کنگره بین المللی سندرم متابولیک، دیابت و چاقی
سال:1388 | دوره:2 |تعداد مقالات:13

OBESITY IS A KEY COMPONENT OF METABOLIC SYNDROME. THESE METABOLIC ABNORMALITIES INCREASE THE RISK OF DEVELOPING CHRONIC DISEASES INCLUDING TYPE 2 DIABETES. DIETARY CARBOHYDRATES MAY DIFFERENTIALLY OPTIMIZE INSULIN ACTION AND THEREBY AFFECT THE DEGREE OF INSULIN RESISTANCE, WHICH IS A KEY UNDERLYING METABOLIC FEATURE OF THIS SYNDROME. THE GLYCEMIC INDEX, A MEASURE OF THE GLYCEMIC RESPONSE TO CARBOHYDRATE-CONTAINING FOODS, HAS BEEN USED TO PHYSIOLOGICALLY CLASSIFY DIETARY CARBOHYDRATE. THIS CONCEPT WAS PROPOSED IN 1981 AND SINCE THEN, MANY STUDIES HAVE BEEN PUBLISHED ON THE TOPIC. HOWEVER, CLINICAL SIGNIFICANCE OF THE GLYCEMIC INDEX REMAINS THE SUBJECT OF DEBATE. THE PURPOSE OF THIS PRESENTATION IS TO EXAMINE THE POTENTIAL ROLE OF GLYCEMIC INDEX IN THE MANAGEMENT OF CARDIO METABOLIC DISEASES INCLUDING DIABETES, OBESITY AND METABOLIC SYNDROME.

THE METABOLIC SYNDROME IS A CONSTELLATION OF TRAITS THAT INCLUDES OBESITY, DYSLIPIDEMIA, GLUCOSE INTOLERANCE AND HYPERTENSION. IT HAS BEEN OBSERVED THAT THESE TRAITS CLUSTER TOGETHER IN AN INDIVIDUAL MORE OFTEN THAN WOULD BE EXPECTED TO OCCUR BY CHANCE. IN DEVELOPING COUNTRIES, THE RAPID INCREASE IN THE PREVALENCE OF THESE DISORDERS HAS BEEN ACCOMPANIED BY AN EQUALLY RAPID INCREASE IN MORBIDITY AND MORTALITY FROM CARDIOVASCULAR DISEASE DRIVEN JOINTLY BY GENETIC PREDISPOSITION AND AN INCREASINGLY PERMISSIVE ENVIRONMENT. EACH OF THE METABOLIC SYNDROME COMPONENTS SHOW STRONG AND STATISTICALLY SIGNIFICANT HERITABILITY, THAT IS THEY TEND TO "RUN IN FAMILIES". NUMEROUS EFFORTS HAVE BEEN MADE TO IDENTIFY THE GENETIC BASIS OF THIS FAMILIAL RISK INCLUDING CANDIDATE GENE STUDIES, GENOME WIDE LINKAGE IN FAMILIES AND MORE RECENTLY GENOME WIDE ASSOCIATION STUDIES. MUCH HAS BEEN ACHIEVED, BUT THE MAJORITY OF THE FAMILIAL RISK REMAINS TO BE IDENTIFIED. ELUCIDATING THE GENETIC AND ENVIRONMENTAL COMPLEXITY IS KEY TO UNDERSTANDING THE PATHOGENESIS OF THE METABOLIC SYNDROME, AND TO BRING ABOUT THE DEVELOPMENT EFFECTIVE TREATMENTS FOR THOSE AFFLICTED.

THE METABOLIC SYNDROME IS A CLUSTER OF CARDIAC RISK FACTORS ASSOCIATED WITH OBESITY AND INSULIN RESISTANCE. THOUGH DIFFICULT TO DEFINE IN YOUTH, THERE IS A CLEAR ASSOCIATION OF OBESITY AND INSULIN RESISTANCE WITH THESE FACTORS IN CHILDREN. THIS RISK CLUSTERING IS ASSOCIATED WITH ACCELERATED ATHEROSCLEROSIS IN YOUTH AND WITH THE PRESENCE OF SUBCLINICAL ATHEROSCLEROSIS IN YOUTH. RISK CLUSTERING TRACKS INTO ADULTHOOD SO CHILDREN WITH RISK BECOME ADULTS WITH RISK FACTORS. MOST IMPORTANT, METABOLIC SYNDROME FACTORS IN YOUTH PREDICT RISK IN ADULTHOOD, SUBCLINICAL ATHEROSCLEROSIS IN ADULTHOOD, AND EARLY CARDIOVASCULAR MORBIDITY AND MORTALITY.

