NCM 211 NUTRITION AND DIET THERAPY (LECTURE)

Father Saturnino Urios University

Prepared by: REANNE MAE C. ABRERA SN
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❖ It is the formation of glycogen, the primary carbohydrate stored in the liver and muscle
cells of animals, from glucose.
DIABETES MELLITUS
GLUCOSE REGULATING HORMONES
❖ Diabetes, in Greek, means “to flow through”. Mellitus, in Latin, means “honeyed”.
Arataeus and Cappadocian, 1st century AD → “the melting down of flesh into urine”. ❖ INSULIN
❖ It is a disorder of CHO, CHON, and Fat metabolism resulting from an imbalance betweein ➢ It is regulated by blood glucose.
insulin availability and insulin needed. ➢ It is secreted in the β cells of the Islets of Langerhans in the pancreas.
❖ It is characterized by hyperglycemia. ➢ Three (3) fold actions of insulin:
❖ Its’ epidemiology are: 1. Promotes glucose uptake by target cells and promotes glycogenesis.
➢ Prevalence of high FBS (fasting blood sugar) equal or greater than 126mg/dl 2. Prevents fat and glycogen breakdown.
among adults was 8.2%, peaking at age 50 to 69 years. 3. Inhibits gluconeogenesis and increases CHON synthesis.
➢ Prevalence of Impaired Fasting Blood Sufar (IFBS 100mg/dL to 125mg/dL) is ○ Gluconeogenesis (GNG) is a metabolic pathway that results in the
29.1%. generation of glucose from certain non-carbohydrate carbon
➢ Hyperglycemia of high FBS (fasting blood sugar) level (50 to 59 years old.) substrates.
increases from 2013 (10.6%) to 2018 (12.9%), and present data (13.9%) but the
increase was not significant.

GLYCOGENESIS

❖ It takes place when blood glucose levels are sufficiently high to allow excess glucose to be
stored in liver and muscle cells.
 ➢ Two (2) actions of glucagon:
1. Initiates glycogenolysis to raise blood glucose.
○ Glycogenolysis is the biochemical breakdown of glycogen to
glucose.
2. Stimulates gluconeogenesis of CHON and fat (at high concentrations).
○ Gluconeogenesis (GNG) is a metabolic pathway that results in the
generation of glucose from certain non-carbohydrate carbon
substrates.

❖ GLUCAGON
➢ It is regulated by blood glucose.
➢ It is secreted by the α cells of the Islets of Langerhans in the pancreas.
❖ Other glucose regulating hormones include:
CLASSIFICATION OF DIABETES MELLITUS
1. Catecholamines (epinephrine and norepinephrine)
❖ TYPE 1 DIABETES MELLITUS (DM)
○ Catecholamine can serve as neurotransmitters transferring signals from
➢ β-cell destruction (mostly immune-mediated) and absolute insulin deficiency;
neuron to neuron, as well as hormones, which regulate physiological
onset most common in childhood and early adulthood.
functions such as your heartbeat and breathing rate.
❖ TYPE 2 DIABETES MELLITUS (DM)
2. Growth Hormones
➢ Most common type, various degrees of β-cell dysfunction and insulin resistance;
○ Growth Hormones stimulate growth, cell production, and cell
commonly associated with overweight and obesity.
regeneration in humans.
➢ A condition of fasting hyperglycemia that occurs despite the availability of insulin.
3. Glucocorticoid Hormones
➢ Metabolic abnormalities that contribute to hyperglycemia include:
○ Glucocorticoids are any steroid hormones that is produced by the adrenal
1. Impaired insulin secretion
gland and known particularly for its’ anti-inflammatory and
○ It happens when cells in your muscles, fat, and liver don’t respond
immunosuppressive actions.
as they should to insulin, a hormone your pancreas makes that is
TYPE OF DIABETES MELLITUS
essential for life and regulating blood glucose (sugar) levels.
❖ Type 1 diabetes occurs because the insulin-producing cells of the pancreas (beta cells) 2. Peripheral insulin resistance
are damaged. ○ The causes are:
i. Abdominal fat and obesity;
ii. Lack of exercise;
iii. Lack of quality sleep;
iv. Excess carbs consumption;
v. Chronic illness and inflammation; and
vi. Genetic susceptibility
3. Increased hepatic glucose production
 PATHOPHYSIOLOGY OF HYPERGLYCEMIA ❖ OTHER SPECIFIC TYPES

