DIABETES

Type 1 diabetes, Type 2 diabetes, and Gestational diabetes, pre-diabetes

By Ms.Anam Zahra
DPN-III Semester
DDNS
UOL(ISLAMABAD CAMPUS):
 INTRODUCTION
 Diabetes mellitus is a group of diseases characterized
by high blood glucose concentrations resulting from
defects in insulin secretion, insulin action, or both.
 Insulin is a hormone produced by the beta-cells of the
pancreas that is necessary for the use or storage of
body fuels (carbohydrate, protein, and fat).
 Persons with diabetes do not produce adequate
insulin; with insulin deficiency, hyperglycemia
occurs.
 CATEGORIES OF GLUCOSE
INTOLERANCE
 Prediabetes
Individuals with a stage of impaired glucose homeostasis that
includes IFG and IGT are referred to as having
prediabetes, indicating their relatively high risk for the
development of diabetes and CVD.
People at risk may have IFG (fasting plasma glucose 100-125
mg/dL), IGT (2-hour post challenge glucose of 140 to 199
mg/dl), both, or a hemoglobin A1c (A1C) of 5.7% to 6.4%
and should be counseled about strategies, such as reduced
energy intake, weight loss, and physical activity, to lower
their risks.
 Type 1 Diabetes
 At diagnosis, people with type 1 diabetes (T1DM)
often experience excessive thirst, frequent
urination, and significant weight loss.
 The primary defect is pancreatic beta-cell
destruction, usually leading to absolute insulin
deficiency and resulting in hyperglycemia, polyuria
(excessive urination), polydipsia (excessive thirst),
polyphagia (excessive hunger), weight loss,
dehydration, electrolyte disturbance, and
ketoacidosis.
 DKA
 Diabetic ketoacidosis (DKA) is a life-threatening problem
that affects people with diabetes.
 It occurs when the body starts breaking down fat at a rate
that is much too fast.
 The liver processes the fat into a fuel called ketones, which
causes the blood to become acidic.
 The fat is broken down by the liver into a fuel called
ketones.
 Ketones are normally produced by the liver when the body
breaks down fat after it has been a long time since your last
meal.
 DKA
 The fat is broken down by the liver into a fuel called
ketones.
 Ketones are normally produced by the liver when the
body breaks down fat after it has been a long time
since your last meal. These ketones are normally
used by the muscles and the heart.
 When ketones are produced too quickly and build up
in the blood, they can be toxic by making the blood
acidic. This condition is known as ketoacidosis.
 TYPE 1 DIABETES MELLITUS
 The capacity of a healthy pancreas to secrete insulin is far
in excess of what is needed normally.
 Therefore the clinical onset of diabetes may be preceded
by an extensive asymptomatic period of months to years,
during which beta-cells are undergoing gradual
destruction.
 Persons with T1DM are dependent on exogenous insulin to
prevent ketoacidosis and death.
 T1DM can develop at any age. Although more cases are
diagnosed in people before the age of 30 years, it also
occurs in older individuals
 TYPE 1 DIABETES MELLITUS
T1DM has two forms:
 Immune-mediated
 Idiopathic
 Immune-mediated diabetes mellitus results from an autoimmune
destruction of the beta-cells of the pancreas, the only cells in the
body that make the hormone insulin.
 Idiopathic T1DM refers to forms of the disease that have no
known etiology.
 Although only a minority of individuals with T1DM fall into this
category, of those who do, most are of African or Asian ancestry
(ADA, 2014b).
 At this time there are no known means to prevent T1DM.
 Pathophysiology
 Markers of the immune destruction of the beta-cells
include islet cells autoantibodies, autoantibodies to
insulin, autoantibodies to glutamic acid decarboxylase
(GAD65) (a protein on the surface of the beta-cells).