FOOD INTAKE AND ENERGY EXPENDITURE ARE CONTROLLED BY COMPLEX, AND DISTRIBUTED NEUROENDOCRINE SYSTEMS THAT ESTABLISH ENERGY BALANCE. MOST VERTEBRATES CAN STORE A CONSIDERABLE AMOUNT OF ENERGY AS FAT IN THEIR ADIPOCYTES FOR LATER USE. SO, A PREDISPOSITION TO OBESITY CAN RESULT FROM ANY PATHOLOGICAL MALFUNCTION OR LACK OF ADAPTATION TO CHANGING ENVIRONMENTS OF THIS HIGHLY COMPLEX SYSTEM. MANIPULATING ELEMENTS OF THIS REGULATORY SYSTEM, NAMELY THE BRAIN AND THE HORMONAL SIGNALS FROM MIGHT PROVIDE THE BEST OPPORTUNITY FOR US TO COMBAT OBESITY. THE HYPOTHALAMUS AND THE BRAINSTEM ARE THE MAIN BRAIN REGIONS RESPONSIBLE FOR THE REGULATION OF ENERGY HOMEOSTASIS AND AREAS IN THE CORTEX AND LIMBIC SYSTEM ARE IMPORTANT FOR PROCESSING INFORMATION REGARDING PRIOR EXPERIENCE WITH FOOD, REWARD, AND EMOTION, AS WELL AS SOCIAL AND ENVIRONMENTAL CONTEXT. SOME OBESITY THERAPIES TARGET CENTRAL NEUROTRANSMITTERS IN ORDER TO REDUCE BODY WEIGHT. THE HYPOTHALAMUS AND BRAINSTEM RECEIVE NEURAL AND HORMONAL SIGNALS FROM THE PERIPHERY (INCLUDES LEPTIN, ADINOPECTIN AND RESISTIN SECRETED BY THE ADIPOCYTES AND THE PANCREATIC INSULIN) THAT ENCODE INFORMATION ABOUT ACUTE NUTRITIONAL STATE AND ADIPOSITY.INSULIN AND LEPTIN SHARE MANY PROPERTIES AS ADIPOSITY SIGNALS AND THEIR CIRCULATING CONCENTRATIONS ARE PROPORTIONAL TO ADIPOSITY. LEPTIN AND INSULIN ALSO CROSS THE BLOOD-BRAIN BARRIER AND INTERACT WITH SPECIFIC RECEPTORS IN THE HYPOTHALAMUS. MOREOVER, THROUGH INTERACTION WITH SPECIFIC NEURONS IN THE HYPOTHALAMUS, THEY REDUCE FOOD INTAKE AND BODY WEIGHT. OBESITY IS CHARACTERIZED BY HIGHER CIRCULATING LEVELS OF INSULIN AND LEPTIN AND A DEVELOPMENT OF RESISTANCE TO THESE HORMONES. ADIPONECTIN, AND RESISTIN ARE REPORTED TO ENHANCE OR IMPAIR INSULIN SENSITIVITY, RESPECTIVELY. APART FROM THE ABOVE MECHANISMS, NEURAL AND ENDOCRINE SIGNALLING FROM THE GUT IS BELIEVED TO HAVE IMPORTANT ROLES IN THE SHORT-TERM REGULATION OF APPETITE BY MEDIATING FEELINGS OF HUNGER AND SATIETY. GUT HORMONES LIKE CHOLECYSTOKININ, AMYLIN, PEPTIDE YY (PYY), PANCREATIC POLYPEPTIDE, GLP-1, GLP-2, AND OXYNTOMODULIN ACT AS ANORECTIC SIGNALS THAT REDUCE FOOD INTAKE. GHRELIN OFTEN REFERRED TO AS THE.’HUNGER HORMONE’ PRODUCES AN OREXIGENIC SIGNAL AND INCREASES APPETITE. THE GUT HORMONE GENES ARE WIDELY EXPRESSED, NOT ONLY IN ENDOCRINE CELLS, BUT ALSO IN CENTRAL AND PERIPHERAL NEURONS AND CERTAIN TUMOUR CELLS. THESE PEPTIDES THUS ACT AS TRUE BLOOD-BORNE HORMONES AS WELL AS LOCAL GROWTH FACTORS. FOR MANY GUT HORMONES, THE PRECISE MECHANISMS OF CENTRAL ACTION ARE UNKNOWN. A NUMBER OF GUT HORMONES ALSO ACT AS NEUROTRANSMITTERS IN THE BRAIN, WHERE THEY DO NOT NECESSARILY SERVE THE SAME FUNCTIONS AS IN THE PERIPHERY, MAKING IT DIFFICULT TO PINPOINT THEIR ENDOCRINE EFFECTS. GUT HORMONES HAVE A NUMBER OF FUNCTIONS, INCLUDING THE REGULATION