لخّصلي

This lecture on Diet Therapy 1 (NF381) covers endocrine system diseases, focusing on diabetes mellitus. The endocrine system, composed of scattered glands secreting hormones (chemical messengers), regulates bodily functions through hormone interactions. Endocrine diseases stem from hormone hyper/hypofunction or target cell issues. Hormones control growth, homeostasis, metabolism, and reproduction. Three hormone classes exist: peptides/proteins (majority, secreted by various glands), amines (thyroid and adrenal medulla), and steroids (adrenal cortex, gonads, placenta). The lecture details the pituitary, thyroid, adrenal glands, and pancreas, explaining their anatomy, hormone secretions, and roles in energy metabolism. Energy metabolism relies on carbohydrate, fat, and protein, with insulin and glucagon crucial for blood glucose control. Insulin, an anabolic hormone, facilitates glucose uptake and synthesis; glucagon counteracts hypoglycemia. Endocrine disorders arise from hormone imbalances or target organ hyporesponsiveness. Diabetes mellitus, a prevalent global health concern, is categorized into Type 1 (autoimmune beta-cell destruction), Type 2 (insulin resistance and deficiency), prediabetes, gestational diabetes, and other causes. Type 1 diabetes results in acute, potentially fatal consequences (hyperglycemia, ketoacidosis), while Type 2 presents insidiously. Diagnosis involves FPG, random plasma glucose, OGTT, and A1C tests. Treatment for Type 1 necessitates insulin administration; Type 2 involves lifestyle changes and medication (metformin initially). Nutrition therapy emphasizes individualized plans, considering carbohydrate counting, food lists, and meal planning to achieve glycemic control and prevent complications. Monitoring involves self-monitoring blood glucose (SMBG) and A1C tests.

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Jordan University of Science & Technology
Faculty of Agriculture
Department of Nutrition & Food Technology

Course: DIET THERAPY 1 (NF381)
Course Lectures (Chapter 6)
Instructor: Naseem Alshwaiyat

Student Name: …………………………………………
Student No.: …………………………………………

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CHAPTER 6: Diseases of the Endocrine System

INTRODUCTION

Endocrine system is made up of endocrine glands that are not attached anatomically but
scattered throughout the body. These glands make up a system in a functional sense because
their regulatory activities are often interdependent and must be closely coordinated.

Endocrine glands carry out their functions by secreting hormones (chemical messengers)
into the blood and by the numerous interactions that occur between the various glands.

Hormones is defined as a blood-borne chemical messengers that act on target cells located
in a different part of the body from the endocrine gland that produces them.

Once released into the blood, hormones travel to target organs (the intended recipients of
the chemical message). A single hormone can have more than one type of target organ and
thus can generate more than one type of effect.

For example, insulin is secreted from pancreas, and act on muscle, liver, and adipose tissue
to regulate the storage of nutrients after absorption.

ANATOMY AND PHYSIOLOGY OF ENDOCRINE SYSTEM

Hormones released from endocrine glands regulate activities throughout the body. In a
healthy state, hormones are released when their actions are required and inhibited when
effects are achieved.

Endocrine diseases manifest through either hyperfunction (exceptionally high blood
concentrations of a hormone), hypofunction (depressed levels of hormones in the blood),
or abnormal target cell responsiveness.

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The functions of hormones may be grouped into four categories:

1. Growth and development


2. Homeostasis


3. Regulation of metabolism and nutrient supply


4. Reproduction and sexual differentiation

Figure 1: The Endocrine System

Endocrine system is made up of Pineal, Hypothalamus, Pituitary, Thyroid, Parathyroid,
Thymus, Adrenal gland, Pancreas, Heart, Liver, Stomach, Duodenum, Kidney, Adipose tissue,
Skin, Ovaries in female, Placenta in pregnant female, and Testes in male.

