“

Obesity, MetS, & Diabetes

Mellitus

2017
Naufal Muharam Nurdin
Naufalmn.ipb@gmail.com
08998269369
 References
Understanding Normal and Clinical Nutrition 8th Edition
Sharon Rady Rolfes, Kathryn Pinna, Ellie Whitney

1. Chapter 8 : Energy Balance and Body

Composition
2. Chapter 9 : Weight Management Overweight,
Obesity and Undernutrition
3. Chapter 26 : Diabetes Mellitus

Nutrition Therapy &

Patophysiology
Marcia Nahikian Nelms, Kathryn
Sucher, Karen Lacey, Sara Long
Roth
Obesity & Energy
Balance
Let’s start with the first set of slides
 Energy Balance

Energy Balance : Energy In – Energy out

Past and Future
 Fat cell development

Obesity due to an increase in the number of

fat cells is hyperplastic obesity. Obesity due
to an increase in the size of fat cells is
hypertrophic obesity.
 Fat Cell Development

1. excess energy is stored in the fat cells of adipose

tissue
2. The amount of fat in a person’s body reflects
both the number and the size of the fat cells
3. fat cells increases most rapidly during the
growing years of late childhood and early puberty
4. When energy intake exceeds expenditure, the fat
cells accumulate triglycerides and expand in size
5. When the cells enlarge, they stim- ulate cell
proliferation so that their numbers increase again
 Fat cell Metbolism

The enzyme lipoprotein lipase (LPL) :

promotes fat storage in both adipose and
muscle cells.

When weight loss, LPL increase -> regain

weight -> set point of weight
 Obesity
“ cause “

1. Genetics
2. Leptin :
1. gen ‘ob’ expressed leptin,
2. leptin act in hypotalamus -> suppressing appetite
and increasing energy expenditure
3. Defective ob gen -> not produce leptin -> obesity
3. Ghrelin
4. Uncoupling proteins
1. two types of fat: white and brown adipose tissue.
2. Uncoupling proteins : influence the basal metabolic
rate (BMR) and oppose the development of obesity
 Obesity
“ Fat distribution “
 Obesity
Consequences

Diseases associated with

Obesity :
• type 2 diabetes
• hypertension,
• stroke,
• coronary heart disease,
• sleep apnea,
• gallbladder disease,
• osteoarthritis, and
• cancer of the endometrium, breast, Time bomb
prostate, and colon.
Metabolic Syndrome
(MetS)
Let’s continues with the second set of
slides
 MetS
“Definition”

Definition :
Metabolic syndrome is a group of syndrome
criteria in a form of metabolicabnormalities
connected with obesity and insulin resistance
resulted in an increased risk of cardiovascular
diseases, stroke, and diabetes mellitus
(Alberti et al. 2005).
 MetS
” Criteria “
 MetS

1. Obesity causes a reduced secretion of

adiponectin, a hormone that improves insulin
sensitivity.
2. resistin, a hormone that con- tributes to insulin
resistance, is released in greater amounts.
3. production of certain cytokines that induce the
synthesis of liver proteins that promote
inflammation and blood coagulation
4. elevated levels of C-reactive protein, a marker
of inflammation linked to an increased risk of
CVD
5. Insulin resistance interferes vasodilatation
6. Hyperinsulinemia promotes reaborption of
sodium by the kidneys,
 MetS
Consequences

The metabolic syndrome are at increased

risk of developing cardiovascular diseases.
1. insulin resistance and elevated lipoprotein
levels can cause damage to blood vessels,
promoting inflammation and accelerating the
progression of atherosclerosis
2. Induced liver secretion of fibrinogen (a
protein that promotes blood clot formation)
3. Inhibits Nitric Oxide (a vasodilator)
4. Overproduced plasminogen activator
inhibitor-1 (a procoagulant)
Diabetes Mellitus
Let’s continues
 INSULIN
an Anabolic Hormone
 INSULIN
an Anabolic Hormone

Control metabolic of carbohydrate, protein and

lipid
Stimulated by :
○ Increase level of blood glucose
○ Action of counter-regulatory hormones
(catabolic hormone) including growth
hormone
Function :
○ Promote the UPTAKE of glucose into hepatic,
muscle, and adipose cell (via GLUT
Receptor)
○ Stimulate the SYNTHESIS of glycogen,
triglyceride and Protein
 INSULIN
Role on Blood Glucose Regulation
 INSULIN
Role on Glucose Uptake
 Diabetes Mellitus
“ Definition and Types“

