1. Glucose Metabolism & Diabetes
How does diabetes disrupt the homeostatic levels of glucose in the blood?

2. Objectives
Describe the major structures and functions of the liver and pancreas.
Explain the intricacies of glucose, protein, and fat metabolism.
Explain the roles of insulin and glucagon in maintaining homeostasis.
Explain the processes of lipolysis, deamination glycogenolysis, and gluconeogenesis.
Define the terms glycosuria, polyuria, polydipsia, and polyphagia and explain why diabetes causes these conditions.
State the medical complications associated with diabetes and explain why these occur.

3. PART I
LIVER & PANCREAS:
STRUCTURE
FUNCTION

4. THE LIVER: Structure
Largest visceral organ in the body 1.5 kg (3.3 lb.), 4 lobes
Sinusoids (blood vessels-similar to capillaries) between liver cells (hepatocytes) empty into the central vein

5. THE LIVER: Structure
Functional unit of the liver: Liver lobule (50, ,000): cylindrical structure, several mm long 1-2 mm in diameter
Central vein in center of lobule

6. THE LIVER: Structure
Hepatocytes in a liver lobule form a series of irregular plates arranged like the spokes of a wheel
Portal area between lobules: hepatic artery, interlobular portal vein, interlobular bile duct

7. Sinusoid with red blood cell and Kupffer cell
LIVER
Blood flowing from the intestinal capillaries picks up many bacteria from the intestines.
When bacterium comes into contact with a Kupffer cell (phagocytic cell: engulf pathogens, cell debris, and damaged blood cells) in less than 0.01 sec it passes inward through the cell membrane and gets lodged until it is
digested.
Less than 1% of incoming bacteria
escapes to circulation.
Sinusoid with red blood cell and Kupffer cell

8. HEPATIC PORTAL CIRCULATION
Blood from the spleen,
pancreas, stomach & intestines
enters the liver via the hepatic
portal vein.
Blood from the intestines is
very high in glucose.
Liver cells remove excess
glucose, amino acids, toxins,
bacteria.
Blood leaves the liver by
means of the hepatic vein, now
with normal levels of glucose.

9. LIVER: Function Filtration and storage of blood.
Metabolism of carbohydrates, proteins, fats, and hormones.
Storage of vitamins and minerals.
Synthesis of plasma proteins.
Synthesis and secretion of bile.
PHAGOCYTE

10. Filtration of the blood

11. THE PANCREAS: Structure
The pancreas is approximately 20 cm (8 in) and weighs about 80g (3 oz)
The pancreas has two major types of tissues: the acini
(secrete digestive juices to duodenum) and the islets of
Langerhans (secrete insulin and glucagon directly into blood)
Human pancreas has 1 – 2 million islets of 0.3 mm in diameter, although the islets account for only about 1% of the pancreatic cell population

12. THE PANCREAS: Structure
Ref:
Islets of Langerhans contain 3 types of hormone-secreting cells
Alpha cells (25%) Beta cells (60%)
Delta cells (10%) F cells (PP cells) (5%)
The islets are organized around small capillaries into which the cells secrete their hormones

13. THE PANCREAS: Structure/Function
Alpha cells secrete glucagon elevates blood glucose concentrations
Beta cells secrete insulin reduces blood glucose concentrations
Delta cells secrete somatostatin- slows the rate of food absorption and digestive enzyme secretion
F cells/PP cells secrete pancreatic polypeptide
Close interrelation among various cell types allow regulation of secretion of some hormones by other hormones: insulin inhibits glucagon secretion, somatostatin inhibits insulin and glucagon secretion

14. PART II
HOW DO THE LIVER & PANCREAS ALLOW US TO UTILIZE THE NUTRIENTS WE CONSUME?

15. Glucose: the preferred nutrient
Carbohydrates are the preferred source of energy for the body.
Final products of carbohydrate digestion in the digestive tract are monosaccharides (glucose [80%], fructose and galactose)
Much of fructose and all galactose are converted to glucose in the liver and released back into the blood.
Glucose is a large molecule that must be broken down into a form of energy usable by the cell (ATP).
health.howstuffworks.com/diabetes1.htm