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There are three chemical classes of hormones:

1. Peptides and proteins hormones: the majority of hormones fall into the category of
   peptides and proteins, which are amino acid derivatives. Peptide hormones are secreted
   by the following glands: hypothalamus, anterior and posterior pituitary glands, pineal
   gland, pancreas, parathyroid gland, gastrointestinal (GI) tract, kidney, liver, thyroid C
   cells, heart, and thymus.


2. Amines hormones: they are secreted by the thyroid gland and adrenal medulla.


3. Steroid hormones: they are derived from cholesterol, are secreted by the adrenal cortex,
   gonads, and placenta.

Endocrine Function

1. Pituitary Gland:
   The pituitary gland is located in the bony cavity at the base of the brain just below the
   hypothalamus. It is connected to the hypothalamus by a thin connecting stalk called the
   pituitary stalk. The pituitary gland actually consists of two anatomically and functionally
   distinct glands: the anterior pituitary and the posterior pituitary.

Figure 2: Anatomy of the Pituitary Gland

A. Anterior pituitary secretes six hormones (Thyroid-stimulating hormone (TSH),
Adrenocorticotropic hormone (ACTH), Growth hormone, Prolactin, Follicle-stimulating
hormone (FSH), Luteinizing hormone (LH)) that in turn control secretion of various other
hormones. None of the hormones is secreted at a constant rate; rather, secretion is
regulated by hypothalamic hormones and feedback from target gland hormones.

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B. Posterior pituitary releases two hormones (vasopressin and oxytocin). These
hormones are synthesized by the hypothalamus.

2. Thyroid Gland:
   The thyroid gland, which is responsible for controlling metabolic rate, lies over the trachea
   just below the larynx and consists of two lobes connected by a thin strip called the isthmus.

Figure 3: Anatomy of the Thyroid Gland

The thyroid hormones are two iodine-containing hormones derived from the amino acid
tyrosine: thyroxine or tetraiodothyronine (T4) and triiodothyrone (T3).
T4 is the major hormone secreted by the thyroid, but T3 is more active. The conversion of
T4 to T3 within the anterior pituitary, liver, and kidney accounts for approximately two-
thirds of T3 production.

3. Adrenal Glands:
   The two adrenal glands are embedded above each kidney and are encapsulated in fat. Each
   adrenal gland is composed of two endocrine organs:
   A. Adrenal medulla: the inner portion of the glands, forms part of the sympathetic nervous
   system and secretes three hormones (epinephrine, norepinephrine, and
   catecholamines).
   B. Adrenal cortex: the outer layers of the glands, compose 80%–90% of the adrenal gland
   and produce over 50 known adrenocortical hormones such as Aldosterone and Cortisol.
   Structural variations in these hormones confer different functional capabilities and allow
   them to perform different primary actions.
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Figure 4: Anatomy of the Adrenal Glands

4. Endocrine Pancreas
   The pancreas is located in the abdominal cavity adjacent to the upper part of the small
   intestine. Different groups of cells within the pancreas carry out different functions. Cells
   making up the exocrine pancreas are responsible for secretion of fluid and various
   digestive enzymes that are secreted via the pancreatic duct into the duodenum.

Figure 5: Anatomy of the Pancreas

The endocrine cells of the pancreas include:

1. Alpha cells: which secrete glucagon and glucagon-like-peptide 1 (GLP-1).


2. Beta cells: which secrete insulin.


3. Delta cells: which secrete somatostatin.


4. F cells: which secrete pancreatic polypeptide.

These cells called (Islet of Langerhans), and make up an anatomically small portion of the
pancreas (2%), but the hormones they secrete play a vital role in energy regulation and fuel
homeostasis.
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Figure 6: Anatomy of the Endocrine Cells of the Pancreas

Endocrine Control of Energy Metabolism
Energy use in the body is constant, but ingestion of energy-yielding nutrients is sporadic.
This means that excess energy taken in meals must be stored for later use between meals.