Definition Diabetes Mellitus :

a group of metabolic disorders characterized by
hyperglycemia and disordered insulin
metabolism.
Diabetes = excessive passage of urine
Mellitus = sweet, honey-like

Types of Diabetes Mellitus

• Type 1 diabetes : Insulin deficience caused
by autoimmune destruction of the pancreatic
beta cell
• Type 2 diabetes : Insulin resistance
• Gestational Diabetes : diabetes in
pregnancy -> macrosomia
 Diabetes Mellitus
“ overview“

DIABETES : insulin disorder

Hyperglycemia : a marked elevation in blood

glucose levels -> Damage to blood vessels,
nerves, and tissues

Defect Insulin metabolism :

- Increase fatty acid and tryglycerida
- Muscle wasting
Diabetes Mellitus
“ overview“
 Diabetes Mellitus
“ Sign and Symptom “

- Glycosuria : presence of glucose in the urine

- polyuria
- Dehydration : hyperosmolar
- polyphagia : nutrient depletion
- blurred vision : he exposure of eye tissues to
hyperosmolar fluids
- Increased infections : hyperglycemia, impaired
circulation, or weakened immune function.
- constant fatigue : altered energy metab- olism,
dehydration, or other effects of the disease.
 Diabetes Mellitus
Diagnosis

Diagnosis DM
• Fasting blood gluocose (FBG) > 126 mg/dl (fasting at least 8
hours)
• Random blood glucose > 200 mg/dl + classic symptom DM
(polyuria, polydipsia, unexplained weigh loss)
• 2 hours post prandial glucose (2hPPG) > 200 mg/dl (after 2
hours after a 75 gram glucose load)
Prediabetes (between normal and diabetic)
• FBG between 100– 125 mg/dl
• 2hPPG between 140 – 200 mg
Oral Glucose Tolerance test : he individual ingests a 50- or
75-gram glucose load, and plasma glucose is measured at one
or more time intervals following glucose ingestion (minute: 0,
30, 60, 90, 120)
 Diabetes Mellitus
Diagnosis

Diagnosa Tambahan SCORE HBA1C

○ Kadar insulin
○ Kadar pro insulin
○ Kadar C-peptide
○ Kadar HBA1C  Glycosilated
Hemoglobin
□ Prinsip : oksidasi akibat hiperglikemia
pada HB
□ Menunjukkan konsentrasi glukosa
plasma pada periode waktu yang lama : 1 –
3 bulan
□ Untuk mengukur tingkat kepatuhan
 Diabetes Mellitus
Natural History of Diseases

Tipe 1 Diabetes
 Diabetes Mellitus
Natural History of Diseases
NATURAL HISTORY of TYPE-2 DM
OBESE
NORMAL DIABETES
Overweight Metabolic
syndrome

Blood glucose

Insulin resistance

Insulin secretion

Achmad Rudianto. 2007. patophysiology Metabolic Diseases (Kuliah Gizi Kesehatan FKUB). Malang: Dep. Internal Medicine, FKUB

Tipe 2 Diabetes
 Diabetes Mellitus
Acute Complications

Diabetic Ketoacidosis in Type 1 Diabetes

• Severe lack of insulin, blood glucose > 250 mg/dl may rise
above 1000 mg/dl + ketosis
• Breakdown of triglycerides (TG) -> increased fatty acid
oxidation -> excessive production ketone body ->
• Ketonuria + acetone breath + diabetic coma

Hyperosmolar Hyperglycemic State in Type 2 Diabetes

• Severe hyperglycemia, dehydration and hyperosmolarity.
(absence of significant ketosis)
• Blood glucose > 600 mg/dl may rise above 2000 mg/dl
• Extreme hyperglycemia -> fluid loss -> electrolyte
imbalance -> neurogical abnormalities
 Diabetes Mellitus
Acute Complications

Hypoglicemia (low blood glucose)

• Side efect antidiabetic drugs or insulin
• Symptom : sweating, shakiness, heart
palpitations, slurred speech, double vision,
and irritability.
○ Severe : koma -> brain damge
 Diabetes Mellitus
Acute efect of Insulin defeciency
 Diabetes Mellitus
Chronic Complication of Diabetes
Mellitus

Glucose nonenzymatically combines with proteins

produce advanced glycation end products
(AGEs). AGEs can accumulate and cause damage
to cells and blood vessels.

Excessive glucose also promotes the production and

accumulation of sorbitol, which increases oxidative
stress and alters molecular structures and
functions.