16. A P P P Structure of ATP: Adenosine Triphosphate High-energy bonds
Phosphate groups
adenosine

17. A P P P A P P P + C6H12O6 CATABOLISM: Molecule Breakdown
Glucose is broken down into many molecules of ATP
(higher # if O2 present) A P P P
When bond is broken, energy is released to do cellular work A P P P +
Adenosine
Diphosphate

18. Glucose Metabolism
The process of glucose metabolism involves 1) glycolysis, ) the citric acid cycle (Krebs cycle) ) electron transport.
1-cytoplasm;
2, 3-mitochondria
Complete reaction:
C6H12O6 + 6O2 >>
6CO2 + 6H2O
Net gain = 36 ATP

19. Only 40% of the energy released through catabolism of glucose is captured in ATP.
The remaining 60% escapes as heat that warms the interior of the cells and the surrounding tissues.
If cells have inadequate amounts of glucose to catabolize, the immediately shift to the catabolism of fats for energy.
In starvation, proteins are used for energy after carbohydrate and fats are depleted.

20. Fat & Protein Metabolism
Triglycerides >> Fatty acids & Glycerol (lipids)
Proteins >> amino acids
Lipids and amino acids are broken down into molecules that can enter the citric acid cycle
LIPOLYSIS: catabolism of lipids
DEAMINATION: catabolism of amino acids
Fatty acids or glycerol or amino acids
>>intermediate compounds
>>Citric Acid Cycle >> ETS >> ATP

21. Alternative Catabolic Pathways
Triglycerides
Glycogen
Proteins
Fatty Acids
Glycerol
Glucose
Amino Acids
Pyruvic
acid
cytoplasm
Acetyl-CoA
mitochondrion
Citric
Acid
Cycle
Electron Transport
ATP Production

22. REGULATION OF NUTRIENTS
Insulin regulates the uptake of nutrients into the cells, the storage of nutrients not being used, and the conversion of one nutrient type to another.

23. Metabolic Efficiency: Glucose
Cells rely on insulin for efficient absorption of glucose from the blood (except brain cells)
Insulin also enhances ATP production
Without insulin not enough glucose is supplied to tissues for energy metabolism

24. A SIMPLIFIED VIEW OF THE
MECHANISM OF INSULIN
SIMPLY PUT, insulin can be thought of as the funnel that allows glucose to pass through the receptors into cells.
S= SUGAR (glucose)

25. Insulin & its chemistry
Insulin is a small protein (MW of human insulin 5808) composed of two amino acid chains connected by two disulfide linkages.
Secreted by beta cells, insulin circulates in blood in unbound form.
It has a plasma half-life of about 6 min and is cleared from circulation in 10 – 15 min
Insulin not combined with receptors
in target cells are degraded by
insulinase -mostly in liver and
also in kidneys and muscles
Connecting peptide (white)
joins the two chains

26. INSULIN MOLECULE Protein of 21 amino acid A chain and
30 amino acid B chain, Disulfide linkages 21
A Chain
B Chain 30

27. Mechanism of Action of Insulin*
The insulin receptor is a combination of 4 subunits held together by disulfide linkages: two α-subunits
lying outside the cell membrane and two β- subunits protruding into the cell cytoplasm.

28. Mechanism of Insulin
When insulin binds to the α-subunit in target tissues, the β- subunits in turn become activated.

29. Mechanism of Action of Insulin*
Activation of the β-subunits triggers a series of reactions that draw the glucose transporter to the cell membrane.
Cells (liver, muscle, adipose, but not brain) are now able to increase their uptake of glucose. (w/in seconds after insulin binds with its membrane)
The cell membrane also becomes more permeable to many amino acids.

30. Mechanism of Action of Insulin*

31. Mechanism of Action of Insulin
Ref:

32. Insulin: Glucose Storage
Only enough ATP for immediate cellular requirements is made at any one time
Glucose that is NOT needed for ATP is ANABOLIZED into glycogen and stored for later use in the liver and in muscles.
GLYCOGENESIS: synthesis of glycogen from glucose molecules
Insulin
stimulates glycogenesis (glycogen anabolism)
inhibits glycogenolysis (glycogen catabolism)

33. Why is glucose stored as glycogen?
Glucose is in liquid form. As the number of glucose molecules increases, the pressure inside the cell increases.
Converting glucose to glycogen
(in solid form) relieves pressure inside the cell.