Carbohydrate are stored as in the form of glucose (circulating in blood) and as glycogen (in
liver and muscle cells). Carbohydrate is the body’s primary energy source and the preferred
source of energy for brain cells. Excess carbohydrate (beyond what is used for glucose and
glycogen) is converted to and stored as fat (triglycerides).

Fat is the body’ primary energy reservoir. Fat is stored in adipose tissue in the form of
triglycerides and also circulates in the blood as free fatty acids.

Protein is not stored as an energy source in the same manner as carbohydrate and fat but
can be used for energy as a last resort. Protein can be converted to glucose
(gluconeogenesis) to provide energy for the brain during a prolonged fast.

Following meals, ingested nutrients are absorbed and enter the bloodstream; this period is
termed the “fed state”. During this time, glucose functions as the main energy source
because most cells preferentially use glucose. Additional amounts of glucose or fat not
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immediately used for energy or structural repairs are converted into their storage forms:
glycogen or triglycerides, respectively.

It takes approximately 4 hours for a typical meal to be absorbed. During the time period
when no nutrients are in the GI tract (fasting state), endogenous energy stores are
mobilized for energy. Synthesis of protein and fat is minimized, and stored forms of these
nutrients are catabolized for glucose formation and energy production, respectively.
Through mechanisms of gluconeogenesis and glucose sparing, the blood glucose level is
sustained to nourish the brain.

Figure 7: Summary of Major Pathways Involving Nutrient Absorption and Metabolism

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Hormones play an important role to manage and control fuel homeostasis. Insulin and
glucagon are the primary hormones that maintain normal blood glucose concentration (70
to 110 mg/100 mL).

1. Insulin:
   Insulin is initially secreted as a prohormone called preproinsulin. Preproinsulin is processed
   first to proinsulin and then, active insulin is produced. Active insulin enters the blood via the
   portal vein and has an approximate half-life of 5 minutes. It is then degraded back into the
   two separate chains and is inactive.

Figure 8: Structure of Insulin

Insulin is an anabolic hormone that controls the metabolic fates of carbohydrate, protein,
and lipid. In general, insulin promotes the uptake of glucose into hepatic, muscle, and adipose
cells as well as the stimulation of glycogen, triglyceride, and protein synthesis. Insulin
secretion is stimulated by an increased level of blood glucose and by the action of counter-
regulatory hormones including Growth Hormone.

In order for glucose, fructose, or galactose to be absorbed into the cell, transport molecules
are necessary (GLUT-1, GLUT-2, GLUT-3, GLUT-4, and GLUT-5). Most tissues in the body
depend on insulin for transportation of glucose from the bloodstream into cells to be used
for energy. There are exceptions: cells of the brain, and liver, are readily permeable to
glucose even in the absence of insulin.

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The GLUT-4 transporter (which is insulin dependent) is present in skeletal and cardiac
muscle and in the adipocytes. Insulin allows the translocation of the GLUT-4 from the interior
of the cell to the cell membrane, where it transports glucose into the cell. The net effect of
insulin is to promote glucose oxidation, glycogen storage, and triglyceride storage.

Figure 9: Role of Insulin in Cellular Uptake of Glucose

The most pronounced effect of insulin on protein metabolism is seen in skeletal muscle and
the liver. It promotes active transport of amino acids from the blood into muscle and other
tissues, thus promoting protein synthesis within cells. These effects demonstrate the
importance of insulin in tissue growth.

2. Glucagon:
   Glucagon is the hormone released from alpha cells of the pancreas when blood glucose levels
   fall below the normal range, demanding a source of energy to maintain homeostasis.
   Glucagon stimulates the breakdown of stored glycogen (glycogenolysis) and the production
   of new glucose from amino acids (gluconeogenesis), and thus raises blood glucose.
   Glucagon also stimulates breakdown of triglycerides (lipolysis), which provides additional
   substrate to meet energy requirements.
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Figure 10: Summary Interactions of Insulin and Glucagon

PATHOPHYSIOLOGY OF ENDOCRINE SYSTEM
The endocrine disorders are the result of hyposecretion or hypersecretion of hormones,
or of hyporesponsiveness of target organs.

