DM & Komplikasi

Dr Budi Enoch SpPD

Diabetes Estimates and Projections 1994 - 2010

1994 2000 2010

98.9 million 157.3 million 215.6 million

Type 2 Diabetes
DIABETES BECOMES MORE & MORE
IMPORTANT AS A GLOBAL PROBLEM
DUE TO :

1. The Steaply Rising Prevalence

2. The Disvastating Complications
3. High Number of Risk Factors
for Vascular Dysfunction
4. Difficulties in Preventing
Complications
Patogenesis dan Evolusi DM tipe 2
 Normal Glucose Metabolism
LIVER PANCREAS

GLYCOGENOLYSIS

Insulin
G LYCOGEN
Glucose
uptake +
HGP
GLUCOSE G L UC O S E

GLUCONEO
GENESIS
MUSCLE
NORMAL

- = Suppression
+ = Stimulation
Regulasi glukosa darah

•Puasa
kebutuhan glukosa diperoleh:
produksi glukosa oleh hati (80%)
•Setelah makan
Glukosa darah ditekan oleh sel
beta pankreas : insulin
otot :meningkatkan glucose uptake
Pathophysiology of Type 2 Diabetes

Impaired insulin action

Impaired insulin secretion

Hyperglycemia

Increased glucose production Decreased glucose uptake

 HYPERGLYCEMIA GENETIC
GENETIC OBESITY
ENVIRONMENT LIFE STYLE
INSULIN
 CELL RESISTANCE

HYPERINSULINEMIA

ANGIOPATHY etc

NORMAL NGT
DECOMPENSATION - 1 IGT-DIABETES

DECOMPENSATION - 2 DIABETES
 Primary defects in type 2 diabetes

Primary defects in type 2 diabetes1-3

ß-cell Insulin signalling

dysfunction defect
The development of type 2
diabetes is the result of a
combination of -cell
GLUCOSE TOXICITY

Loss of early phase

Insulin resistance
insulin release
dysfunction and insulin
resistance
Postprandial Increased basal
glucose spikes glucose levels

Hyperglycaemia

Adapted from Lebovitz, Ward and Yki-Järvinen

1 Lebovitz HE. Diab Rev 1999; 7: 139-153. 2 Ward W, et al. Diab Care 1984; 7: 491-502. 3 Yki-Jarvinen H. Endocrine Revs 1992; 13: 415-431.
Normal Pancreatic Islets:
ß cells Glucagon cells
Islets in Type II Diabetes:
Loss of ß cells
Amyloid deposits
Hyalinization
 Patogenesis DM tipe 2

• DM defek berupa :
1. Defisiensi insulin (hiperglikemia post prandial)
2. Resistensi insulin (hiperglikemia puasa)

• Pemahaman patogenesis
memudahkan pendekatan terapi.
 DM tipe 2 Multifaktor
Sekresi insulin terganggu
Kegagalan Sel beta
Deposisi amiloid
Obat2 & hormon yang abnormal
Malnutrisi in utero and early childhood
Mutasi glukokinase
Mutasi insulin
Mutasi mitokondria DNA
Resistensi insulin
 DM tipe 2 Multifaktor
Resistensi insulin
Insulin signalling
Obesitas dan diet
Penyakit Endokrin
Kehamilan
Obat-obat
Malnutrisi in utero and early childhood
Mutasi (jarang)
Reseptor insulin
Komponen Post reseptor
Defek Sekresi Insulin
 Physiology of insulin secretion
Ca++

S
Voltage-dependent
ATP-sensitive U
R Depolarization Ca2+ channel
K+ channel

Ca2+
↑ ATP/ADP
Islet
transcription
Mitochondria
factors
Insulin
Pyruvate

Glucose-6-Phosphate Nucleus
Glucokinase Secretory
granules
Glucose

GlucoseGLUT2
 Biphasic Insulin Response to Constant
Glucose stimulus
Stimulation by glucose
Level of insulin secretion