Diabetes accelerates artherosclerosis and

increased tendencies for thrombosis and abnormal
ventricle function
 KELAINAN METABOLIK PD DM

MET. KH MET. PROTEIN MET. LEMAK

MET. POLIOL SINTESA PROTEIN LIPOGENESIS
KATAB. PROTEIN LIPOLISIS
GLIKOLISIS
GLIKOGENESIS
AS. AMINO DRH
GLUKONEOGENESIS
GLIKOGENOLISIS GLISEROL
LUKA FFA DRH
SUKAR SEMBUH

SAPONIFIKASI,
HEPAR
SORBITOL

R.O.S
GLUKOSA VISKOSITAS BENDA VLDL
GLIKOSILASI

DARAH DARAH KETON

LDL
GLUKOSURIA dehidrasi KOMA
STS PL
KERUSAKAN P.j.k
ENDOTEL mikroangiopati
PEMBULUH DRH sklerosis DEGENERASI
SYARAF
 Diabetes Mellitus
Macrovascular Complication
Chronic complication diabetes:
1. Macrovascular Complications
1. Claudication
2. Gangrene
3. CAD (coronary artery diseases)
4. Stroke (trombosis)
2. Microvascular Complications
1. Diabetic retinophaty
2. Diabetic nephropathy – microalbuminuria
3. Nervous System (diabetic neurophatic)
1. Numbness and loss sensation in hands and feets
- Higher Risk of infection (gangren)
1. Gastroparesis
2. Sexual dysfunction
 Diabetes Mellitus
Microvascular Complication
 Diabetes Treatment
Medical Nutritional Therapy

Nutrition Recommendation
○ Total carbohydrate intake :
○ based on metabolic needs,
○ carbohydrate intake must be fairly
consisten (help reduce fluctuation in
blood glucose)
○ Carbohydrate source : consider low
glycemic index
○ Fiber : Similar to general population
 Diabetes Treatment
Medical Nutritional Therapy

Nutrition Recommendation
○ Sugars
○ Similar to general population
○ Dietary fat :
○ saturated fat < 7%,
○ trans fat minal,
○ cholesterol < 200 mg/day
○ Protein : 15-20 % from total kcalories
○ Micronutrients : same with general
population, chromium may improve
glycemic control
 Diabetes Treatment
Medical Nutritional Therapy

Meal Planning Strategies

○ Carbohydrate counting
The user only need concerned carbohyrate
consumption
○ Exchange list for meal planning
More complex, based on proportion of
carbohydrate, fat and protein.
 Diabetes Treatment
Oral anti-Diabetic Drug (OAD)

OAD Mode of Action

○ Delay carbohydrate absorption =
○ Alfa-glucosidase inhibitor
○ Stimulate insulin secretion
○ sulfonylureas
○ Decrease insulin resistence (improves
gluocse utilization)
○ biguanides (metformin)
○ thiazolidinediones
Drug-Diet Interactions
Diabetes Treatment
Insulin
 Insulin Therapy

Insulin Preparations
○ Rapid Acting (lispro, aspartat, glulisine
○ Short acting (regular)
○ Intermediate acting (NPH)
○ Long acting (glargine, detemir)

Mealtime : Rapid acting and Short acting

Between meals and during the night :
Intermediate and long acting
 Diabetes Treatment
“ physical activity “

Regular physical activity can improve

glycemic control
Regular exercise program
□ improves insulin sensitivity
□ lower blood lipid levels
□ lower blood pressur
□ lower body weight
□ improve cardiovascular functioning
Frequentcy :
Moderate-intensity : 150 minutes/week and/or
Vigoroues activity : 90 minutes/week
 Diabetes Treatment
“ physical activity “

Physical Activity and Insulin Therapy

○ Risk of hypoglycemia
○ insulin should not be injected immediately before exercise
○ during activity, injected insulin promotes rapid consumption of
glucose by exercising muscles and also blocks glucose synthesis
by the liver
Physical Activity in Type 2 Diabetes
○ Regular physical activity can improve the metabolic outcomes
associated with type 2 diabetes
○ Before an exercise program is planned, a medical evaluation
should screen for problems
○ retinopathy should avoid heavy lifting or straining, which may
raise blood pressure and damage eye tissue.
○ nephropathy often have reduced capacity for physical activity,
and strenuous exercise is discouraged
○ Peripheral neuropathy precludes repetitive weight-bearing
exercises such as jogging and step exercises, because these
activities may lead to foot ulcerations.