 The rate of clinical beta-cell destruction is quite
variable, being rapid in some individuals (mainly
infants and children) and slow in others (mainly
adults). Hyperglycemia and symptoms develop only
after greater than 90% of the secretory capacity of the
beta-cell mass has been destroyed
 Pathophysiology
 Latent autoimmune diabetes of aging (LADA) may
account for as many as 10% of cases of insulin-requiring
diabetes in older individuals and represents a slowly
progressive form of autoimmune diabetes that frequently
is confused with T2DM.
 Adults with LADA have HLA genetic susceptibility as
well as auto-antibodies. Their diabetes may be controlled
initially with nutrition therapy but within a relatively
short period of time glucose-lowering medication and
progression to insulin treatment are required
 Type 2 Diabetes
 Type 2 diabetes (T2DM) accounts for 90% to 95%
of all diagnosed cases of diabetes and is a
progressive disease that, in many cases, is present
long before it is diagnosed.
 Hyperglycemia develops gradually and is often not
severe enough in the early stages for the person to
notice any of the classic symptoms of diabetes.
 Most persons with T2DM are obese, and obesity
itself causes some degree of insulin resistance.
Persons who are not obese
 Type 2 Diabetes
 Most persons with T2DM are obese, and obesity
itself causes some degree of insulin resistance.
Persons who are not obese by traditional weight
criteria may have an increased percentage of
body fat distributed predominately in the
abdominal region.
 However, many obese persons never develop
T2DM.
 Type 2 Diabetes
 Therefore obesity combined with a genetic
predisposition may be necessary for T2DM to
occur.
 Other risk factors include genetic and
environmental factors, including a family history
of diabetes, older age, physical inactivity, a prior
history of gestational diabetes, prediabetes,
hypertension or dyslipidemia, and race or
ethnicity
 Pathophysiology(T2DM)
 T2DM is characterized by a combination of insulin resistance and
beta-cell failure.
 Endogenous insulin levels may be normal, depressed, or elevated,
but they are inadequate to overcome concomitant insulin
resistance (decreased tissue sensitivity or responsiveness to
insulin.)
 As a result, hyperglycemia ensues.
 The inflammatory response to excess weight, insulin resistance,
and beta-cell failure occurs approximately 5 to 10 years before
the elevation of glucose above normal.
 When T2DM is diagnosed, it is estimated that people already
have lost approximately 50% of their beta-cell function
 Pathophysiology(T2DM)
 There is disagreement among researchers whether this
is loss of beta-cell mass or function.
 Persons in the upper tertile of IGT before the diagnosis
of T2DM are reported to have lost more than 80% of
their beta-cell function.
 Insulin resistance is demonstrated first in target
tissues, mainly muscle, liver, and adipose cells.
 Initially there is a compensatory increase in insulin
secretion (hyperinsulinemia), which maintains glucose
concentrations in the normal or prediabetic range.
 Pathophysiology(T2DM)
 In many persons the pancreas is unable to
continue to produce adequate insulin,
hyperglycemia occurs, and the diagnosis of
diabetes is made.
 Therefore insulin levels are always deficient
relative to elevated glucose levels before
hyperglycemia develops.
 Pathophysiology(T2DM)
 Hyperglycemia is first exhibited as an elevation of
postprandial (after a meal) blood glucose caused by insulin
resistance at the cellular level and is followed by an
elevation in fasting glucose concentrations.
 As insulin secretion decreases, hepatic glucose production
increases, causing the increase in preprandial (fasting) blood
glucose levels.
 The insulin response is also inadequate in suppressing alpha-
cell glucagon secretion, resulting in glucagon hypersecretion
and increased hepatic glucose production.
 Compounding the problem is glucotoxicity, the deleterious
effect of hyperglycemia on insulin sensitivity and insulin
secretion.
 LIPOTOXICITY
 Insulin resistance also is demonstrated at the adipocyte level,
leading to lipolysis and an elevation in circulating free fatty
acids.
 In particular, excess intraabdominal obesity, characterized by an
excess accumulation of visceral fat around and inside abdominal
organs, results in an increased flux of free fatty acids to the liver,
leading to an increase in insulin resistance.