❖ Insulin secretion from the pancreas normally reduces glucose output by the liver, 1. Genetic defects in β cell function

enhances glucose uptake by skeletal muscle, and suppresses fatty acid release from fat 2. Genetic defects in insulin function

tissue. The various factors shown that contribute to the pathogenesis of type 2 diabetes 3. Diseases of the exocrine pancreas

mellitus affects both insulin secretion and insulin action. Decreased insulin secretion will 4. Endocrinopathies

reduce insulin signalling in its target tissues. Insulin resistant pathways affect the action 5. Drug- or chemical-induced

of insulin in each of the major target tissues, leading to increased circulating fatty acids 6. Infections

and the hyperglycemia of diabetes. In turn, the raised concentrations of glucose and fatty 7. Uncommon forms of immune-mediated diabetes

acids in the bloodstream will feed back to worsen both insulin secretion and insulin 8. Other genetic syndromes are sometimes associated with diabetes

resistance. 9. Hybrid forms of diabetes

10. Unclassified diabetes
11. Hyperglycemia first detected during pregnancy
❖ GESTATIONAL DIABETES
➢ Glucose intolerance that is detected first during pregnancy
➢ There are two (2) subtypes of gestational diabetes:
1. Diabetes mellitus in pregnancy
○ Type 1 or type 2 diabetes first diagnosed during pregnancy
2. Gestational diabetes mellitus

MANIFESTATIONS OF DIABETES MELLITUS (DM)

❖ Type 1 DM symptoms arise suddenly.

❖ Type 2 DM symptoms develop more insidiously (gradual and subtle but has harmful
effects).
❖ The most commonly identified symptoms of diabetes mellitus are referred to as the three
(3) polys:
1. Polyuria → excessive urination
2. Polydipsia → excessive thirst
3. Polyphagia → excessive hunger
DIAGNOSIS FOR DIABETES MELLITUS

❖ Fasting Blood Glucose Test

➢ Glucose level measured after food is withheld for 8 to 12 hours.
➢ Normal value is ≤ 100mg/dl.
❖ Random Blood Glucose Test
➢ Done without regard to meals or time of day.
➢ CPG ≥ 200mg/dl in the presence on the three (3) polys
❖ Glycosylated Hemoglobin Test
➢ Measures the concentration of HbA1c
➢ Normal value of less than 7%.
❖ Urine Test
➢ Considered to be obsolete for people with diabetes mellitus (DM).

ACUTE COMPLICATIONS OF DIABETES MELLITUS

❖ Diabetic Ketoacidosis (DKA)

➢ It occurs when ketone production by the liver exceeds cellular use and renal
excretion.
➢ Common in individuals with Type 1 DM.
➢ S/S: Dehydration, Ketoacidosis (liver process fat into fuel – ketones – body breaks
fat too fast – acid blood), compensatory response (Kussmaul’s respiration).
■ Kussmaul’s respiration → fruity odor of breath because of ketones.
■ Deep and labored breathing pattern.
❖ Hypoglycemia
➢ A.K.A insulin reaction, occurs from a relative excess of insulin in the blood and is
characterized by below normal blood glucose level.
➢ S/S Impaired cerebral function and autonomic nervous system response (hunger,
anxiety, hypotension, etc.)
➢ Tx: Immediate ingestion of a concentrated CHO source
■ Shakiness
■ Sweating
■ Irritability
■ Dizziness
 MANAGEMENT OF DIABETES MELLITUS

❖ Treatment is intended to:

1. Control blood glucose levels.
2. Provide optimal nourishment for the client.
3. Prevent symptoms and thus delay the complications of the disease.
❖ Treatment can be diet alone or by diet combinde with insulin or an oral glucose-lowering
medication plus regulated exercise and the regular monitoring of the client’s blood
glucose.