34. Glucose Conversion to Fat
Excess glucose is preferentially stored as glycogen BUT
When cells are saturated with glycogen (liver cells store 5 to 8% of their weight as glycogen, muscle cells 1 to 3%) additional glucose is converted to fat in the liver and stored as fat in adipose cells.

35. Insulin: Glucose>>Fat Storage
Insulin promotes the conversion of all excess glucose in liver that cannot be stored as glycogen into fatty acids
Fatty acids are packaged as triglycerides in low density lipoproteins transported by blood to adipose tissue
Insulin activates lipoprotein lipase in the capillary walls of adipose tissue, which splits triglycerides into fatty acids. This enables them to be absorbed into adipose cells where they are converted again to triglycerides and stored.

36. Insulin: Protein Metabolism
Insulin (like growth hormone) stimulates transport of amino acids into cells.
Insulin increases the translation of messenger RNA, thus forming new proteins.

37. Insulin: Protein & Fat Metabolism
Insulin and growth hormone interact synergistically to promote growth
Insulin stimulates the absorption of fatty acids and glycerol by adipocytes, where they are stored as triglycerides.

38. Summary: Metabolic Effects of Insulin
Increases rate of glucose transport into target cell
Increases rate of glucose utilization and ATP formation
Increases conversion of glucose to glycogen (liver, skeletal muscle)
Increases amino acid absorption and protein synthesis
Increases triglyceride synthesis (adipose tissue)
*DECREASES HIGH BLOOD GLUCOSE LEVELS*

39. THE REGULATION OF BLOOD GLUCOSE
Beta Cells in Islets of Langerhans
Receptors
↑Blood Glucose
Stimulus

40. THE REGULATION OF BLOOD GLUCOSE
Increased Insulin secretion and synthesis
Intracellular communication
Beta Cells in Islets of Langerhans
Receptors
↑Blood Glucose
Stimulus

41. THE REGULATION OF BLOOD GLUCOSE
Increased Insulin secretion and synthesis
Insulin carried in blood
Intracellular communication
Muscle and fat cells throughout body
Liver cells
Beta Cells in Islets of Langerhans
Receptors
↑Glucose uptake
↓Glucose synthesis
Glycogen
synthesis
Response
↑Blood Glucose
Stimulus
↓Blood Glucose
↓Blood Glucose

42. THE REGULATION OF BLOOD GLUCOSE
Increased Insulin secretion and synthesis
Efferent Pathway
Insulin carried in blood
Intracellular communication
Muscle and fat cells throughout body
Liver cells
Effectors
Beta Cells in Islets of Langerhans
Receptors
↑Glucose uptake
↓Glucose synthesis
Glycogen
synthesis
Response
↑Blood Glucose
Stimulus
↓Blood Glucose
Negative Feedback
↓Blood Glucose

43. …and LOW blood glucose…
After the meal is over and blood glucose level begins to fall to a low level:
The pancreas decreases insulin secretion
Glycogen synthesis in liver is stopped
Glucose uptake by liver from blood is prevented
If blood glucose levels continue to fall,
- GLUCAGON will increase the RELEASE of glucose from the cells

44. …and for more glucose… GLUCAGON also causes:
GLYCOGENOLYSIS: Breakdown of glycogen into glucose
GLUCONEOGENESIS: Increase of synthesis of glucose from amino acids and the glycerol portion of fat

45. FOR ADDITIONAL NUTRIENTS…
GLUCAGON causes:
LIPOLYSIS: Activation of adipose cell lipase making fatty acids available for use as energy source
GLUCAGON is a large polypeptide composed of a chain of 29 amino acids and has a molecular weight of Secreted by alpha cells.

47. Somatostatin
A polypeptide with 14 amino acids with a 3 min half-life in blood. Same chemical substance as growth hormone inhibitory hormone. Secreted by delta cells.
All factors related to ingestion of food stimulate somatostatin secretion
Somatostatin has many inhibitory effects: Depresses secretion of insulin and glucagon
Decreases motility of stomach, duodenum and gallbladder
Decreases secretion and absorption in GI tract
It extends the period of time for assimilation of food

48. Pancreatic Polypeptide
Secreted by F cells
Inhibits gallbladder contractions
Regulates the production of some pancreatic enzymes
May help control the rate of nutrient absorption by the digestive tract