First(acute)
Phase on
release
Second
Phase

Baseline

Time
Diabetes Care 1984;7:491-502
Loss of Early- phase Insulin Secretion
in Type 2 Diabetes

Pattern of insulin secretion is altered early in type 2 diabetes

Normal Type 2 diabetes

120
Plasma insulin (µU/ml)

120

Plasma insulin (µU/ml)

20g
20g glucose
glucose
100 100
80 80
60 60
40 40
20 20
0 0
–30 0 30 60 90 120 –30 0 30 60 90 120
Time (minutes) Time (minutes)
Ward WK, et al. Diabetes Care 1984;7:491–502.
Resistensi Insulin
 Resistensi Insulin

Defek utama pada sebagian besar Diabetes Melitus tipe 2

Definisi :

Terganggunya respon terhadap efek fisiologis Insulin,

termasuk pula metabolisme glukosa, lemak, protein
dan fungsi endotelial pembuluh darah

Resistensi insulin terjadi pada : Otot

Hepar
Jaringan adiposa
 EVOLUSI DIABETES
Pada saat diagnosis, kedua mekanisme tersebut telah terjadi

Resistensi
Insulin

Glukosa darah
puasa

Sekresi
Insulin

Normal Fase kompensasi Diabetes

 DOUBLE DEFECTS OF TYPE2 DM

Insulin Type 2 -cell

Resistance Diabetes Dysfunction

-cell Failure
Insulin
Concentration

Insulin
Resistance

Euglycaemia
Normal IGT ± Obesity Diagnosis of Progression of
type 2 diabetes type 2 diabetes
DeFronzo et al. Diabetes Care 1992;15:318-68
 Pada kondisi resistensi insulin, insulin tidak
mampu menggerakkan jumlah GLUT 4 yang cukup
ke permukaan sel
Environmental factors Environmental factors
•Overeating Genetic factors Genetic factors •Pregnancy
•Inactivity •Endocrine diseases
•Smoking Unknown Unknown
•Diabetogenic drugs
•Diabetogenic drugs •Malnutrition in utero

Insulin resistance B- cell defects

Glucose toxicity

Hyperglycaemia

Impaired glucose Worsening B-cell functions

tolerance
• ? Amyloid deposition
•Malnutrition in utero

NIDDM
KOMPLIKASI KRONIK DM
 Complications:
• Short term Complications: (metabolic)
– Hypoglycemia
– Diabetic Ketoacidosis
– Non Ketotic hyperosmolar diabetic coma
– Lactic acidosis
• Long term Complications:(microangiopathy)
– Angiopathy, Retinopathy, Nephropathy,
Neurophathy
 Chronic Complications: Angiopathy
• Macro Angiopathy
– Atherosclerosis
– Stroke / MI
• Micro Angiopathy
– Hyaline arteriolosclerosis
– Diabetic pathies…!
• Immunosuppression.
– Inflam, Infections,
• Retinopathy
– Microaneurysms,
– Dot blot hemorrhages
– Hard and soft exudates
– Cotton wool – infarcts
– Proliferative retinopathy.
• Nephropathy
– Nodular glomerulosclerosis
• Neuropathy
• Dermopathy
– Necrobiosis, gangrene
– Grannuloma
DM COMPLICATIONS
MICROVASCULAR
RETINOPATHY
NEPHROPATHY
CARDIOMYOPATHY
NEUROPATHY
AUTONOMIC CARDIAC
GASTRIC
UROGENITAL
DM COMPLICATION
MACROVASCULAR
CHD RISK
2–4x
DEATH  60 %
CEREBROVASCULAR
STROKE : 4x
PERIPHERAL VD
40 – 50 % NON-TRAUMATIC AMPUTATION
 MAKROANGIOPATI
(Komplikasi Pembuluh Darah Besar)
 FAKTOR-FAKTOR PERLUKAAN ENDOTEL