DIETARY TREATMENT

CHRONIC COMPLICATIONS OF DIABETES MELLITUS
❖ “There is no one ‘diabetic diet’ that will suit the individual and special needs of a person
with diabetes.”
❖ The goals of nutrition therapy:
1. Maintenance of as near normal blood glucose levels
2. Achievement of optimal serum lipid levels
3. Provision of adequate E° to maintain/achieve desired and regulated body weight
4. Prevention and treatment of the acute complication
5. Improvement of overall health
❖ TOTAL CALORIES

❖ Chronic complications include: ➢ Sufficient to maintain/achieve RBW; depends on age, activity, lean muscle mass,

1. Neuropathy size, and REE (resting energy expenditure).

2. Nephropathy ❖ CARBOHYDRATES

3. Retinopathy → it damages the blood vessels in the retina, leading to new ➢ 50% to 60% of total calories

abnormal blood vessel growth, leakage, and bleeding. ➢ 40% to 50% from complex CHO
➢ 10% to 20% from simple sugars
 ■ Research shows that the total amount of CHO eaten affects blood sugar 4. Reduces or modifies the risk for heart disease with reduces LDL (low density
rather than type. lipoproteins), increases HDL (high density lipoproteins), and lowers blood pressure
❖ PROTEIN (BP).
➢ 10% to 20% of total calories 5. Improves physical fitness.
❖ FATS 6. Improves psychological wellbeing.
➢ 20% to 30% of total calories ❖ POTENTIAL RISKS
❖ ALCOHOL 1. Hypoglycemia in persons or insulin
➢ Moderate amounts may be allowed, contingent on good metabolic control 2. Hyperglycemia may be aggravated in poorly controlled or under-insulinized
❖ VITAMIN AND MINERAL SUPPLEMENT patients with a pre-exercise blood glucose of 250mg/dL and above
➢ Not usually necessary, but may be given to individuals on reduced caloric diets 3. MI or arrhythmia risk for individuals with atherosclerosis
(1400kcal/day or less) 4. Possibility of microvascular complications (neuropathy, nephropathy, and
retinopathy)
SPECIAL CONSIDERATIONS
5. Damage to soft tissues and joints, particularly if peripheral neuropathy is present.
❖ FIBER
MEDICAL MANAGEMENT
➢ It lowers blood glucose which reduces the amount of insulin needed.
➢ It lowers blood cholesterol and TGC (triglyceride) levels. ❖ INSULIN THERAPY
❖ ALTERNATIVE SWEETENERS ➢ Exogenous source of insulin
➢ Sucralose → a sugar molecule altered so that the body will not absorb it. ➢ Dosage related to total calories rather than CHO alone; given for type 1 DM and
➢ Aspartame → the combination of phenylalanine and aspartic acid some cases of type 2
➢ The rationale is given to replace the deficiency of insulin
EXERCISE
❖ ORAL HYPOGLYCEMIC DRUGS
❖ BENEFITS
➢ Sulfonylureas
1. Improves glucose utilization by cells
➢ Replaginide and Nateglinide
2. Increased insulin sensitivity
➢ Biguanides
3. Weight control
➢ α-Glucosidase Inhibitors
 ➢ Thiazolidinediones

MEASURING CARBOHYDRATE EFFECTS CAN HELP GLUCOSE MANAGEMENT

❖ The glycemic index is a value assigned to foods based on how slowly or how quickly those
foods cause increases in blood glucose levels.
❖ Foods low on the glycemic index (GI) scale tend to release glucose slowly and steadily.
❖ Foods high on the glycemic index release glucose rapidly.
❖ Low GI foods tend to foster weight loss, while foods high on the GI scale help with energy
recovery after exercise, or to offset hypo- (or insufficient) glycemia.