49. Part III
Diabetes:
What’s the
problem?

50. Review: Endocrine Effects of Insulin
Stimulates Inhibits
Liver
Skeletal Muscle
Adipose tissue
glycogenesis glycogenolysis
triglyceride synthesis ketogenesis
gluconeogenesis
glucose uptake
protein synthesis protein degradation
glycogenesis glycogenolysis
triglyceride storage lipolysis
Promotes anabolic processes
Inhibits catabolic processes

52. Importance of Insulin
Without insulin, glucose transport into the cells will be insufficient.
Lacking glucose, cells will have to rely on protein and fat catabolism for fuel.
Also, when there is not enough insulin, excess glucose cannot be stored in the liver and muscle tissue.
Instead, glucose accumulates in the blood-- above normal levels.

53. The high concentration of glucose in the blood (resulting from the lack of insulin) is called hyperglycemia, or high blood sugar.

54. Blood Glucose
Fasting blood glucose concentration (person who has not eaten in the past 3- 4 hours)
Normal person: mg / 100 ml
Diabetic patient: mg / 100 ml
After a meal:
Normal person: mg / 100 ml
Diabetic patient: < 200 mg / 100 ml

55. EXCESS OF BLOOD GLUCOSE…
Exerts high osmotic pressure in extracellular fluid, causing cellular dehydration
Excess of glucose begins to be lost from the body in the urine: GLYCOSURIA

56. GLYCOSURIA >>>
Excessive glucose in the kidney filtrate acts as an osmotic diuretic, inhibiting water reabsorption resulting in POLYURIA: huge urine output >>> decreased blood volume and dehydration.
Dehydration stimulates hypothalamic thirst centers, causing POLYDIPSIA: excessive thirst.

57. OTHER SIDE EFFECTS of POLYURIA
The dehydration resulting from polyuria also leads to dry skin.
During a period of dehydration, blurred vision can be caused by fluctuations in the amount of glucose and water in the lenses of the eyes.

58. POLYPHAGIA
POLYURIA, POLYDYPSIA, & POLYPHAGIA= THE 3 CARDINAL SIGNS OF DIABETES
POLYPHAGIA: excessive hunger and food consumption, a sign that the person is “starving in the land of plenty.” That is, although plenty of glucose is available, it cannot be used, and the cells begin to starve.
Without fuel, cells cannot produce energy >> fatigue and weight loss.

59. Insulin deficiency >> metabolic use of FAT
A deficiency of insulin will accelerate the breakdown of the body’s fat reserves for fuel.
Free fatty acids become the main energy substrate for all tissues except the brain.
Increased lipolysis results in the production of organic acids called ketones (KETOGENESIS) in the liver.

60. KETOGENESIS>>KETOSIS
The increased ketones in the blood lower the pH of blood, resulting in a form of acidosis called KETOSIS, or ketoacidosis.
Ketones are excreted in the urine: KETONURIA.

61. Complications of KETOSIS:
Serious electrolyte losses also occur as the body rids itself of excess ketones.
Ketones are negatively charged and carry positive ions out with them.
Sodium and potassium are also lost from the body; because of the electrolyte imbalance, the person get abdominal pains and may vomit, and the stress reaction spirals even higher.
Can result in coma, death

62. Effects of insulin deficiency on metabolic use of fat
Excess fat metabolism
leads to an increase in
plasma cholesterol >>>
increased plaque
formation on the walls
of blood vessels.
Leads to atherosclerosis
& other cardiovascular
problems: cerebrovascular
insufficiency, ischemic heart
disease, peripheral vascular
disease, and gangrene.

63. Effects of insulin deficiency on metabolic use of fat
Degenerative changes in cardiac circulation can lead to early heart attacks. Heart attacks are 3-5 times more likely in diabetic individuals than in nondiabetic individuals. The most common cause of death with diabetes mellitus is myocardial infarction.

64. Other complications of diabetes:
A reduction in blood flow to the feet can
lead to tissue death, ulceration, infection, and loss
of toes or a major portion
of one or both feet.
Damage to renal blood
vessels can cause severe
kidney problems.
(Nephropathy)
Damage to blood vessels
of the retina can also cause
blindness. (Retinopathy)

65. Non-Proliferative Retinopathy
Blood vessels in the retina leak and hemorrhage. Patient may notice a decrease in vision if the swelling and hemorrhage affect the macula.
Macula edema is the most common cause of visual loss in diabetic retinopathy.