4 Peningkatan kadar gula

darah

4 Kelainan lemak

4 Tekanan darah tinggi

4 Merokok

Resistensi insulin
BAGAIMANA TERJADINYA KOMPLIKASI
PADA PEMBULUH DARAH BESAR

Pembentukan sel busa

4 Perlukaan endotel

Terjadinya plak
aterosklerosis

Plak yang mudah pecah

Plak yang pecah

 Diabetic Microangiopathy

Peningkatan kadar gula darah

Penebalan Hilangnya sel-sel Kerusakan sel-sel

membrana basalis epitel/pericyte endotel

Penutupan pembuluh darah

Kerusakan pembuluh darah
Normal Capillary

Diabetic
 Neuropathy
• Sensory  Motor (myelin)
• Peripheral Neuropathy
– Bilateral, symmetric
– Progressive, irreversible
– Paraesthesia, pain, muscle atrophy
• Visceral neuropathy
– Cranial nerve – diplopia, Bell palsy
– GIT- constipation, diarrhoea
– CVS – orthostatic hypotension
 KLASIFIKASI NEUROPATI DIABETIK

1. NEUROPATI FOKAL
 Mononeuropati - neuropati kranial - radikulopati/pleksopati
 Entrapment syndrome - carpal tunnel syndrome
- ulnar nerve entrapment - peroneal neuropathy

2. NEUROPATI DIFUS
Neuropati motorik proksimal
Polineuropati simetrik distal

3. NEUROPATI OTONOMIK
Sistem kardiovaskuler
Sistem pencernaan
Sistem perkencingan
Sudomotor kaki tidak berkeringat
NEUROPATI DIABETIK
Chronic Polyneuropathy
Claw foot – Dermopathy & Neuropathy
Diabetic Amyotrophy
Painful muscle wasting
 Neuropathic ulcer

Callus formation
 Nephropathy
• Most common cause of morbidity
& mortality.
• Deposition of ‘AGE’ Advanced
Glycosylation Endproducts as
nodules.
• Nephrotic syndrome
• Pyelonephritis
• End stage renal failure
Diabetic Glomerulosclerosis
Hyaline nodules
Diabetic Glomerulosclerosis
 PERKEMBANGAN NORMO-MAKROALBUMINURIA

NORMAL MIKROAL- MAKROAL- SINDROM

BUMINURIA BUMINURIA NEFROTIK

10 30 300

Mg/hari

Proteinuria
500 mg/hari
Mikroalbuminuria 30-300 mg/h atau
rasio albumin:kreatinin urin = 2 – 25 mg/mmol pada laki-laki
3 – 30 mg/mmol pada wanita
 DERAJAT NEFROPATI DIABETIK

Derajat 1 : Pembesaran ginjal dan peningkatan fungsi

Derajat 2 : Lesi pada ginjal tanpa tanda-tanda klinis

Derajat 3 : Mikroalbuminuria
DMT2 saat diagnosis terjadi pada 18%, DMT1 6,4%
Fungsi ginjal mulai turun

Derajat 4 : Nefropati diabetik klinis

8% DMT2 saat diagnosis
Proteinuria >0,3 g/h; fungsi semakin turun

Derajat 5 : Gagal ginjal terminal; fungsi semakin turun

Perlu terapi pengganti (dialisis)
 Retinopathy
• Microaneurysms,
• Dot blot hemorrhages
• Hard and soft exudates
• Cotton wool – infarcts
• Neovascularization –
Proliferative retinopathy.
• Fibrosis
• Retinal detachment.
Normal Retina
Diabetic Retinopathy

Cotton wool spots

Diabetic Retinopathy
Dot blot – Hemorrhages / Microaneurysms
Diabetic Retinopathy
Pre retinal Hemorrhage
Diabetic Gangrene
KENDALI GULA DARAH