OF BLOOD GLUCOSE LEVELS, GASTROINTESTINAL MOTILITY AND GROWTH, EXOCRINE SECRETION AND ADIPOCYTE FUNCTION. MOST OF THESE HORMONES ARE SENSITIVE TO GUT NUTRIENT CONTENT. THE APPLICATION OF A RESTRICTED ENERGY AND WEIGHT REDUCING DIET IS BASED ON SOME OF THE PRINCIPLES OF THIS INTERPLAY OF GUT HORMONES. TODAY WE RECOGNIZE MORE THAN 30 PEPTIDE HORMONE GENES, EXPRESSING MORE THAN 100 BIOACTIVE PEPTIDES, AND OTHER HORMONAL FACTS TRULY MAKE THE GUT THE LARGEST ENDOCRINE ORGAN IN THE BODY. GUT HORMONES MAY REPRESENT USEFUL TARGETS FOR FUTURE OBESITY THERAPIES AS THEY CAN ACTIVATE CIRCUITS IN THE HYPOTHALAMUS AND BRAINSTEM FOR THE REGULATION OF ENERGY HOMEOSTASIS. SO AS CLAIMED BY MURPHY AND BLOOM (2006) IT MAY BE SAID THAT, “GUT HORMONES MAY YET PROVE THAT THE WAY TO A MAN. S BRAIN IS THROUGH HIS STOMACH”.

THE METABOLIC SYNDROME IS A MULTI-FACET CONDITION CHARACTERISED BY VISCERAL ADIPOSITY, INSULIN RESISTANCE, DYSLIPIDAEMIA, AND HYPERTENSION, ALL OF WHICH CONTRIBUTES TO THE DEVELOPMENT OF LOW-GRADE INFLAMMATORY STATE, ATHEROSCLEROSIS AND ABNORMAL GLUCOSE INTOLERANCE. VARIOUS HYPOTHESES HAD BEEN PUT FORWARD INCLUDING THRIFTY GENES, APPETITE CONTROL INVOLVING THE LIMBIC-HYPOTHALAMIC SYSTEM AND ALTERED HOMEOSTATIC MECHANISMS TO EXPLAIN THE INTERACTION BETWEEN GENETIC, INTRAUTERINE AND ENVIRONMENTAL FACTORS THAT LEAD TO THE SYNDROME. HOWEVER, INSULIN RESISTANCE REMAINS THE UNIFYING FACTOR UNDERLYING ALL THE CLUSTERS OF THE METABOLIC SYNDROME. EVEN THOUGH EXISTING CLINICAL, EPIDEMIOLOGICAL AND EXPERIMENTAL DATA SUPPORT THE ROLE OF INSULIN RESISTANCE AS AN IMPORTANT AETIOLOGIC COMPONENT OF THIS SYNDROME, CURRENT EVIDENCE SUGGEST THAT NEUROHORMONAL MECHANISMS, INCLUDING AN ENDOCRINE FUNCTION OF ADIPOCYTES HAS A FUNDAMENTAL ROLE TO PLAY. THIS IS SUPPORTED BY THE STRONG RELATIONSHIP BETWEEN CENTRAL ADIPOSITY AND ALL THE COMPONENTS OF THE SYNDROME, UNLIKE THE INCONSISTENT ASSOCIATION BETWEEN THE SYNDROME AND THE MARKERS OF INSULIN RESISTANCE. TRADITIONALLY, ADIPOCYTES STORE EXCESS CALORIES AS TRIGLYCERIDE IN FAT PARTICLES, THUS ACTING AS ENERGY WAREHOUSES. OF LATE ADIPOCYTES HAVE RECENTLY BEEN FOUND TO REGULATE METABOLIC FUNCTION BY PRODUCING A WHOLE RANGE OF CYTOKINES, APTLY NAMED ADIPOCYTOKINES. WHILE SOME ADIPOCYTOKINES, SUCH AS TUMOR NECROSIS FACTOR-ALPHA AND RESISTIN INDUCE INSULIN RESISTANCE, ADIPONECTIN ON THE OTHER HAND IS AN ADIPOCYTOKINE THAT HAS ANTI-DIABETIC AND ANTI-ATHEROGENIC PROPERTIES. ANOTHER VISCERAL FAT-DERIVED ADIPOCYTOKINE, VISFATIN WAS IDENTIFIED RECENTLY WITH INSULIN-LIKE ACTIVITIES. THUS, ADIPOCYTES PLAY AN IMPORTANT ROLE IN THE REGULATION OF ENERGY METABOLISM AND IN THE PATHOGENESIS OF METABOLIC SYNDROME. IN ADDITION TO VISCERAL ADIPOCYTES, INCREASED FREE FATTY ACIDS AND LIPID ACCUMULATION IN CERTAIN ORGANS ALSO CONTRIBUTES TO INSULIN RESISTANCE.