1. Hyposecretion disorders:
   A. Primary hyposecretion: occurs when an endocrine organ releases an inadequate amount
   of hormone to meet physiological needs.
   
   B. Secondary hyposecretion: occurs when secretion of a tropic hormone (a hormone that
   regulates secretion of another hormone) is inadequate to cause an endocrine organ to
   secrete adequate amounts of a hormone.

For example, if the thyroid gland produces inadequate amounts of thyroid hormone, this
would be considered primary hyposecretion, whereas inadequate production of thyroid
hormone that is caused by insufficient secretion of a tropic hormone such as thyroid-
stimulating hormone (TSH) is secondary hyposecretion.

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In a primary thyroid hormone deficiency, for example, thyroid hormone would be low, but
TSH levels would be high. In secondary thyroid hormone deficiency, both thyroid hormone
and TSH levels would be abnormally low.

2. 
   

   Hypersecretion disorders:
   A. Primary hypersecretion: occurs when an endocrine organ releases an abnormally high
   amount of hormone, while the tropic hormone will be at unusually low levels.
   
   B. Secondary hypersecretion: occurs when secretion of a tropic hormone is abnormally high
   to cause an endocrine organ to secrete high amounts of a hormone.

   
   


3. 
   

   Hyporesponsiveness disorders:
   Hyporesponsiveness of the target organ will cause the same symptoms as hyposecretion, but
   hormone levels will be normal or high instead of low. Most cases of hyporesponsiveness are
   caused by a lack or deficiency of hormone receptors on the target cells. An example of this
   type of disorder is type 2 diabetes mellitus (T2DM).

   
   

DIABETES MELLITUS
Diabetes mellitus is defined as a diverse group of disorders that share the primary
symptom of hyperglycemia resulting from defective insulin production, insulin action, or
both.

Diabetes mellitus is the most common of all endocrine disorders and public health concerns
at the world level. The prevalence of diabetes mellitus has increased worldwide, from an
estimated 30 million cases in 1985 to 425 million in 2017. The IDF Diabetes Atlas (2021)
reports that 10% of the adult population (20-79 years) has diabetes. The risk for death
among people with diabetes is about twice that of those without diabetes.

Diabetes mellitus is not a single disease but a diverse group of disorders that differ in origin
and severity. All forms of diabetes share one common characteristic: hyperglycemia
resulting from defects in insulin production, insulin action, or both.

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Chronic hyperglycemia is correlated with organ dysfunction and damage, progressing to
failure of multiple organs, particularly the eyes, kidneys, nerves, heart, and blood vessels.
Diabetes is the leading cause of adult blindness, end-stage renal disease, and nontraumatic
amputations.

Insulin deficiency is generally due to either insufficient insulin secretion by beta cells or
comparative deficient response by target tissue cells to insulin. Whatever the cause of
insulin deficiency, it results in glucose intolerance.

Classifications of Diabetes:

1. Type 1 diabetes: caused by autoimmune beta cell destruction with absolute insulin
   deficiency.


2. Type 2 diabetes: caused by progressive defective insulin secretion with insulin
   resistance.


3. Prediabetes: Category of increased risk of diabetes.


4. Gestational diabetes: a diabetes diagnosed in the second or third trimester of
   pregnancy that is clearly not overt diabetes.


5. Diabetes due to other causes: caused by drug or chemical induced, genetic defects,
   cystic fibrosis or other diseases of the pancreas.

Type 1 Diabetes
Epidemiology:
Type 1 diabetes mellitus (T1DM) accounts for 5% of all diagnosed cases of diabetes. While
this form of diabetes develops most frequently in children and adolescents, it is increasingly
diagnosed later in life, even in older adults. Gender distribution of T1DM is equal.

