

 
 
 
thus is also called the
$   
$ 
Effects on Glucose
Meta[olism

Major Effects
1. [reakdown of liver glycogen    X

2. 
  
in the liver
ther Effects (when conc. rises a[ove maximum
normally found in the [lood

1.activates adipose cell lipase- increasing fatty acids


availa[le to the energy system of the [ody

2.inhi[its storage of triglycerides in the liver

3. enhances the strength of the heart

4. increases [lood flow in some tissues, esp. kidneys

5. enhances [ile secretion

6. inhi[its gastric acid secretion


Regulation of Glucagon Secretion

a. Increased Blood Glucose Inhi[its Glucagon Secretion

Ñ the most potent factor that controls glucagon secretion


Ñ 


 
 


 

 
 
%

 
  





 
  
 

[. Increased Blood Amino Acids Stimulate Glucagon


Secretion (especially   

  X
SOMATOSTATIN INHIBITS GLUCAGON
AND INSULIN SECRETION

Factors Related to Ingestion of Food Stimulate


Somatostatin Secretion:

1. Increased [lood glucose


2. Increased amino acids
3. increased concentrations of GI hormones
4. increased fatty acids
Inhi[itory Effects of Somatostatin:

1. Acts on the islets of Langerhans to depress the


secretion of insulin and glucagon

2. decreases the motility of the stomach, duodenum and


gall[ladder

&
  
' 

  ( is to
extend the period of time over which the
food nutrients are assimilated into the
[lood
SUMMAR Y F BLD GLUCSE REGULATIN
Mechanisms:

1. The liver functions as an important [lood glucose [uffer


system
2. Both insulin and glucagon function as important
feed[ack control systems for maintaining a normal
glucose concentration
3. Severe hypoglycemia stimulates the sympathetic nervous
system
ë Growth hormone and cortisol are secreted in response to
prolonged hypoglycemia, decreasing the rate of glucose
utilization by most cells
Importance of Blood Glucose Regulation:

1. Glucose is the only nutrient that normally can [e used


[y the  
  and  
  





2. Blood glucose should not too high (reasonsX


a. glucose exert a large amount of osmotic pressure in
the ECF causing cellular dehydration
[. high levels of [lood glucose concentration causes loss
of glucose in the urine
c. causing osmotic diuresis [y the kidneys
d. long-term increase in [lood glucose cause damage to
many tissues, esp. [lood vessels. Vascular injury
leads to heart attack, stroke, end-stage renal
failure and [lindness
DIABETES MELLITUS

It is a syndrome of impaired
car[ohydrate, fat, and protein meta[olism
caused [y either  
 or 

   
 
 

 
Types of Diabetes Mellitus:

1. & 
)
* - also called   dia[etes
mellitus (IDDMX, is caused [y lack of insulin secretion.

2. & 

*  ± also called   
 dia[etes
mellitus (NIDDMX , is caused [y decreased sensitivity of
target tissues to insulin. This reduced sensitivity to
insulin is often referred to as  
 
Type I Dia[etes- Lack of Insulin
Production [y Beta cells of the Pancreas

CAUSES:

1. Viral Infection or Autoimmune Disease ± may [e


involved in the destruction of the [eta cells

2. Heredity

   
      0 
    

 
 
Principal Sequelae:

0Y   

Y   



 
 


 
   

Y  
     
Blood Glucose Concentration Rises to Very
High Levels in Dia[etes Mellitus

Increased Blood Glucose Causes Loss of Glucose in


the Urine

Increased Blood Glucose Causes Dehydration


"  
  
  
  


%  
  


    +
Chronic High Glucose Concentration
Causes Tissue Injury:

Blood vessels function a[normally resulting


to inadequate [lood supply to tissues
leading to risk 

,   

 
 ,   and  , and
  and 



Damage to tissues causing  

(a[normal function of peripheral nerves, and
 
  
  

$  
secondary to renal injuryX
and     (secondary to
a[normal lipid meta[olismX
Dia[etes Mellitus Causes Increase Utilization of Fats
and Meta[olic Acidosis leading to coma and death

As a result the patient develops severe meta[olic


acidosis leading to coma and death

Ñ     ± increased deposition of cholesterol


in the arterial walls
Ñ A  
 Ñ rapid and deep breathing ±
physiologic compensation in metabolic acidosis
Dia[etes Causes Depletion of Body¶s
proteins

- rapid weight loss and   (lack of


energyX despite of eating large amounts of food
  X
Type II Dia[etes ± Resistance to Meta[olic
Effects of Insulin

Ñmore common than type I ± to 90% of all cases of


dia[etes
Ñnset occurs after the age of 30, often [etween 50 t0 60
years
 referred to as  
"
* 
 related mainly to the increasing prevalence of   




 


 

 


 

,

 

Obesity, Insulin Resistance and ³Metabolic


Syndrome´ Usually Precede Development of Type II
Diabetes
Features of Metabolic Syndrome

0Y      





Y    
Y    
Y !     
   "
     "  
#Y    
Other Factors That cause Insulin
Resistance and Type II Diabetes

0Y $   % &$'%(


Y )* 
 
  
&' % (+ 
& (

Development of Type II Diabetes During


Prolonged Insulin Resistance
Physiologic Diagnosis of Diabetes
Mellitus

1 Urinary Glucose
u Fasting Blood Glucose and Insulin Levels
- in the early fasting blood glucose level is
normally 80 to 90 mg/100 ml
-110 mg/100 ml to be the upper limit
Ô 

 
 
 
 
 
Ñ type I dia[etes ± plasma insulin levels are
very low or undetecta[le during fasting and
after a meal
type II dia[etes ± plasma insulin concentration
is higher than normal

3. Glucose Tolerance Test

4. Acetone [reath
TREATMENT F DIABETES:

A.Type I dia[etes ±administer enough insulin

B. Type II dia[etes
Ñdieting and exercise
Ñdrugs
Insulinoma ± Hyperinsulinism

Ñ occurs from an adenoma of an islet of Langerhans

Ñ insulin shock and hypoglycemia

Ñ as [lood glucose level falls into the range of 50 to 70


mg/dl the CNS [ecomes excita[le leading to
hallucinations, extreme nervousness, trem[les
all over, [reaks out in a sweat
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