UNDERSTANDING THE STRUCTURE AND METABOLISM OF HDL IS ESSENTIAL FOR COMPREHENSIVE MANAGEMENT OF DYSLIPIDAEMIA. EPIDEMIOLOGICAL STUDIES HAVE ESTABLISHED THE RELATIONSHIP OF LOW-HDL WITH INCREASED INCIDENCE OF CORONARY ARTERY DISEASE. HOWEVER, THUS FAR, LESS CERTAINTY IS OBSERVED ON THE EFFECT OF HDL REDUCING THERAPY IN THE SUBSEQUENT REDUCTION OF CAD. HDL RAISING CAN BE OBTAINED VIA DIETARY, EXERCISE AND OTHER NON-PHARMACOLOGICAL MEANS. PHARMACOLOGICAL TREATMENT AVAILABLE CURRENTLY ARE NICOTINIC ACID, FIB RATE AND STATINS (EITHER AS MONOTHERAPY OR COMBINATION). THERE ARE OTHER AGENTS THAT HAVE BEEN SHOWN TO INCREASE HDL, UNFORTUNATELY WITH PARADOXICAL OUTCOMES. IN SHORT, CURRENT TREATMENT OF LOW HDL IS STILL FAR FROM SATISFACTORY. HOWEVER, TREATING THE OVERALL PROFILE OF DYSLIPIDAEMIA (INCLUDING TARGETING THE LDL AND TG) HAS BEEN PROVEN TO BE MORE PRODUCTIVE.

IT IS MY PLEASURE TO WELCOME ALL PARTICIPANTS FROM IRAN AND THE OTHER PARTS OF THE WORLD TO THE 2ND INTERNATIONAL CONGRESS OF METABOLIC SYNDROME, OBESITY AND DIABETES. RUNNING HIGH QUALITY SCIENTIFIC MEETINGS IN COLLABORATION WITH OTHER INSTITUTIONS AND ORGANIZATIONS IS OF THE UNIVERSITY POLICY AND PRIORITIES AS A STEP TO CONTRIBUTE TO THE MEDICAL SCIENCE DEVELOPMENT AND HEALTH PROMOTION WITH THE MAXIMUM TECHNICAL AND MANAGEMENT CAPACITY. THE 2ND INTERNATIONAL CONGRESS OF METABOLIC SYNDROME, OBESITY AND DIABETES HAS BEEN PLANNED TO PROVIDE AN OPPORTUNITY FOR THE EXCHANGE OF RECENT DEVELOPMENTS IN CLINICAL INTERVENTIONS AND GUIDELINES AMONG THE PHYSICIANS AND OTHER SCIENTISTS INVOLVED IN THIS IMPORTANT MEDICAL FIELD. THE PROGRAM INCLUDES GOOD SYMPOSIA AND WORKSHOPS COVERING SEVERAL IMPORTANT MAJOR SUBJECTS IN METABOLIC DISORDERS; ALSO A VARIETY OF RESEARCH PAPERS HAVE BEEN SELECTED FOR ORAL OR POSTER PRESENTATION. I AM SURE ALL PARTS OF THE PROGRAM WILL FRUITFULLY ADD TO THE KNOWLEDGE AND EXPERIENCES OF ALL PARTICIPANTS, IN PARTICULAR YOUNG PHYSICIANS AND RESEARCHERS. IN ADDITION TO YOUR CONGRESS PARTICIPATION, I HOPE YOU ENJOY VISITING ZANJAN, UNDER WELCOME SUPPORTS OF THE LOCAL GOVERNING AGENTS AND WARM HOSPITALITY OF THE PEOPLE OF ZANJAN.