PENTINGNYA KENDALI GULA

DARAH YANG OPTIMAL

IDF WPR/WHO Diabetes Guidelines, 2

Terapi
 Symptom of Diabetes

Classical Symp (+) Classical Symp (-)

FBG FBG
>126 <126 >126 110 - <126 <110
or or
2h pp >200 <200 2h pp >200

140-199
Repeat FBG or 2h pp
OGTT
FBG 2h pp
>126 <126
or
2h pp >200 <200

>200 140 - 199 <140

DIABETES MELLITUS IGT IFG NORMAL

 Glucose Tolerance Categories
2-h PG
Fasting PG On OGTT

Diabetes Diabetes
Mellitus Mellitus
126 mg/dL 200 mg/dL
IFG IGT
110 mg/dL 140 mg/dL

Normal Normal

55
 Targets for Glycemic Control
ADA1 IDF2 ACE3

HbA1c (%) <7.0 6.5 6.5

Fasting/preprandial 80-120 mg/dL <100 mg/dL <110 mg/dL

(mg/dL) 4.4-6.7 mmol/L <5.6 mmol/L <6.1 mmol/L

2-hr postprandial <135 mg/dL <140 mg/dL

–
(mg/dL) <7.5 mmol/L <7.8 mmol/L

1American Diabetes Association. Diabetes Care. 1999;22(Suppl 1):S1-S114.

2 European Diabetes Policy Group. Diabet. Med. 1999;16:716-730.
3Endocrine Pract. 2002;8(Suppl 1):5-11.
 PERKENI: Tight glycemic target

A1c (%) <6.5

FBG (mg/dl) 80-<100

2-hpp (mg/dl) 80-144

Professionals Who Treat People With
Diabetes Means To …
• Set treatment goals
• Assess the quality of diabetes treatment
provided
• Identify areas where more attention or self-
management training is needed
• Define timely and referral patterns patients
to appropriate specialist

58
 Management Plan
• Statement of short- and long-term goals
• Medication (insulin OHA, antihypertensive,
lipid-lowering agents, aspirin therapy, and others
• Individualized nutrition recommendation
• Recommendations for appropriate lifestyle
changes
• Patient and family education

59
 Laboratory Tests
• Fasting plasma glucose, 2 hPP, HbA1C
• Fasting lipid profile – total-C (total
cholesterol), HDL-C, LDL-C, TG
(triglycerides)
• Serum creatinine (if proteinuria present)
• Urinalysis – glucose, ketones, protein,
sediment
• Test for microalbuminuria
• ECG
60
 ADA/EASD Consensus Algorithm

Call to action if HbA1c is 7%

Tier 1:
well-validated therapies Lifestyle + Lifestyle + Metformin
Metformin + Intensive insulin
+ Basal insulin
At diagnosis:
Lifestyle +
Metformin
Lifestyle + Metformin
+ Sulfonylurea

STEP 1 STEP 2 STEP 3

Lifestyle +
Metformin Lifestyle + Metformin
Tier 2: + Pioglitazone +
Less well validated No hypoglycaemia
therapies Oedema/CHF
Bone loss

Lifestyle +
metformin Lifestyle + metformin
+ GLP-1 agonist +
No hypoglycaemia
Weight loss
Nausea/vomiting
Nathan DM, et al. Diabetes Care 2009;32 193-203.
 HbA1c reflects
FPG and mealtime glucose spikes

Relative contributions of FPG and mealtime glucose spikes to 24-hour

glycemic control
300
Plasma glucose (mg/dl)

200 Mealtime
glucose
spikes
Fasting
100 hyperglycemia

Normal

0
6 am 12 pm 6 pm 12 pm 6 am
Time of day
Riddle MC. Diabetes Care 1990;13:676–686.
 BERDASARKAN TARGETNYA TERAPI DM DAPAT
DIGOLONGKAN MENJADI