66. Non-Proliferative Diabetic Retinopathy
Fundus photo of normal macula
Hemorrhages in non-proliferative
diabetic retinopathy

67. Proliferative Retinopathy
New blood vessels grow in the eye.
These new blood vessels tend to bleed and leak causing vision loss.
These new blood vessels may also pull on the retina causing retinal detachment.

68. Proliferative Diabetic Retinopathy
New blood vessel growth
around optic nerve in
proliferative diabetic retinopathy
Hemorrhage from new
blood vessel growth in
proliferative diabetic retinopathy

69. Side Effects of Excess Sugar
Loss of vision due to cataracts: Excessive blood sugar chemically attaches to lens proteins, causing cloudiness.
Skin infections sometimes occur because excess sugar in the blood suppresses the natural defense mechanism like the action of white blood cells. And sugar is an excellent food for bacteria for food to grow in.
BACTERIA CELLS

70. Periodontitis
High blood glucose also helps bacteria in the mouth to grow, making tooth and gum problems worse.
Gingivitis: bacteria grow in the shallow pocket where the tooth and gum meets; gum begins to pull away from the tooth. Progresses to:
Periodontitis: infection causes actual bone loss, teeth begin to pull away from the jaw itself

71. Latter Stages of Periodontitis

72. Damage to the Nerves
Numbness and tingling in feet and night leg cramps may result from nerve damage due to prolonged high glucose levels that cause changes in the nerves and “neuron starvation” from lack of cellular glucose.
Nerve damage can also lead to a loss of the ability to feel pain in the feet, leading to undue pressure>>calluses>> ulceration. (Neuropathy)

73. Diabetic Neuropathy
Neuropathy can result in two sets of what appear to be contradictory problems. Most patients who have neuropathy have one these problems but some can be affected by both:
1) symptoms of pain, burning, pins and needles or numbness which lead to discomfort
2) loss of ability to feel pain and other sensation which leads to neuropathic ulceration

74. Diabetic Neuropathy
Patients with neuropathy lose their sensation of pain. As a result, they exert a lot of pressure at one spot under the foot when they walk, building up a callus at that site without causing discomfort.
The pressure becomes so high that eventually it causes breakdown of tissues and ulceration.

75. A TYPICAL NEUROPATHIC ULCER IS…
1) PAINLESS
2) SURROUNDED BY
CALLUS
3) ASSOCIATED WITH GOOD FOOT PULSES
(BECAUSE THE CIRCULATION IS NORMAL)
4) AT THE BOTTOM
OF THE FOOT
& TIPS OF TOES

76. EFFECTS OF DECREASED INSULIN
Hyposecretion of
Insulin
Undiscovered
mechanisms
Malfunction of hormone
signal in target cells
Decreased insulin
effects
Increased blood glucose
level
(hyperglycemia)
Decreased glucose
available
for cellular respiration
Kidney’s ability to
conserve
glucose is exceeded
Increased glucose in
interstitial fluid
Water follows glucose
into
urine by osmosis
Increased urine glucose
level (glycosuria)
Provides nutrients for
microorganisms
Net water loss from
body
Increased volume of
urine (polyuria)
Increased
susceptibility
to infection
Thirst
(polydipsia)
EFFECTS OF DECREASED INSULIN
= signs & symptoms

77. Decreased insulin effects Neurons “starve” Production of Coma
Hyposecretion of
Insulin
Undiscovered
mechanisms
Malfunction of hormone
signal in target cells
Decreased insulin
effects
Increased blood glucose
level
(hyperglycemia)
Decreased glucose
available
for cellular respiration
Neurons
“starve”
Shift from using
carbohydrates to
using fats
Nerve diseases
Production of
ketone bodies
Coma
Increased blood
lipid levels
(hyperlipidemia)
Weight
Loss
EFFECTS OF
DECREASED
INSULIN
Acidosis
Gallstones
Cardiovascular
Disorders
= signs & symptoms
Eye (retina)
damage
Ulcers &
Gangrene
Kidney
damage
Heart
Disease
Blindness