THE SERUM TRIGLYCERIDE CONCENTRATION CAN BE STRATIFIED IN TERMS OF CORONARY RISK. NORMAL < 150 MG/DL, BORDERLINE HIGH 150 TO 199 MG/DL, HIGH 200 TO 499 MG/DL, VERY HIGH ≥ 500 MG/DL. THE ROLE OF TRIGLYCERIDES IN PROMOTING CARDIOVASCULAR DISEASE (CVD) IS STILL DEBATED MORE THAN 60 YEARS AFTER A RELATIONSHIP WAS FIRST POSTULATED. RECENT DATA FOCUSING ON THE POTENTIAL IMPORTANCE OF NONFASTING TRIGLYCERIDE LEVELS SEEM TO SETTLE THIS DEBATE BY ESTABLISHING A CONSISTENT STRONG RELATION OF TRIGLYCERIDES WITH CVD RISK. A RECENT META-ANALYSIS USING 29 PROSPECTIVE STUDIES CONDUCTED IN WESTERN POPULATIONS AGAIN NOTED THAT TG CONCENTRATIONS WERE AN INDEPENDENT RISK FACTOR FOR CORONARY HEART DISEASE IN BOTH SEXES. MOREOVER CHANGE IN TG CONCENTRATIONS HAS BEEN SHOWN TO RESULT IN CHANGE IN THE RISK OF DEVELOPING INCIDENT CORONARY HEART DISEASE. HOWEVER TWO IMPORTANT QUESTIONS REMAIN UNANSWERED. 1) HOW CAN DISTINGUISH THE EFFECTS OF TRIGLYCERIDES ON CHD RISK FROM THAT OF LOW HDL-C, OR FROM THAT OF INSULIN RESISTANCE PER SE. 2) IS IT APPROPRIATE TO ADJUST FOR HDL-C, WHICH IS STRONGLY INVERSELY CORRELATED WITH TRIGLYCERIDES AND ALSO BIOLOGICALLY LINKED TO INSULIN RESISTANCE IN MULTIVARIABLE ANALYSES. RECOMMENDATIONS FOR THE THERAPY OF HYPERTRIGLYCERIDEMIA HAVE BEEN LIMITED BY PREVIOUSLY INCONSISTENT EPIDEMIOLOGIC STUDIES, THE INTERRELATIONSHIP BETWEEN TRIGLYCERIDES WITH HDL AND OTHER RISK FACTORS, AND THE LACK OF CONCLUSIVE DATA THAT TRIGLYCERIDE LOWERING CAN REDUCE CHD RISK. A MAJOR QUESTION IN MANAGEMENT IS WHETHER THERAPY SHOULD BE DIRECTED SOLELY TOWARD REDUCTION OF TRIGLYCERIDE LEVELS OR TOWARD THE MODIFICATION OF ASSOCIATED ABNORMALITIES OF INTERMEDIATE-DENSITY LIPOPROTEIN, LDL, AND HDL CHOLESTEROL. THE BENEFIT OF TREATING MILD-TOMODERATE ELEVATIONS IN TRIGLYCERIDE LEVELS IS LESS CLEAR.