 Increased fatty acids also cause a further decrease in insulin
sensitivity at the cellular level, impair pancreatic insulin
secretion, and augment hepatic glucose production (lipotoxicity).
 The above defects contribute to the development and progression
of T2DM and are also primary targets for pharmacologic therapy
 Pathophysiology(T2DM)
 The progressive loss of beta-cell secretory
function means that persons with T2DM require
more medication(s) over time to maintain the
same level of glycemic control; eventually
exogenous insulin will be required.
 Insulin is also required sooner for control during
periods of stress-induced hyperglycemia, such as
during illness or surgery.
TYPE 1 DIABETES MELLITUS
TYPE II DIABETES MELLITUS
 Gestational Diabetes Mellitus
 Gestational diabetes mellitus (GDM) occurs in about 7% of all
pregnancies (ranging from 1% to 14% depending on the population
studied), resulting in more than 200,000 cases annually (ADA, 2014a).
 After delivery, about 90% of all women with GDM become
normoglycemic but are at increased risk of developing GDM earlier in
subsequent pregnancies.
 Immediately after pregnancy, 5% to 10% of women with GDM are
diagnosed with T2DM.
 Women who have had GDM have a 35% to 60% chance of developing
diabetes in the next 5 to 10 years (CDC, 2014).
 Lifestyle modifications aimed at reducing or preventing weight gain
and increasing physical activity after pregnancy may reduce the risk of
subsequent diabetes
Gestational Diabetes Mellitus
 Gestational Diabetes Mellitus
 birth the extra glucose is no longer available to the fetus, but
until his or her pancreas can adjust, the neonate may require
extra glucose through intravenous feedings for a day or two to
keep blood glucose levels normal.
 GDM does not cause congenital anomalies.
 Such malformations occur in women with diabetes before
pregnancy who have uncontrolled blood glucose levels during
the first 6 to 8 weeks of pregnancy when fetal organs are being
formed.
 Because GDM does not appear until later in pregnancy, the
fetal organs were formed before hyperglycemia became a
problem.
 Gestational Diabetes Mellitus
 When optimal blood glucose levels are not being
maintained with MNT or the rate of fetal growth is
excessive, pharmacologic therapy is needed (AND,
2008b).
 Research supports the use of insulin, insulin analogs,
metformin, and glyburide during pregnancy.
 Women with GDM should be screened for diabetes 6
to 12 weeks postpartum and should have lifelong
screening for the development of diabetes or
prediabetes at least every 3 years (ADA, 2014b).
Medical Nutrition Therapy
 Carbohydrates
 As noted earlier, blood glucose levels after eating are
determined primarily by the rate of appearance of glucose from
carbohydrate digestion and absorption into the bloodstream,
and the ability of insulin to clear glucose from the circulation.
 Low-carbohydrate diets may seem to be a logical approach to
lowering postprandial glucose.
 However, foods that contain carbohydrates (whole grains,
legumes, fruits, vegetables, and low-fat milk) are excellent
sources of vitamins, minerals, dietary fiber, and energy and are
encouraged over other sources of carbohydrates, or sources
with added fats, sugars, or sodium to improve overall nutrient
intake
 Carbohydrates
 The glycemic effect of carbohydrate foods cannot be predicted
based on their structure (i.e., starch versus sugar) owing to the
efficiency of the human digestive tract in reducing starch
polymers to glucose.
 Starches are rapidly metabolized into 100% glucose during
digestion, in contrast to sucrose, which is metabolized into only
approximately 50% glucose and approximately 50% fructose.
 Fructose has a lower glycemic response, which has been
attributed to its slow rate of absorption and its storage in the liver
as glycogen.
 Sucrose-containing foods can be substituted for isocaloric
amounts of other carbohydrate foods.
 Carbohydrates
 However, as for the general population, care
should be taken to avoid excess energy intake and
to avoid displacing nutrient-dense food choices.