Etiology:
Type 1 diabetes mellitus (T1DM) results from a cell-mediated autoimmune response causing
a gradual decline in β cell mass within genetically susceptible individuals.

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The primary gene for T1DM is located in the human leukocyte antigen (HLA) region of
chromosome 6. More than 50 different gene associations have been linked to risk for this
disease and are estimated to account for 85% of the inheritability of the disease. The genetic
components of T1DM support our understanding of the increased risk for relatives of
individuals with T1DM.

Pathophysiology:
Type 1 diabetes mellitus (T1DM) is characterized by the deficiency of insulin due to
destruction of pancreatic beta cells, resulting in the inability of cells to use glucose for energy.
By the time clinical symptoms occur, 60%–80% of β cells have been destroyed.

Figure 11: Acute Effects of Insulin Deficiency
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Clinical Manifestations:
As shown in Figure 11, the acute consequences of an insulin deficit are numerous and
potentially fatal. Clinical manifestations can be summary in the following changes:

1. When glucose cannot enter cells, two things happen: plasma glucose levels rise
   (hyperglycemia, #1) and cells starve.


2. This signals an increase in gluconeogenesis in the liver as well as stimulation of
   glycogenolysis. These further contribute to the hyperglycemic state.


3. To compensate for the hyperglycemia, excess glucose is filtered out into the urine
   because the kidneys can filter only small amount of glucose from the blood. As a result,
   glycosuria (#2) and frequent urination (polyuria, #3) occur.


4. Loss of fluid stimulates the thirst mechanism and leads to polydipsia (#10).


5. Cells dependent on glucose for energy have none available. In turn, the body responds to
   this emergency by promoting hunger (polyphagia, #11).


6. As the insulin deficiency persists, production of additional hormones (catecholamines,
   cortisol, glucagon, and Growth Hormone) increases, leading to lipolysis (#12).


7. As the body breaks down fat stored in adipose tissue, the resulting fatty acids are
   transformed into keto acids in the liver (ketosis #13).


8. In the non-diabetes state, keto acids can be used for energy by muscle and brain cells. As
   increased production of keto acids occurs, pH falls (7.3 to 6.8), and ketone bodies are
   secreted in the urine.


9. Metabolic acidosis (#14) develops as bicarbonate concentration is reduced, and
   ketoacidosis results.


10. The body tries to offset metabolic acidosis through deep, labored respirations
    (Kussmaul respirations, #16).


11. Due to increased urination and a shift of vascular volume in response to hyperosmolality,
    potassium, sodium, magnesium, and phosphorus are also lost in urination. Serum levels
    of these ions may be normal or elevated due to decreased blood volume in the body
    (hypovolemia, #5).


12. Hypovolemia also accounts for increased hematocrit, hemoglobin, protein, white blood
    cell count, creatinine, and serum osmolality. Hypovolemia and muscle catabolism are the
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causes for considerable, imminent weight loss in persons with ketoacidosis (#17), and
often present at the diagnosis of T1DM.

13. Hypovolemic shock can lead to death if left untreated (#6 and #7).

Type 2 Diabetes
Epidemiology:
• About 90% of all diagnosed cases of diabetes are Type 2 diabetes mellitus (T2DM). T2DM
occurs most frequently in adults but is being diagnosed with increasing frequency in
children and adolescents as well. Gender distribution of T2DM is equal, but prevalence
increases with age.

• The risk characteristics for T2DM include obesity, family history, history of gestational
DM, impaired glucose metabolism, and physical inactivity.

Etiology:
• Type 2 diabetes mellitus (T2DM) evolves from a combination of abnormal insulin
secretion and insulin resistance.
• The environmental factors include poor nutrition, and physical inactivity are the primary
factors contributing to T2DM development.
• Obesity (body fat distribution) also appears to play a role in development of T2DM.
Central body adiposity increases the degree of insulin resistance.
• Physical inactivity increases risk of T2DM unrelated to body weight, whereas exercise
seems to reduce risk of T2DM by enhancing whole-body insulin sensitivity.