DEAR COLLEAGUES:OVER THE YEARS, THE FIELD OF OBESITY AND ITS METABOLIC CONSEQUENCES HAS UNDERGONE ENORMOUS EXPANSION IN CLINICAL AND BASIC DATA. WITH THE PROBLEM OF SOME MORBIDITY RELATED TO OBESITY AND METABOLIC SYNDROME REACHING EPIDEMIC DIMENSIONS, INTERVENTIONS POSSIBILITIES HAVE DIVERSIFIED. THESE DEVELOPMENTS HAVE CREATED A NEED FOR DEBATES ON THE NUMBER OF CONTROVERSIAL ISSUES AND TO ATTAIN CLINICAL CONCLUSIONS. THE INTENTION OF THE 2ND INTERNATIONAL CONGRESS ON METABOLIC SYNDROME, OBESITY & DIABETES'S TO FUNCTION AS AN EXCLUSIVE FORUM FOR EXPERTS TO SHARE AND COMPARE EXPERIENCES IN ORDER TO OUTLINE APPROPRIATE TREATMENTS. IT IS EMBARKED UPON PRIMARILY TO FACILITATE EFFECTIVE DEBATE ON UNRESOLVED CLINICAL AND THERAPEUTIC DILEMMAS, SUBSTANTIATED BY EVIDENCE BASED DATA. WE LOOK FORWARD TO AN EXCITING SCIENTIFIC EVENT IN THE BEAUTIFUL CITY OF ZANJAN, IRAN.

C-REACTIVE PROTEIN (CRP) PLAYS A CRUCIAL ROLE AT ALL STAGES OF ATHEROGENESIS. IT DEMONSTRATES IMMUNE MODULATING EFFECTS AND WAS FOUND IN THE ATHEROSCLEROTIC PLAQUE, FACILITATING ITS DESTABILIZATION AND RUPTURE. IN SOME CHRONIC INFLAMMATORY DISORDERS THIS INFLAMMATORY AGENT IS RECOGNIZED AS A SPECIFIC MARKER OF ACTIVITY. THE CLASSIC EXAMPLE, IN THIS REGARD, IS RHEUMATOID ARTHRITIS, WHERE SUPPRESSION OF CRP PRODUCTION IN THE RETICULOENDOTHELIAL SYSTEM BY STATINS AND DISEASE-MODIFYING ANTI-RHEUMATIC DRUGS SUCH AS METHOTREXATE IS ASSOCIATED WITH AMELIORATION OF THE DISEASE COURSE AND PREVENTION OF CARDIOVASCULAR MORBIDITY AND MORTALITY. OVER THE PAST YEARS, IT HAS BECOME CLEAR THAT CRP IS A MARKER OF SYSTEMIC INFLAMMATION WITH A STRONG PREDICTIVE CARDIOVASCULAR VALUE. IN FACT, THE PHYSICIANS' HEALTH STUDY (PHS) AND THE JUSTIFICATION FOR THE USE OF STATINS IN PREVENTION-AN INTERVENTION TRIAL EVALUATING ROSUVASTATIN (JUPITER) PROVED THAT CRP CAN PREDICT OCCURRENCE OF CARDIOVASCULAR EVENTS IN APPARENTLY HEALTHY SUBJECTS AND INDICATED THE NEED TO MODIFY AVAILABLE GUIDELINES FOR PRIMARY PREVENTION. BASED ON THESE LANDMARK TRIALS, IT IS NOW CLEAR THAT ASPIRIN AND STATINS EXERT THEIR CARDIO PROTECTIVE EFFECT VIA SUPPRESSION OF LOW-GRADE INFLAMMATION IN SUBJECTS BURDENED WITH CARDIOVASCULAR RISK FACTORS. THE SEARCH FOR OTHER DRUGS WITH CARDIO PROTECTIVE AND ANTI-INFLAMMATORY EFFECTS IS UNDERWAY AND IT IS HOPED THAT METHOTREXATE AND COLCHICINES WILL BE INCLUDED IN THE ARMAMENTARIUM OF PREVENTIVE MEASURE FOR SUBJECTS AT HIGH RISK CARDIOVASCULAR EVENTS AND THOSE UNDERGOING CONORARY INTERVENTIONS.

