Diabetes Milletus

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At the end of this report, the class will
be able to:
1. Know the biosynthesis of Insulin
Specifically:
h Its release from Beta cells;
h Its role in Carbohydrates, Protein, and Fat
Metabolism;
h Its relationship with glucagon, epinephrine,
and cortisol;
_. What Diabetes Milletus is and its causes;
3. The clinical types of Diabetes Milletus;
4. The mechanism behind the development of
Polyuria, Polydipsia and Polyphagia in DM;
5. The biochemical events that lead to the
formation of HbA1c;
6. The complications in DM and the end- organ
damage, and;
7. The treatment in DM.
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6 lucose is liberated from dietary carbohydrate such
as starch or sucrose by hydrolysis within the small
intestine, and is then absorbed into the blood.
6 Elevated concentrations of glucose in blood stimulate
release of insulin, and insulin acts on cells
throughout the body to stimulate
of glucose.
6 The effects of insulin on glucose metabolism vary
depending on the target tissue.

6 Two important effects are:

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the major transporter used for uptake of

glucose (called T4) is made available in
the plasma membrane through the action of
insulin.

large fraction of glucose absorbed from the small

intestine is immediately taken up by hepatocytes,
which convert it into the storage polymer glycogen.
(+) hexokinase, phosphofructokinase and glycogen

synthase
(-) glucose-6-phosphatase
Physiologic Action of Insulin on CHO
Metabolism

lucose transport Increase Muscle, adipose tissue
lycolysis Increase Muscle, adipose tissue
lycogen synthesis Increase iver muscle, adipose
tissue
lycogen degradation Decrease iver muscle, adipose
tissue
luconeogenesis Decrease iver and kidney
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Insulin͛s relationship with glucagon

6 is a hormone, secreted by the pancreas, that
raises blood glucose levels.
6 The pancreas releases glucagon when blood
glucose levels fall too low.
6 lucagon causes the liver to convert stored
glycogen into glucose, which is released into
the bloodsteam.
Insulin͛s relationship with glucagon
6 lucagon also stimulates the release of
insulin, so that glucose can be taken up and
used by insulin-dependent tissues.
6 Thus, glucagon and insulin are part of a
feedback system that keeps blood glucose
levels at the right level.
Insulin͛s relationship with epinephrine
6 Epinephrine acts by binding to a variety of
adrenergic receptors. Binding to ɲ-adrenergic
receptors inhibits insulin secretion by the
pancreas,
6 ÿ in the liver and muscle, and

in muscle.
Insulin͛s relationship with epinephrine
6 ɴ-Adrenergic receptor binding triggers
glucagon secretion in the pancreas, increased
adrenocorticotropic hormone (ACTH)
secretion by the pituitary gland, and increased
lipolysis by adipose tissue.
6 Results to an increase blood glucose and fatty

acids
Insulin͛s relationship with cortisol
6 counteracts insulin, contributes to
hyperglycemia-causing hepatic
gluconeogenesis and inhibits the peripheral
utilization of glucose (insulin resistance) by
decreasing the translocation of glucose
trasporters (especially T4) to the cell
membrane.
6 ÿ (glycogenesis) in the
liver.
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6 is a group of metabolic diseases characterized by

hyperglycemia. This can result from defects in insulin
secretion, defects in insulin receptor and action, or both.
6 Because glucose is a chemically reactive molecule, the

chronic hyperglycemia of diabetes is associated with long-
term damage, dysfunction, and, ultimately, failure of
various organs.
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Following is a comprehensive list of
other causes of diabetes:
6 enetic defects of ɴ-cell Function 6 Endocrinopathies
Maturity onset diabetes of the young rowth hormone excess
(MODY) (acromegaly)
Mitochondrial DNA mutations
Cushing syndrome
6 enetic defects in insulin processing or Hyperthyroidism
insulin action
Defects in proinsulin conversion Pheochromocytoma
Insulin gene mutations lucagonoma
Insulin receptor mutations 6 Infections
6 Exocrine Pancreatic Defects Cytomegalovirus infection
Chronic pancreatitis
Pancreatectomy
Coxsackievirus B
Pancreatic neoplasia 6 Drugs
Cystic fibrosis lucocorticoids
Hemochromatosis Thyroid hormone
Fibrocalculous pancreatopathy
ɴ-adrenergic agonists
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CADA, Kristel Joy S.