Pathophysiology:
• Individuals with T2DM produce insulin, but their tissues are insulin resistant. This
increases the need for insulin, so the pancreas increases production. Over time, the
pancreas is not able to maintain such high insulin production levels.

• Consequently, two metabolic defects are observed in individuals with T2DM: 1) insulin
resistance and 2) relative insulin deficiency.

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• Although insulin resistance develops many years before onset of diabetes in individuals
with predisposition to T2DM, clinical onset is correlated with the diminishing pancreatic
release of insulin.
• Insulin resistance is caused by a cell receptor defect resulting in the body’s inability to
use insulin. When cells cannot respond to insulin by translocating glucose transporters
to their outer membrane, they are unable to take up glucose from the blood for fuel.

• Since insulin normally serves to inhibit glycogenolysis and gluconeogenesis when blood
glucose is high, defective insulin secretory response results in excessive hepatic
gluconeogenesis.

• For T2DM to manifest, both defects must be present. At first, postprandial glucose levels
rise due to the inability of the cells to utilize glucose; subsequently, hepatic
gluconeogenesis increases to compensate for the lack of glucose within cells, resulting in
fasting hyperglycemia.

Clinical Manifestations:
• The onset of T2DM is insidious. Many individuals will be asymptomatic for as long as 6-
10 years but present with complications associated with diabetes such as retinopathy.

• The estimate that as many as one-third of all individuals with T2DM are undiagnosed,
therefore, screening of individuals at high risk is needed.

Prediabetes (Increased Risk for Diabetes)
• The diagnosis of prediabetes is made for individuals who present with impaired fasting
glucose or impaired glucose tolerance (FPG: 100-125 mg/dL, or AIC: 5.7%-6.4%). These
individuals are at high risk for development of diabetes.

• Early and aggressive intervention with nutrition and lifestyle changes can be crucial to
prevent the further development of diabetes.

• Nutrition therapy focused on weight loss when needed is an important first step and
evidence analysis has supported that their physiological impact may prevent the onset of
T2DM. Further dietary modifications should include changes in dietary patterns to
follow DASH diet or Mediterranean dietary pattern.
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Diagnosis of Diabetes
There are four ways to diagnose diabetes:

1. Fasting plasma glucose test (FPG) ≥ 126 mg/dL (7.0 mmol/L).


2. Random plasma glucose concentration test ≥ 200 mg/dL (11.1 mmol/L).


3. Oral glucose tolerance test (OGTT) of ≥ 200 mg/dL (after 2-hour plasma glucose).


4. Glycosylated hemoglobin test (A1C or HbA1c) ≥ 6.5%.

Glycosylated hemoglobin test (A1C or HbA1c)
• It measures the amount of glucose bound to hemoglobin protein.

• The higher the glucose concentration in the blood, the more hemoglobin is glycated (via
addition of a glucose molecule to amino acid side chains), thus making it a valid test to
measure degree of hyperglycemia.

• Because red blood cells have a life span of 120 days, A1C can measure the average glucose
concentration for the previous 2–3 months.

Medical Treatment of Diabetes
• Treatment goals for both T1DM and T2DM include avoiding hyperglycemia and
retarding development of complications within an acceptable level of treatment side
effects.

• The closer to the normal range blood glucose can be maintained over the long term, the
lower the risk of complications such as cardiovascular disease, nephropathy,
retinopathy, peripheral neuropathy.

Type 1 diabetes mellitus (T1DM):
To survive, individuals with T1DM must depend on daily administration of exogenous
insulin in conjunction with nutrition therapy and physical activity to mimic the insulin
secretion in an individual without diabetes.

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Type 2 diabetes mellitus (T2DM):
Treatment of T2DM utilizes a variety of medications (including insulin), nutrition therapy,
and lifestyle changes. The first step in treatment for T2DM is weight loss and increased
physical activity. The next step of treatment includes the initiation of pharmacological
agents.