RAPID CHANGES IN LIFESTYLE HABITS, NOTABLY IN DIET AND PHYSICAL ACTIVITY, EXPOSED THE POPULATION OF CHILDREN AND ADOLESCENTS TO OBESITY AND ITS CONSEQUENCES. IT IS WELL DOCUMENTED THAT THIS PROBLEM IS INCREASING IN BOTH DEVELOPED AND DEVELOPING COUNTRIES. OBESITY IS A MAJOR RISK FACTOR FOR DEVELOPING TYPE 2 DIABETES MELLITUS (T2DM). COMPARED TO ADULT POPULATION, THE DATA ABOUT THE PREVALENCE OF T2DM ARE LIMITED IN THE PEDIATRIC AGE GROUP; HOWEVER, IT IS SHOWN THAT T2DM HAS AN INCREASING TREND IN THIS AGE GROUP. TAKEN INTO ACCOUNT THAT MICRO- AND MACRO VASCULAR COMPLICATIONS OF T2DM COULD BE DEVELOPED IN YOUNG AGE SIMILAR TO ADULTS, PREVENTION AND EARLY DETECTION OF THIS DISORDER IS OF HIGH IMPORTANCE. IN IRAN, AS A DEVELOPING COUNTRY STILL GRAPPLING WITH UNDER NUTRITION AND MICRONUTRIENT DEFICIENCIES, THE PREVALENCE OF OVERWEIGHT AND OBESITY IN CHILDREN AND ADOLESCENTS IS ESTIMATED TO BE 13.4%. ACCORDING TO THE RECOMMENDATION OF AMERICAN DIABETES ASSOCIATION (ADA), THE BEST SCREENING TEST FOR DM IN CHILDREN IS FASTING PLASMA GLUCOSE (FPG). ORAL GLUCOSE TOLERANCE TEST (OGTT) IS A SUITABLE TEST TOO, BUT FPG IS MORE FEASIBLE AND FAST; FURTHERMORE IT IS MORE CONVENIENT AND ACCEPTABLE FOR PATIENTS AND LESS EXPENSIVE.

THE METABOLIC SYNDROME IS DEFINED AS CLUSTERING OF SEVERAL CARDIOVASCULAR RISK FACTORS ALONG WITH OBESITY, OCCURRING IN A SINGLE INDIVIDUAL. GENERALLY, INSULIN RESISTANCE IS THE CENTRAL FEATURE OF THE METABOLIC SYNDROME. SEVERAL CONDITIONS AND DISEASES ARE LINKED TO INSULIN RESISTANCE, AND THOSE WITH METABOLIC SYNDROME ARE MORE PREDISPOSED TO DEVELOP THEM. THE PREVALENCE OF OBESITY AND THE METABOLIC SYNDROME IS RAPIDLY INCREASING GLOBALLY, IN INDIA, SOUTH ASIAN COUNTRIES, AND MIDDLE EAST, LEADING TO INCREASED MORBIDITY AND MORTALITY DUE TO TYPE 2 DIABETES MELLITUS (T2DM) AND CARDIOVASCULAR DISEASE (CVD). THE MAIN DRIVERS ARE RAPID NUTRITION, LIFESTYLE AND SOCIO-ECONOMIC TRANSITIONS, CONSEQUENT TO INCREASING AFFLUENCE, URBANIZATION, MECHANIZATION, AND RURAL-TO-URBAN MIGRATION IN MANY COUNTRIES OF THIS REGION. LESS INVESTIGATED DETERMINANTS OF THE METABOLIC SYNDROME INCLUDE PSYCHOLOGICAL STRESS IN URBAN SETTING, GENETIC PREDIPOSITION, ADVERSE PERINATAL ENVIRONMENT, AND CHILDHOOD. CATCH UP OBESITY. DATA SHOW ATHEROGENIC DYSLIPIDEMIA, GLUCOSE INTOLERANCE, THROMBOTIC TENDENCY, SUBCLINICAL INFLAMMATION, AND ENDOTHELIAL DYSFUNCTION ARE HIGHER SOUTH ASIANS THAN WHITE CAUCASIANS. MANY OF THESE MANIFESTATIONS ARE MORE SEVERE IN EVEN AT AN EARLY AGE IN SOUTH ASIANS THAN WHITE CAUCASIANS. METABOLIC AND CARDIOVASCULAR RISK IN SOUTH ASIANS IS ALSO HEIGHTENED BY THEIR HIGHER BODY FAT, TRUNCAL SUBCUTANEOUS FAT, INTRA-ABDOMINAL FAT, AND ECTOPIC FAT DEPOSITION (LIVER FAT ETC.). FURTHER, CARDIOVASCULAR RISK CLUSTER MANIFESTS AT A LOWER LEVEL OF ADIPOSITY AND ABDOMINAL OBESITY. THE CUT-OFFS OF BODY MASS INDEX AND WAIST CIRCUMFERENCE FOR DEFINING OBESITY AND ABDOMINAL OBESITY, RESPECTIVELY, HAVE BEEN LOWERED AND DEFINITION OF THE METABOLIC SYNDROME HAVE BEEN REVISED FOR ASIAN INDIANS IN A RECENT CONSENSUS STATEMENT, SO THAT PHYSICIANS COULD INTERVENE EARLY WITH LIFESTYLE MANAGEMENT. DATA FROM A MAJOR INTERVENTION PROGRAM CONDUCTED BY US ON URBAN ADOLESCENT SCHOOLCHILDREN IN NORTH INDIA FOR PREVENTION OF OBESITY (PROJECT. MARG.) HAS SHOWN ENCOURAGING RESULTS, MAKING IT A MODEL FOR ANY FUTURE INTERVENTION PROGRAM IN SOUTH ASIANS AND IN OTHER COUNTRIES AS WELL. THE SCOURGE OF THE METABOLIC SYNDROME CONTINUES IN SOUTH ASIA AND MIDDLE-EAST. PRIMARY PREVENTION PROGRAMS SHOULD BE DIRECTED TO SCHOOLCHILDREN, AS HAS BEEN DONE IN INDIA, UAE AND IRAN.