1. Post Pandrial hiperglikemia , mis Diet, Rapid Acting

Insulin, acarbose, meglitinid, GLP-1 inhibitor, DPP
IV Inhibitor, dan Amylin analogues

2 Basal hiperglikemia, mis : Basal Insulin dan SU

3 Basal hiperglikemia dan resistensi insulin, mis :

Exercise, Metformin, Thiazolidinedione dan Inlacin
 BASICS OF TYPE2 DM THERAPY
1 2 1

EDUCATION EXERCISE DIET

4 5

HYPOGLYCEMIC ISLET TRANSPLANT

 Sites of Action of Current OAD
GLUCOSE ABSORPTION

INTESTINE

a-glucosidase inhibitors
GLUCOSE
PRODUCTION PERIPHERAL GLUCOSE
UPTAKE & UTILIZATION
LIVER
Glucose
MUSCLE
Biguanides
Thiazolidinediones
ADIPOSE TISSUE

Thiazolidinediones
INSULIN SECRETION Biguanides
Sulphonylureas
Meglitinides
ref version 2.1 PANCREAS Modified: Ann Intern Med 1999;131:281
 ANTI DIABETES
LAMA : BARU
1. Sulfonilurea 1. meglitinid
– klorpropamid 2. Golongan thiazolidinedione
– glibenklamid 3.GLP-1 inhibitor
– glipisid 4.DPP IV Inhibitor
– glikasid 5. Amylin analogues
– glimepirid 6. Inlacin
– glikuidon

2. Metformin
3. α glukosidase inhibitor
4. Insulin
 Sulfonilurea :

 Bekerja dengan cara memacu sel Beta Pankreas untuk

menghasilkan insulin

 Relatif cepat menurunkan kadar gula darah

 Lebih ditujukan untuk basal hiperglikemia

 Kebutuhan insulin kurang dari 20 U per hari

 Belum pernah mengalami ketoasidosis dan berat badan

normal atau lebih
 Tidak dianjurkan untuk terapi DM dengan komplikasi yg berat
 METFORMIN

1. Meningkatkan efektifitas kerja insulin.

Pemberian merformin pada penderita IDDM dapat
mengurangi
kebutuhan insulin sampai 25,8%
2. Mengurangi produksi gula hati.
3. Meningkatkan glikolisis yang anaerobe
4. Menurunkan glukoneogenesis.
5. Menghambat absorpsi glukose di usus.

Biguanide tidak menurunkan gula darah pada orang normal

 INDIKASI PENGGUNAAN METFORMIN

1. DMTTI :
– OBEIS
– GAGAL MONOTERAPI
– DISERTAI DISLIPIDEMIA, HIPERINSULINEMIA

2. DM DENGAN GANGGUAN RESEPTOR

3. NON-DM DISERTAI DISLIPIDEMIA, HIPERINSULINEMIA,

GANGGUAN RHEOLOGI
 KONTRAINDIKASI METFORMIN

• GAGAL GINJAL KREATININ > 1,5 MG%

• GANGGUAN FUNGSI HEPAR
• GANGGUAN OKSIGENASI JARINGAN
– DEKOMPENSASI KORDIS
– PENYAKIT PARU MENAHUN
• ALKOHOL ABUSE
• GRAVIDITAS
 Acarbose

 Acarbose menghambat pencernaan dari karbohidrat rantai

panjang di bagian atas jejunum sehingga karbohidrat tersebut
dicerna sepanjang usus halus. Pengaruh utamanya adalah
menurunkan glukosa darah sesudah makan.

 Acarbose dapat menurunkan glukosa darah postprandial 30-60

mg% , glukosa darah puasa 15-20 mg% dan HbA 1c 0,5-1 %.
 Repaglinid

 Repaglinid adalah derivat dari carbamoyl methyl benzoic acid.