78. INSULIN DEFICIENCY Polyphagia Hyperglycemia Increased lipolysis
Glycosuria
EFFECTS OF
DECREASED
INSULIN
Increased
free fatty acids
(FFA)
Polyuria
Increased FFA
oxidation (liver)
Polydipsia
Volume
depletion
DIABETIC
COMA
Ketoacidosis

79. Glucose and insulin secretion
BLOOD GLUCOSE
PLASMA
INSULIN
CONCENTRATION 5 10 15 20
TIME (MIN)

80. GLUCOSE TOLERANCE
Glucose tolerance is the body’s ability to manage its
blood sugar level within normal range. The Cori cycle is a strategy used by the body to accomplish
this.
The blood sugar of
normal individuals
can sometimes drop
to the hypoglycemic
level.
This can even be
caused by ingesting
too much sugar, trig-
gering the release
of extra insulin.

81. TOO MUCH OF A GOOD THING…
Diabetics use insulin injections to treat high blood glucose levels. It is essential that blood glucose levels always be maintained above a critical level.
Brain cells use only glucose for energy. When blood glucose levels fall too low (20 to 50 mg/ml), symptoms of hypoglycemic shock develop – nervous irritability leading to fainting, seizures and coma

82. Part Iv
Diabetes:
Type I Vs. Type II

83. History of Diabetes Mellitus
TIME
EVENT
1500 BC
Ebers Papyrus first describes diabetes
400 BC
Susruta records diabetes symptoms and classifies types of diabetes. Charaka refines this work in 6AD.
10 AD
Celsus develops a clinical description of diabetes
20 AD
Aretaeus coins the term diabetes.
1869
Langerhans describes clusters of cells (islets) in the pancreas.
1889
von Mering and Minkowski observe that diabetes develops when an animal's pancreas is removed.
1921
Banting and Best obtain and purify islets of Langerhans from an animal pancreas, inject the material (insulin) into a diabetic animal, and find a fall in blood sugar level.

84. The disease’s name was derived from two terms:
Diabetes– Greek for siphon or fountain for the characteristic frequent urination
Mellitus– Latin for sweet as honey. In 1679, a physician tasted the urine of a person with diabetes and described as sweet like honey.

85. Type II or Non-Insulin Dependent Diabetes Mellitus (NIDDM)
TYPES OF DIABETES
Type I or Insulin-Dependent Diabetes Mellitus (IDDM)
The pancreas makes no insulin. It is a result of progressive and irreversible destruction of the islets by the patient's immune system.
Treatment:
Blood Glucose
Measurements
Daily Insulin Injections
Exercise & Diet
Type II or Non-Insulin Dependent Diabetes Mellitus (NIDDM)
The pancreas produces some insulin, but often, not sufficient to lower the blood glucose level to normal.
Blood Glucose Measurements
Oral Medication
Insulin Injections

86. Classification of Diabetes Mellitus
Type 1 (previously called Type I; Insulin-dependent diabetes mellitus, IDDM, juvenile diabetes)
Pathophysiology
Immune-mediated destruction of ß cells
Idiopathic
Absolute insulin deficiency- insulin therapy required
Accounts for 5 to 10 percent of cases
Diabetes Control and Complications Trial (DCCT) showed that control of glycemia slows the onset and progression of eye, kidney, and nerve complications

87. Pathophysiology of IDDM
Juvenile (14 years of age)
Age (years)
Stages in the Development of Diabetes Mellitus
Genetic predisposition
Overt Immunologic
abnormalities
Normal insulin
release
Progressive
loss of insulin
Glucose
normal
Overt
diabetes
C-peptide
present No
β-cell
mass

88. Classification of Diabetes Mellitus
Type 2 (Type II; Non-insulin-dependent diabetes mellitus, NIDDM)
Ranges from predominantly insulin resistance with relative insulin deficiency to a predominantly secretory defect with insulin resistance
Insulin therapy required in 20-30% patients; oral hypoglycemic drugs used in most cases; diet and exercise sufficient in mild cases
Accounts for 90 to 95 percent of the 18 million cases in the United States.