Insulin Delivery Regimens
Insulin that is used for diabetes treatment is recombinant human insulin. One method for
determining a starting insulin dose is multiplying the weight in kilograms by 0.55.

There are three basic types of insulin delivery regimens:

1. 
   

   Conventional therapy (Fixed therapy):
   It consists of a premixed or fixed insulin plan. This type of insulin therapy is prescribed less
   often and when it is prescribed, it is usually for T2DM. Individuals using conventional
   therapy must synchronize administration of their insulin and food intake to avoid
   hypoglycemia.
   Usually, a prescribed dose of basal or intermediate-acting insulin is combined with short- or
   rapid-acting insulin. Typically, these regimens prescribe 2/3 of total insulin dose in the
   morning (2/3 long acting and 1/3 short acting), and the rest is given in the evening (1/2 long
   acting and 1/2 short acting). This is referred to as a mixed dose and the individual may use
   premixed insulins (e.g., 30 units of 70/30 insulin).

   
   


2. 
   

   Intensive insulin therapy (Flexible therapy):
   It is much more common today than other regimens, requires multiple daily injections of
   rapid-acting insulin before meals in addition to basal insulin dose once daily. This regimen
   can use actual syringes, or pens to deliver the insulin.
   Nutrition interventions for individuals using this typical regimen should incorporate the
   following: Insulin should be taken prior to eating at mealtime.

   
   

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3. Continuous subcutaneous insulin infusion (CSII):
   This method is an external closed-loop pump that provides a 24-hour programmable basal
   rate of insulin. The rate can be individualized for changes in insulin sensitivity, sleep, and
   activity. Additional boluses of insulin are given before meals and snacks.

Figure 12: Insulin Delivery Regimens According to Acting Periods

Medications for T2DM
As T2DM progresses, use of glucose-lowering medications is indicated if glycemic control
cannot be achieved with lifestyle management: nutrition therapy and regular physical
activity. Metformin is the preferred initial drug to treat T2DM. It acts to lower hepatic
glucose production.

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Nutrition Therapy for Diabetes

Nutritional Implications:
The impact of dietary modification on overall health, metabolic control, and treatment for
acute and chronic complications is substantial. Individualized nutrition therapy is required
to achieve treatment goals.

Nutrition Assessment:
A comprehensive nutrition assessment, a self-care treatment plan, and the client’s health
status, learning ability, readiness for change, and current lifestyle should be the basis for
nutrition therapy.

Nutrition Diagnosis:
Common nutrition diagnoses associated with diabetes include inadequate energy intake,
inappropriate intake of types of carbohydrates, inconsistent carbohydrate intake,
inadequate fiber intake, altered GI function, altered nutrition-related laboratory values,
food-medication interaction, underweight, food- and nutrition-related knowledge deficit,
not ready for diet/lifestyle change, self-monitoring deficit, undesirable food choices, physical
inactivity, or inability or lack of desire to manage self-care.

Nutrition Intervention:

1. There is no one diet for diabetes. Instead, basic nutrition principles will be incorporated
   to address an individual’s nutritional needs with regard to personal and cultural
   preferences and lifestyles while respecting the individual’s wishes and willingness to
   change.


2. Other interventions that are generally included in the nutrition intervention are
   carbohydrate-to-insulin dosing, prevention of acute complications such as hypoglycemia,
   blood glucose monitoring, and physical activity with specific attention to coordination
   with food and medications.

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Nutrition Prescriptions:

1. There is no single ideal dietary distribution of calories among carbohydrates, fats, and
   proteins for people with diabetes; therefore, macronutrient distribution should be
   individualized.


2. The registered dietitian could start with the dietary guidelines that suggest
   approximately 45% of kcal from carbohydrate, 15-20% from protein, and 20-30% of
   total kcal from fat.