PO YRIA
6 condition usually defined as excessive or
abnormally large production and/or passage
of urine
6 Frequent urination
6 may also be termed diuresis.
6 appears in conjunction with polydipsia
(increased thirst)
PO YRIA in Diabetes Mellitus
6 Diabetes mellitus
disorder of blood glucose regulation, which results
from a deficiency in the action of the hormone insulin
autoimmune destruction of the insulin-secreting cells
of the pancreas (type 1 diabetes mellitus)
problem in the responsiveness of tissues to insulin,
known as insulin resitance (type _ diabetes mellitus

HYPER YCEMIA
6 Hyperglycemia
causes excessive urine production
6 RINE PRODCTION involves
filtration and reabsortion.
rine Production
6 first step in the production of urine is a
process called
6 there is bulk flow of water and small
molecules from the plasma into Bowman͛s
capsule (the first part of the nephron).
6 nonspecific nature of filtration, useful small
molecules such as glucose, amino acids, and
certain ions end up in the forming urine,
which flows into the kidney tubules
6 To prevent the loss of these useful substances
from the body, the cells lining the kidney
tubules transfer these substances out of the
forming urine and back into the extracellular
fluid. This process is known as

Filtration and Reabsorption.
6 nder normal circumstances, 100% of the
glucose that is filtered is reabsorbed
6 lucose reabsorption involves transport
proteins that require specific binding
6 diabetic that has hyperglycemia
filtered load of glucose (amount of glucose
filtered) can exceed the capacity of the kidney
tubules to reabsorb glucose, because the
transport proteins become saturated
result is glucose in the urine
lucose is a solute that draws water
into the urine by osmosis. Thus,
hyperglycemia causes a diabetic to
produce a high volume of glucose-
containing urine.
Normal lucose Handling and Polyuria
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6 medical symptom in which the patient
displays excessive thirst
6 symptom is characteristically found in

diabetics
6 appears in conjunction with O!)*

6 caused by a change in the osmolality of the
extracellular fluids of the body, hypokalemia,
decreased blood volume (as occurs during
major hemorrhage), and other conditions that
create a water deficit
6 usually a result of %*

PO YPHAIA
6 Excessive hunger or increase in appetite
6 abnormal behavior of eating or the need to
eat
6 a common symptom of diabetes
6 referred to as disorder of hyperalimentation
commonly associated with diabetes
6 causative factors of polyphagia or hyperphagia
are depression, uncontrolled diabetes,
increased exercise, growth spurt, injury to the
hypothalamus, medication and drugs and
bulimia nervosa.
6 Insulin is the hormone that regulates the
blood glucose levels
produced by the islets of angerhans in the
pancreas
Patients with diabetes mellitus also experience
excessive thirst (polydipsia) and increase in urine
output (polyuria)
hyperglycemia
6 Hyperglycemia
ack of insulin results in increased blood glucose
levels
This is not used for energy and causes starvation
of the cells
sugar build up is passed out in the urine

Build up of glucose in the
bloodstreaqm
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Cabungcal, Kristine Mae

Diagnostic Procedures:
6 Fasting Plasma lucose (FP)
6 Oral lucose Tolerance Test (OTT)
6 2