89. Type I vs. Type II Diabetes
Type I (IDDM)
Type II (NIDDM)
Age at onset
Usually under 40
Usually over 40
Body weight
Thin
Usually overweight
Symptoms
Appear suddenly
Appear slowly
Insulin produced
None
Too little, or it is ineffective
Insulin required
Must take insulin
May require insulin
Other names
Juvenile onset diabetes
Adult onset diabetes

90. CAUSES OF DIABETES
Two factors especially important in the development of diabetes:
1) Heredity: About a 5% risk of developing Type II diabetes if mother, father, or sibling has diabetes. Higher risk (up to 50%) if overweight.
2) Obesity: 80% of people w/ Type II diabetes are overweight when diagnosed and symptoms disappear in many of the obese patients when they lose weight.

91. Other causes/triggers of diabetes:
Age: As people age, their bodies may have fewer insulin- producing beta cells.
Faulty immune system: Scientists now believe that there is not one cause of diabetes, but multiple factors that may trigger the immune system to destroy beta cells.
Viruses: Certain viruses
may destroy beta cells
in susceptible people.

92. Other causes/triggers of diabetes:
Physical trauma: An accident or injury may destroy the pancreas, where insulin is normally produced.
Stress: Hormones released during periods of stress may block the effect of insulin.
Pregnancy: Hormones produced
during pregnancy may block the effect
of insulin.
Drugs: Drugs prescribed
for another condition may
unmask diabetes.

93. Maintaining Control
Protect heart, nerves, blood vessels, eyes, and kidneys by controlling blood glucose level.
Maintain schedule for checking blood glucose level and taking insulin.
Maintain well-balanced meal plan, exercise program, and healthy weight.

94. How does exercise help? Most of the time muscle tissue
depends on fatty acids for energy
Under two conditions muscles use large amounts of glucose:
During moderate or heavy exercise (muscle fibers become permeable to glucose even in the absence of insulin– important in Type I)
During the few hours after a meal (while pancreas is secreting more insulin– important in Type II). Most of the glucose is stored as muscle glycogen.

95. The Diabetic Meal Plan
Under this plan, 60 to 70 percent of your total daily calories should come from grains, beans, and starchy vegetables, with the rest being meat, cheese, fish and other proteins.
Fats, oils, and sweets should be used sparingly. The Diabetes Food Pyramid suggests the following daily servings of food for people with diabetes:

96. DIABETES
FOOD
PYRAMID

97. The Diabetes Food Pyramid differs from the standard Food Guide Pyramid in the way that it groups different foods together.
Because blood glucose is of primary concern to people with diabetes, the Diabetes Food Pyramid focuses on the way in which certain foods affect blood glucose levels.
For example, in the standard pyramid, beans and legumes are grouped with meats, due to their protein content. In the diabetes pyramid, however, beans are grouped with starches, because they affect blood glucose in the same way that starchy foods do.

98. And ONE LASE TIME, why are…
Maintaining a well-balanced meal plan, exercise program, and healthy weight
AND
Maintaining a schedule for checking blood glucose levels taking insulin SO
IMPORTANT??????

99. Heart Disease and Stroke
Heart disease is the leading cause of diabetes-related deaths. Adults with diabetes have heart disease death rates about two to four times higher than adults without diabetes.
The risk for stroke is two to four times higher among people with diabetes.
About 65 percent of deaths among people with diabetes are due to heart disease and stroke.

100. Blindness
Diabetes is the leading cause of new cases of blindness among adults aged years.
Diabetic retinopathy causes 12,000 to 24,000 new cases of blindness each year.

101. Kidney Disease
Diabetes is the leading cause of end-stage renal disease, accounting for 44 percent of new cases.
In 2001, 42,813 people with diabetes began treatment for end-stage renal disease.
In 2001, a total of 142,963 people with end- stage renal disease due to diabetes were living on chronic dialysis or with a kidney transplant.

102. Nervous System Disease
About 60 percent to 70 percent of people with diabetes have mild to severe forms of nervous system damage. The results of such damage include impaired sensation or pain in the feet or hands, slowed digestion of food in the stomach, carpal tunnel syndrome, and other nerve problems.
Severe forms of diabetic nerve disease are a major contributing cause of lower-extremity amputations.

103. Amputations More than 60 percent of non-
traumatic lower-limb amputations
occur among people with diabetes.
In , about 82,000 non-traumatic lower-limb amputations were performed annually among people with diabetes.

104. homeostatic mechanism
One final look at the
homeostatic mechanism
in question:
In diabetes, where is
the missing link?
Can you remember
all of the
biochemical
consequences???
The physical
consequences??