3. Carbohydrate and available insulin are the most influential factors affecting glycemic
   response; thus, the amounts and types of carbohydrate should always be considered
   when planning interventions to control hyperglycemia. Carbohydrates from fruits,
   vegetables, legumes, low-fat dairy products, and whole grains are emphasized.


4. Sucrose-containing foods should not necessarily be substituted for other carbohydrates
   and foods, and as is recommended for all individuals (including those without diabetes),
   simple sugars should provide 5%) achievable by the combination of reduction of calorie intake and
   lifestyle modification benefits overweight or obese adults with type 2 diabetes and also
   those with prediabetes.


5. People with diabetes and those at risk should avoid sugar-sweetened beverages in order
   to control weight and reduce their risk for CVD and fatty liver and should minimize the
   consumption of foods with added sugar that have the capacity to displace healthier, more
   nutrient-dense food choices.

Meal Patterns and Planning:

1. 
   

   Numerous meal patterns discussed within the literature can be used to achieve glycemic
   and metabolic goals. These include the Mediterranean diet, the DASH diet, and vegetarian
   or vegan diets.

   
   


2. 
   

   Personal choice and individual metabolic parameters will assist in using these patterns
   to make individual food choices.
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3. 
   

   Coordinating food with each type of medication should be a component of all nutrition
   therapy interventions. Individuals receiving conventional insulin therapy must be
   consistent with the timing of their meals and amounts of food consumed. Those receiving
   intensive insulin therapy have more flexibility in when and what they eat.

   
   

Carbohydrate Counting:

1. The basic concept of carbohydrate counting is that the carbohydrate found in foods is the
   major macronutrient influencing postprandial glucose variations and that it influences
   premeal insulin requirements more than the protein and fat content of the meal.


2. The total amount of daily carbohydrate intake, not its source, is the focus of this meal
   planning approach. Emphasis on eating consistent amounts of carbohydrate at meals and
   snacks can make carbohydrate counting a simpler method of meal planning.


3. Food carbohydrate sources are starches, fruits, milk/yogurt, and sweets. Non-starchy
   vegetables do not need to be counted unless eaten in servings containing >15 g of
   carbohydrates.


4. Carbohydrates can be counted in any of the following ways: The serving of food
   containing 15 g carbohydrate counts as one carbohydrate choice.


5. For individuals with diabetes who takes exogenous insulin, insulin-to-carbohydrate
   ratio (ICR) should be calculated to adjust premeal insulin doses for variable
   carbohydrate intake.


6. The insulin-to-carbohydrate ratio (ICR) is typically calculated by dividing 500 by the
   total daily dose (TDD) of insulin. For example, if a patient is taking 50 units of insulin
   per day, you would divide 500 by 50 to get 10. This means that 1 unit of rapid acting
   insulin will cover the spike in blood glucose after the patient eats 10 g of carbohydrate.

Food Lists:

1. 
   

   This method uses the concept of choosing different foods within each of three groups:
   carbohydrate (starch, fruit, milk, nonstarchy vegetables, and other carbohydrates),
   protein (lean meats, medium-fat meats, high-fat meats, and plant-based proteins), and
   fats (monounsaturated, polyunsaturated, saturated).
   
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2. 
   

   Each food portion on a particular list can be exchanged with any other food portion on
   the same list.

   
   

Figure 13: Food Lists Meal Plan

Nutrition Monitoring and Evaluation:

1. Progress can be monitored using self-monitoring records and laboratory tests.
   Evaluation may reveal a need for further education or adjustment of insulin dosages
   based on self-monitoring.


2. Glycemic control is fundamental to the management of diabetes and provides the basis
   for monitoring and evaluation of the condition.


3. Improved glycemic control is correlated with sustained reduced rates of microvascular
   and macrovascular complications.


4. The combination of Self-monitoring of blood glucose (SMBG) and A1C is the best
   indicator of glycemic control. A typical SMBG test includes a drop of blood obtained via a
   finger prick that is then analyzed using a blood glucose meter.