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Fasting Plasma lucose
È done to measure the blood glucose in a person who has not eaten anything for at least 8
hours. This test is used to detect diabetes and pre-diabetes
È The FP test is said to be most reliable when done in the morning.
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È OTT is more sensitive than the FP test for diagnosing pre-diabetes
È requires fasting for at least 8 hours before the test and _ hours after the person is made to drink a glucose-containing
beverage.
È The plasma glucose level is measured immediately before and _ hours after a person drinks a liquid containing 75 grams of
glucose dissolved in water.
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Summary of Diagnostic Procedures that confirms positive for diabetes mellitus
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HbA1c
È Hemoglobin A1c is a minor component of hemoglobin to
which glucose is bound. HbA1c is also sometimes referred
to as glycosylated or glycosylated hemoglobin or
glycohemoglobin.
È HbA1c is a form of hemoglobin used primarily to identify
the average plasma glucose concentration over prolonged
periods of time. It is formed in a non-enzymatic glycation
pathway by hemoglobin's exposure to plasma glucose.
Normal levels of glucose produce a normal amount of
glycated hemoglobin. As the average amount of plasma
glucose increases, the fraction of glycated hemoglobin
increases in a predictable way.
6 Higher amounts of glycated hemoglobin,
indicating poorer control of blood glucose
levels, have been associated with
cardiovascular disease, neuropathy and
retinopathy. Monitoring the HbA1c in Type-I
diabetic patients may improve treatment
( arsen et al., 1990).

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HbA1c
È HbA1c levels depend on the blood glucose concentration in which the
higher the glucose concentration in blood, the higher the level of HbA1c.
È Not influenced by daily fluctuations in the blood glucose concentration
but reflect the average glucose levels over the prior six to eight weeks.
Thus, HbA1c is a useful indicator of how well the blood glucose level has
been controlled over the duration of _-3 months.

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È Cannot be used to monitor day-to-day blood
glucose concentrations to adjust insulin doses
È Cannot detect the day-to-day presence or absence
of hyperglycemia or hypoglycemia
È May increase falsely in: uremia (kidney failure),
chronic excessive alcohol intake, and
hypertriglyceridemia.
È May falsely decrease in: acute or chronic blood loss,
sickle cell disease or thalassemia.
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Bustos, Precious Nikki

group of cells that need insulin:
6 those in muscle, liver, and fat
6 do not become exposed to high internal
glucose levels when the blood sugars are high
and insulin levels are low. The lack of insulin
slows the movement of glucose into these
cells
6 cells such as those in the brain, nervous
system, heart, blood vessels and kidneys pick
up glucose directly from the blood without
using insulin.
6 reason why damage tends to occur in these
areas of the body (nerve and kidney cells, and
in small blood vessels like those in the eyes.)
Complications of Diabetes Mellitus:
1.Cardiovascular Disease
_0% of patients with CVD are Diabetics.
75% of these patients died due to CVD
magnified by high blood sugars
_.Nephropathy
sually begins as recurrent TI
rinalysis: presence of rbc, protein, sugar.
when people have had diabetes > 10 years
Diabetes is the most common cause of kidney
failure in some parts of the world, where it may
affect as many as 40% of dialysis patients.
3.Retinopathy
sually there is blurry vision
Retinopathy may lead to permanent blindness.
4.Neuropathy
sually there is numbness on extremities
longest nerves going to the feet are the first to be
damaged
Occasionally there is ͞tingling sensation͟
Worse is loss of sensation
5. Skin Infections
There is itchiness
There is drying of skin
Recurrent wounds/ non healing wounds
Non healing wound/diabetic ulcer
lcers with gangrene
ong Term Complications of DM
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Cabantac, Katherine Rhea D.

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6 Carbohydrates
Should comprise 60-70% of the calories needed
Fructose should be avoided except those from
fruits
6 Protein
Type _ diabetics has higher than normal protein
consumption
6 Fat
Saturated fat should be <7% of daily calories
Cholesterol consumption should be <_00mg/day
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6 Should first undergo cardiovascular disease
screening before doing moderate to high
intensity exercise
6 Type 1 diabetics should monitor their blood
glucose level during and after exercise

6 Increase insulin production
6 Sulfonylureas ʹ stimulate the pancreas to secrete insulin
6 DPP-IV inhibitors ʹ inhibit enzymatic degradation of glucagon
like peptide 1
6 Enhance insulin effect
6 Thiazolidenediones ʹ increases insulin sensitivity
6 Reduce blood glucose level
6 Biguanides ʹ decreases hepatic glucose output
6 Interfere with glucose absorption
6 ɲ glucosidase inhibitor ʹ slows down carbohydrate
absorption

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6 Two important effects are:

the major transporter used for uptake of

large fraction of glucose absorbed from the small

(+) hexokinase, phosphofructokinase and glycogen

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