 Obat in efeknya serupa dengan nateglinid, yaitu memacu

sekresi
insulin secara cepat dan aksinya juga hilang dengan cepat.

 penggunaannya tepat sebelum makan (one meal one dose, no

meal no dose)

 Eksresinya terutama lewat saluran empedu dan hanya

sebagian
kecil lewat urin.
 Nateglinide
 Nateglinide adalah derivat asam amino D-phenylalanine

 Nateglinide menyebabkan pelepasan insulin yang cepat dari

sel 
pankreas dan aksinya juga hilang dengan cepat

 Cara kerjanya menyerupai sulfonilurea, yaitu melalui ATP

dependent kalium channel.

 Penggunaannya adalah tepat sebelum makan, dan dapat

menurunkan terutama glukosa darah postprandial.

 Pacuan terhadap sekresi insulin hanya terjadi saat adanya

hiperglikemi, sehingga resiko hipoglikemi sangat kecil.
 Thiazolidinedione

 memperbaiki resistensi insulin.

 terikat pada Peroxisome Proliferator-Activated Receptor (PPARY)

 deferensiasi preadiposit  sel lemak matak

 aktivasi transkripsi gena  ekspresi protein spesifik  regulasi

K.H. & lipid - aksi insulin 

 ada 2 : trogglitazone & pioglitazone.

 Kegunaan Klinis Thiazolidinedione

 Troglitazone menurunkan kebutuhan isulin pada DM tipe-2 yang

mendapat insulin (Buse dkk. 1988).

 Perubahan preadiposit  sel lemak matang disubkutan -

troglitazone 6 bl ratio lemak visceral/subkutan  (Mori dkk, 1999)

 Pioglitazone - sensivitas insulin di hepar & jaringan  (Miyazaki

dkk, 2001).
Plasma glucose multihormonal
regulation of glucose
 GLP-1 Inh, DPP IV Inh,
Amylin analogues
• Menurunkan kadar glukosa darah post pandrial
• Stimulasi sekresi insulin
• Supresi kadar glukagon
• Memperlambat pengosongan usus  menimbulkan
rasa cepat kenyang
• Penurunan Berat Badan (DPP IV Inh Netral)
• Efek samping mual
• Sediaan injeksi (kecuali DPP IV inh; oral)
• Unpredictable hypoglycaemic (Amylin Analouge)
 Inlacin

• Made in Indonesia
• Memperbaiki resistensi insulin
• Menginduksi ekspresi gen PPAR y pada tingkat mRNA
• Meningkatkan expresi GLUT 4
 Summary of glucose-lowering interventions
Intervention dec A1C Advantages Disadvantages
Tier 1: well-validated core
Step 1: initial therapy
Lifestyle to
decrease weight Insufficient for most
1.0-2.0 Broad benefits
and increase within first year
activity
GI side effects,
Metformin 1.0-2.0 Weight neutral contraindicated with
renal insufficiency
Step 2: additional therapy
One to four injections
No dose limit, rapidly
daily, monitoring, weight
Insulin 1.5-3.5 effective,
gain, hypoglycemia,
improved lipid profile
analogues are expensive
Weight gain,
Sulfonylurea 1.0-2.0 Rapidly effective hypoglycemia ( gliben-
clamide chlorpropamide)
Tier 2: less well validated
Improved lipid profile Fluid retention, HF, weight gain,
(pioglitazone), bone fractures, expensive,
TZDs 0.5-1.4
potential decrease in potential increase in MI
MI (pioglitazone) (rosiglitazone)
Two injections daily, frequent
GLP-1 agonist 0.5-1.0 Weight loss GI side effects, long-term safety
not established, expensive
Other therapy
α-Glucosidase Frequent GI side effects, three
0.5-0.8 Weight neutral
inhibitor times/day dosing, expensive
Weight gain, three times/day
Glinide 0.5-1.5* Rapidly effective dosing, hypoglycemia,
expensive
Three injections daily, frequent
Pramlintide 0.5-1.0 Weight loss GI side effects, long-term safety
not established, expensive
 TERAPI GIZI MEDIK