The ADA advises that people with or at risk for
diabetes avoid sugar-sweetened beverages (soft
drinks, fruit drinks, energy and vitamin-type water
drinks containing sucrose, high-fructose corn
syrup, and/or fruit juice concentrates) to reduce the
risk of worsening the cardiometabolic risk profile
and to prevent weight gain
 GLYCEMIC INDEX
 Glycemic Index and Glycemic Load The glycemic index
(GI) of food was developed to compare the physiologic
effects of carbohydrates on glucose.
 The GI measures the relative area under the postprandial
glucose curve of 50 g of digestible carbohydrates
compared with 50 g of a standard food, either glucose or
white bread.
 When bread is the reference food, the GI value for the food
is multiplied by 0.7 to obtain the GI value that is
comparable to glucose being used as the reference food
(GI of glucose % 100; GI of white bread % 70
 GLYCEMIC LOAD
 The estimated glycemic load (GL) of foods,
meals, and dietary patterns is calculated by
multiplying the GI by the amount of available
carbohydrate (divided by 100) in each food and
 Then totaling the values for all foods in a meal or
dietary pattern.
 MAIN CONCEPT
 What is the Glycemic index?
The glycemic index (GI) is a tool to measure how individual foods
are expected to impact blood sugar levels.
What is the glycemic load?
The glycemic load (GL) is an equation that takes into account the
planned portion size of a food as well as the glycemic index of
that food.
Glycemic Load = GI/100 multiplied by the net grams of planned
carbohydrate (net carbohydrate is the total grams of carbohydrate
minus the dietary fiber).
In theory, a large amount of a low GI food may increase your blood
sugar as much as a small amount of a high GI food
 Fiber and Whole Grains
 It is unknown if free-living individuals can daily
consume the amount of fiber needed to improve
glycemia.
 However, consuming foods containing 25 g fiber
per day for adult women and 38 g per day for
adult men is encouraged (Evert et al, 2013).
 As with the general population, individuals with
diabetes should consume at least half of all grains
as whole grains.
 Protein Intake
 The amount of protein usually consumed by
persons with diabetes (15% to 20% of energy
intake) has minimal acute effects on glycemic
response, lipids, and hormones, and no long-term
effect on insulin requirements.
 Although nonessential amino acids undergo
gluconeogenesis, in well-controlled diabetes, the
glucose produced does not appear in the general
circulation; the glucose produced is likely stored in
the liver as glycogen
 Protein Intake
 When glycolysis occurs, it is unknown if the
original source of glucose was carbohydrate or
protein.
 Although protein is just as potent a stimulant of
acute insulin release as carbohydrate, it has no
long-term effect on insulin needs
 Fats Intake
 Monounsaturated fatty acid (MUFA)-rich foods as a
component of the Mediterranean-style eating pattern are
associated with improved glycemic control and improved
CVD risk factors in persons with type 2 diabetes.
 Controversy exists on the best ratio of omega-6 to omega-
3 fatty acids; however, polyunsaturated fatty acids
(PUFAs) and MUFAs are recommended as substitutes for
saturated fatty acids (SFAs) or trans fatty acids.
 The amount of SFAs, cholesterol, and trans fat
recommended for people with diabetes is the same as for
the general population.
 Exercise
 Physical activity involves bodily movement
produced by the contraction of skeletal muscles
that requires energy expenditure in excess of
resting energy expenditure.
 Exercise is a subset of physical activity: planned,
structured, and repetitive bodily movement
performed to improve or maintain one or more
components of physical fitness
 Exercise
 Despite the increase in glucose uptake by muscles during
exercise, glucose levels change little in individuals without
diabetes. Muscular work causes insulin levels to decline.
 In persons with T1DM, the glycemic response to exercise
varies, depending on overall diabetes control, plasma glucose
and insulin levels at the start of exercise; timing, intensity, and
duration of the exercise; previous food intake; and previous
conditioning.
 An important variable is the level of plasma insulin during and
after exercise. Hypoglycemia can occur because of insulin-
enhanced muscle glucose uptake by the exercising muscle.