AGUSSALIM BUKHARI

Place/Date of Birth : Bulukumba, 21 Agustus 1970

Office : Dept. of Nutrition, Medical Faculty, Hasanuddin University, Clinical Nutrition Unit,
Dr. Wahidin Sudirohusodo Hospital, Makassar
Education
1996 : Medical Doctor, Hasanuddin University, INDONESIA
2002 : Master of Clinical Nutrition, Monash University, AUSTRALIA
2004 : Clinical Nutrition Specialist, CN Collegiate, Jakarta, INDONESIA
2008 : Ph.D in Diabetology, Dept. of Internal Medicine, Univ. of Toyama, JAPAN

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 Mechanisms of
Nutritional-related
Diseases
Agussalim Bukhari, MD, Ph.D
Nutrition Department School of Medicine
Hasanuddin University
@2008
 Objective Learning
 To understand mechanism of Nutritinal related
Diseases
 To be able to explain types of Malnutrition
 To comprehend Basic of Clinical Nutrition
 To Understand Metabolism of Macronutrients
(Carbohydrate Protein, and Fat)
 To Understand Metabolism of Micronutrients
(Vitamin dan Mineral) and water
 To comprehend Nutrient Interrelation
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 Disease

Agents:
Host: Microorganism
Genetic Chemical
Immunity substance
Nutrition Nutrition
Psychological Trauma
factor Physical stressor

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CORRELATION BETWEEN NUTRITIONAL STATUS AND IMMUNE FUNCTION

Immune suppression Normal Immune

Susceptible to Infection Function Immune activation,
Susceptible to
Inflammatory disease
Undernutrition Optimal
Nutritional status
Overnutrition

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 Pathogeneses of Nutritional
related Diseases
 Malnutrition
 Starvation
 Undernutrition
 Specific Deficiency
 Imbalance
 overnutrition
 Toxicity
 Vitamin
 Mineral
 Amino acid

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 Malnutrition-related Diseases
Undernutrition Overnutrition
 PEM: marasmus,  Obesity related diseases :
kwashirkor Metabolic syndrome
 Vitamin deficiency (diabetes, CVD,
diseases: Beriberi (B1), Hyperlipidemia,
scurvy (vit C), Hypertension),
xerophthalmia (vit A) Osteoarthritis, Gout,
 Mineral deficiency Cancer,
diseases: Anemia (Fe),  Hypervitaminosis
Osteoporosis (Ca)  Mineral toxicity
Food Allergy, Food Intolerance, Food Poisoning
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 Pathogeneses of Nutritional
related Diseases
OVERNUTRITION
S
P E
R C
I O
NUTRIENTS M N BODY
A D
R A
Y R
Y

UNDERNUTRITION

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Ethiology of Nutritional
Deficiency
1. Inadequate Intake (Primary Cause)

Secondary Cause
2. Malabsorption
3. Inadequate Utilisation--- lack of enzymes
4. Increased Requirement (Pregnancy)
5. Increased Excretion (Liver Disease)
6. Inadequate mobilisation from storage (i.e
Ferritin in inflammatory disease)
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THE PATHOGENESIS OF NUTRITIONAL DEFICIENCY DISEASE

Secondary
Inadequacy

Nutritional Tissue Biochemical Functional

Inadequacy Depletion Lesions Changes

Nutrients
reserve

Primary Anatomic
Inadequacy Lesions

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 ESTIMATION OF SOME NUTRIENTS RESERVE

Nutrients Reserve Time

Asam amino Bbrp jam
KH 13 jam
Lemak (12% BB) 27 hari
Thiamin 30-60 hari
Ascorbic acid 60-120 hari
Niacin 60-180 hari
Riboflavin 60-180 hari
Vit A 90-365 hari
Iron (menstruating women) 125 hari
Iron (post menopausal women and men) 750 hari
Iodine 2500 hari

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SEVERE PROTEIN ENERGY MALNUTRITION (PEM)

MARASMUS

KWASHIORKOR
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 MARASMIC-KWASHIORKOR
KWASHIRKOR
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KWASHIORKOR MARASMIC-KWASHIORKOR

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 Hospital malnutrition
 Malnutrition characterized by
HYPOALBUMINEMIA is associated with：
 Increased morbidity,

 Increased mortality and

 Prolonged hospital length of stay

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Types of Malnutrition

• Marasmus
• Kwashiorkor
• Mixed

Because this is a disease with multiple etiologies, the

best terminology would probably be polydeficient
malnutrition.

Green CJ. Clin Nutr 1999;18(s):3-28

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How common is Malnutrition in surgical patients?
25% of surgical patients are malnourished on admission!