• Membantu penyandang diabetes

memperbaiki kebiasaan makan dan olahraga
untuk mendapatkan kontrol metabolik yang
baik
 4 LANGKAH TERAPI GIZI MEDIS

• Pengkajian

• Penentuan Tujuan

• Intervensi

• Evaluasi
 FOKUS

• Gaya hidup
• Pengendalian
Glukosa darah
Dislipidemia
Tekanan darah
Berat Badan
 REKOMENDASI GIZI DIABETES
(PERKENI 2006)

• Karbohidrat : 45-65 %
Sukrose : < 5%
Serat : 25 g (/1000 kal)
Pemanis : Sesuai ADI
• Total lemak : 20-25%
As. Lemak jenuh : < 7 %
PUFA : < 10 %
MUFA : selebihnya
Lemak trans sesedikit mungkin
• Kolesterol : < 200-300 mg
• Protein : 10 -20 %
• Alkohol : < 30 g (L), < 15 g (W) (ADA)
 KARBOHIDRAT
• Mempengaruhi respon glikemik
- Jumlah KH
- Index glikemik
- Glikemik load
- Mengenyangkan / tidak
- Tipe Gula
- Sifat Tepung
- Pemasakan
- Bentuk makanan
- Bahan yang memperlambat pencernaan
- Jenis Karbohidrat : Kompleks/sederhana
- Tidak dianjurkan kurang dari 130 g per hari
 FAKTOR-FAKTOR YG MENENTUKAN
KEBUTUHAN KALORI
1. Jenis Kelamin
2. Umur
3. Aktivitas fisik
4. Kehamilan / lakatasi
5. Komplikasi
6. Tinggi dan berat badan
 PERHITUNGAN BERAT BADAN
RUMUS BROCCA IMT

BB IDEAL (Bbi) 90% X (TB-100) KG BB(KG)/TB2(M2)

BB NORMAL BBI +/- 10 % 18,5-22,5

KURUS < BBI – 10% < 18,5

GRMUK > BBI + 10 % > 23

KEBUTUHAN ENERGI BBI X 25 (w) ; 30 (P) KALORI  DIKURANGI

ATAU DITAMBAH BEBERAPA FAKTOR
kondisi Penambahan energi

Bb lebih 10 %

Bb gemuk 20 %

Bb kuran 30 %

Stres metabolik 10-30%

Hamil trimester i dan ii 300 kalori

Hamil trimester III 500 kalori

 JENIS AKTIVITAS FISIK
aktivitas contoh Penambahan energi

RINGAN PEGAWAI KANTOR, DR, IRT 10%

SEDANG LATIHAN JASMANI RUTIN 20 %

BERAT PETANI, BURUH, ATLIT 30 %

 Tips for healty cooking

• Cook of boil meat insted of frying

• Take the skin of chicken before cooking
• Use less salt and sugar when preparing food
• Avoid fat
 Tips for healty cooking

• Use fresh or frozen fruit and vegetables when

eating or in between meals
• Use low fat chesse instead of regular chesse
• Use low fat milk
• Drink fruit juice instead of powder juice
Physical Activity

z To control diabetes the

recommendation is to increase
physical activity, preferably every
day for 20-60 minutes.
z < 20 min : no effect
z > 60 min : prone to injury
and disease attack
 INTENSITY

z MHR (Maximum Heart Rate)  220 –

Age

z THR (Target Heart Rate)  60 – 70 %

MHR (80%)
 EXERCISE

• C : continuous
• R : rhytmical
• I : interval
• P : progressive
• E : endurance
Physical Activity
z Benefits:

y Lowers glucose levels in blood

y Improves blood circulation in the
entire body
y Contributes to weight loss
y Improves physical and mental
wellbeing
y Helps the body to utilize insulin more
efficiently
TERIMA KASIH