Does it matter?
80
70
60 Well
50 nourished
Moderately
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malnourished
30 Severly
20 malnourished
10
0
P<0.005 (infections)
Infections (%) LOS (days) P<0.0001 (LOS)

McWirther, BMJ 1994;308:945-8. Baker, N Engl J Med 1982;306:969-72 18

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OBESITY AND IMMUNE FUNCTION

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 Medical Nutrition Therapy
of Diseases
 DDT-----  Endocrine & Metab:
anthropometrics DM, Thyroid
 Immunology----allergy &  Cardiovascular
Food intolerance  Musculoscelteal: Gout
 Hematology---  Neuropsychiatry
Nutritional related  Special sense:
anemia xerophhlamia
 Oncology---dietary
prevention and
management
 Gastroenterology
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 Nutrients & Non Nutrients
(Bioactive components)
 Macronutrients: Carbohydrate, Protein, Lipid
 Micronutrients: Mineral, Vitamin
 Phytochemicals (mostly antioxidants):
Carotenoids, Flavonoids, organosulfur,
isothiocyanates, phenolic acids

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 MAKRONUTRIENTS

DIETARY
CARBOHYDRATES, FAT AND PROTEIN

Dr. Agussalim Bukhari, M.Med.,Ph.D ,Sp.GK

Nutrition Department School of Medicine
Hasanuddin University
@2008
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DIETARY CARBOHYDRATES
AND FIBRE

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To see carbohydrate molecular structures go to:
http://www.fao.org/docrep/x5738e/x5738e06.htm

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 INDEKS GLISEMIK (IG)
 Pasien DM dianjurkan untuk mengkonsumsi
makanan dengan IG rendah
 Karbohidrat kompleks/serat tinggi memiliki IG
relatif rendah dibanding Gula sederhana
 IG 70 = tinggi
 IG 56 – 69 = sedang
 IG 55 = Rendah

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Makanan Tinggi IG menaikkan gula darah

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Makanan Tinggi IG menaikkan gula darah
160

140
Blood Glucose (mg/dL)

Potatoes (GI 75)

Kidney Beans(GI 55)
120

100

80

60
0 60 120
Time (min)

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Makanan Tinggi IG menaikkan gula darah
180

160
Blood glucose (mg/dL)

Fructose(GI <50)
140 Sucrose(GI 70-80)
Glucose(GI 100)
120

100

80

60
0 60 120
TIME (min)
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 MAKANAN INDEKS
GLIKEMIK/IG
GLUKOSA 100
KENTANG 85
NASI PUTIH 80
BERAS MERAH 76
ROTI PUTIH 70
ROTI TINGGI SERAT 69
GULA PASIR 65
MADU 58
JAGUNG 55
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 MAKANAN INDEKS
GLIKEMIK/IG
KRIPIK KENTANG 54
KACANG KEDELE 48
MIE INSTAN 46
JUZ JERUK 46
SPAGHETTI 41
JUZ APPEL 40
YOGHURT, RENDAH 33
LEMAK
SUSU SKIM 32
KACANG TANAH 44
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http://en.wikipedia.org/wiki/Dietary_fibre

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DIETARY LIPIDS

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Play a role in blood cholesterol levels. These substances
occur when polyunsaturated oils are altered through
hydrogenation, a process used to harden liquid vegetable oils
into solid foods like margarine and shortening.

One recent study found that trans-monounsaturated fatty

acids raise LDL cholesterol levels, behaving much like
saturated fats.

Simultaneously, the trans-fatty acids reduced HDL

cholesterol readings. Much more research on this subject is
necessary, as studies have not reached consistent and
conclusive findings.
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DIETARY PROTEIN

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SEVERE PROTEIN ENERGY MALNUTRITION (PEM)

MARASMUS

KWASHIORKOR
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 MARASMIC-KWASHIORKOR
KWASHIRKOR
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Fate of Dietary Protein (amino acids) from one meal
during post-absorptive phase (~2 h)

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Regulation of Fuel
Utilization
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 TISSUE-SPECIFIC
METABOLISM
TISSUE FUEL USED FUEL RELEASED
Brain Glucose Lactate (in prolonged
Ketone Bodies starvation; the brain can
utilize lactate under some
pathological conditions）
Skeletal Muscle Glucose, FFA, TG, BCAA Lactate, alanine, glutamine
Heart FFA, TG, Ketone bodies,
Glucose, Lactate
Liver Amino acids, FFA, lactate, Glucose, ketone bodies,
glycerol, glucose, alcohol lactate, TG
Intestine Glucose, glutamine Lactate, alanine
Red blood cells Glucose lactate
Kidney Glucose, FFA, Ketone glucose
bodies, lactate, glutamine
Adipose tissue Glucose, TG Lactate, glycerol, FFA 110
 40 GLUCOSE UTILIZATION VS TIME IN THE 5 PHASES OF GLUCOSE METABOLISM
I II III IV V
Exogenous
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Glucose Used (g/h)

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Gluconeogenesis
Glycogen
10
/
/

/
/
4 8 12 16 20 24 28 2 8 16 24 32 40
/
Hours /
Days
ORIGIN OF
BLOOD : Exogenous Glycogen, hepatic Hepatic gluconeo- Gluconeogenesis Gluconeogenesis
GLUCOSE gluconeogenesis genesis, glycogen Hepatic and renal Hepatic and renal
TISSUES All except liver & All except liver, muscle Brain, RBC, Renal Brain, at a diminished
USING : All
adipose tissue at
& adipose tissue at Medulla, small rate, RBC, Renal
GLUCOSE rates intermediate
diminished rates between II & IV
amount by muscle Medulla
MAJOR
FUEL OF : Glucose Glucose Glucose Glucose, ketone Glucose, ketone 111
GLUCOSE bodies bodies
 40 GLUCOSE UTILIZATION VS TIME IN THE 5 PHASES OF GLUCOSE METABOLISM
I II IIIa IIIb
Exogenous (dietary glucose)
30
Glucose Used (g/h)

total glucose

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Gluconeogenesis
Glycogen
10
/
/

/
/
4 8 12 16 20 24 28 2 8 16 24 32 40
/
Hours /
Days

I Fed state Most glucose is provided by diet

II Fasted state Most glucose is provided by breakdown of liver glycogen stores; increasing
(Post absorptive) amounts are provided by gluconeogenesis
III Starved state Most glucose comes from gluconeogenesis; the breakdown of protein and fat
provides amino acids and glycerol, substrate for gluconeogenesis
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I II IIIa IIIb
Exogenous (dietary glucose)
30
Glucose Used (g/h)

total glucose

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Gluconeogenesis
Glycogen
10
/
/

/
/
4 8 12 16 20 24 28 2 8 16 24 32 40
State Time course Major fuels used / Hormonal control
Hours /
Days
I. Fed 0-4 h following a meal Most tissues use glucose insulin results in; glucose uptake by peripheral
tissues, glycogen, TG, and protein synthesis

II. Fasted 4-12 h after a meal Brain: glucose glucagon and Noradrenaline stimulate breakdown of
(post-absorptive) Muscle and liver: fatty acids liver glycogen and TG
insulin
IIIa. Early starvation 12h-16 days without food Brain: glucose and some ketone bodies glucagon and NoradrenalineTG hydrolysis and
Liver: fatty acids ketogenesis
Muscle:mainly fatty acids and some ketone bodies
cortisolbreakdown of muscle protein, releasing
amino acids for gluconeogenesis

IIIb. Prolonged starvation >16 days without food Brain: uses more ketone bodies and less glucose to preserve body protein glucagon and Noradrenaline
Muscle: only fatty acids
 Three States of glucose homeostasis
State Time course Major fuels used Hormonal control
I. Fed 0-4 h following a Most tissues use glucose insulin results in; glucose
meal uptake by peripheral tissues,
glycogen, TG, and protein
synthesis
II. Fasted 4-12 h after a meal Brain: glucose glucagon and
(post-absorptive) Muscle and liver: fatty acids Noradrenaline stimulate
breakdown of liver glycogen
and TG
insulin
IIIa. Early 12h-16 days Brain: glucose and some glucagon and
starvation without food ketone bodies NoradrenalineTG
Liver: fatty acids hydrolysis and ketogenesis
Muscle:mainly fatty acids and
some ketone bodies cortisolbreakdown of
muscle protein, releasing
amino acids for
gluconeogenesis
IIIb. Prolonged >16 days without Brain: uses more ketone glucagon and
starvation food bodies and less glucose to Noradrenaline
preserve body protein
Muscle: only fatty acids 114
 Fatty acid synthesis: Cytosol
 Pyruvate----Acetyl CoA----Malonyl CoA-FFA-
TG
 Fatty acid oxidation: Mitochondria

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 FATE OF DIETARY CARBOHYDRATE (GLUCOSE) FROM ONE MEAL DURING THE ABSORPTIVE
PHASE (~2 H). GLUCOSE PROVIDES THE GLYCEROL MOETY FOR TRIACYLGLYCEROL SYNTHESIS

CO2

Brain
15-20 g

15 - 20 g

Adipose 2g 20 g
Glucose Liver
Triacylglycerol tissue Glycogen
90 g 20 g
2g

20 - 45 g

Muscle
25 g 20-45 g
20 g

Glycogen ATP 116

Plasma concentrations of fuels during prolonged starvation

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Plasma concentrations of insulin & glucagon during prolonged starvation
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 DIETARY VITAMINS

 Dr. Agussalim Bukhari, M.Med.,Ph.D

 Nutrition Department School of Medicine
 Hasanuddin University

 @2008

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Bitot’s Spot
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DIETARY MINERALS AND WATER

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Increase
absorption

Decrease absorption

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