BACKGROUND: METABOLIC SYNDROME COMPRISES OF A CONSTELLATION OF CARDIOVASCULAR DISEASE RISK FACTORS, INCLUDING ABDOMINAL ADIPOSITY, ABNORMAL GLUCOSE TOLERANCE, DYSLIPIDAEMIA AND HYPERTENSION. THE MAIN PATHOLOGICAL ABNORMALITY IN METABOLIC SYNDROME IS BELIEVED TO BE INSULIN RESISTANCE. OVER THE LAST DECADE, MALAYSIA HAS EXPERIENCED A MARKED ESCALATION IN THE PREVALENCE OF OBESITY AND DIABETES. THE PREVALENCE OF OVERWEIGHT AND OBESITY IN ADULTS HAS RISEN FROM 24% IN 1996 TO 44% IN 2006 WHILE THAT OF DIABETES HAS RISEN FROM 8.3% TO 14.9% AMONG THOSE ABOVE 30 YEARS OLD. DESPITE THIS, THERE HAS NOT BEEN ANY MAJOR STUDY TO LOOK AT THE PREVALENCE OF METABOLIC SYNDROME PER SE IN MALAYSIA. METHODS: BETWEEN 2007 TO 2008, THE MINISTRY OF HEALTH, MALAYSIA THROUGH ITS E-HEALTH INITIATIVE FUNDED THE METABOLIC SYNDROME STUDY OF MALAYSIA (MSSM) WHICH UTILISED A MULTISTAGED SAMPLING PROCEDURE TO RANDOMLY SCREEN (WITH ORAL GLUCOSE TOLERANCE TEST) 4341 ADULTS BETWEEN THE AGES OF 18 TO 70 YEARS OLD THROUGHOUT THE COUNTRY. FIVE MAJOR AREAS WERE SELECTED BASED ON THE GEOGRAPHICAL AS WELL AS ETHNIC COMPOSITION OF THE COUNTRY. THESE WERE FURTHER DIVIDED INTO URBAN AND RURAL AREAS RESPECTIVELY. THE CRITERIA USED TO DEFINE METABOLIC SYNDROME WAS BASED ON THE MODIFIED ASIAN NCEP (ATP III) 2004 CLASSIFICATION. RESULTS: THE PREVALENCE OF METABOLIC SYNDROME WAS 31.7% (95% CI, 30.3-33.1). IT WAS HIGHER IN FEMALES AT 33.1% (95% CI, 31.3 -34.8) COMPARED TO MALES AT 29.2% (95% CI, 26.7- 31.5). THE PREVALENCE IN URBAN AREAS RANGED FROM 22.2% (95% CI, 18.0-26.4) IN KOTA KINABALU TO 36.7% (95% CI, 32.8- 40.7) IN JOHOR BHARU. WHILE IN THE RURAL AREAS IT RANGED FROM 15.8% (95% CI, 12.0-19.6) IN LAHAD DATU, SABAH TO 37.3% (95% CI, 33.1-41.7) IN KUALA SELANGOR, AN HOUR. S DRIVE FROM THE CAPITAL CITY OF KUALA LUMPUR. THE PREVALENCE INCREASED FROM 13.0% (95% CI, 11.1-14.9) IN THOSE BELOW 40 YEARS OLD TO 21.9% (95% CI, 26.5-31.8) IN THOSE BETWEEN 40 TO 49 YEARS OLD, 41.9% (95% CI, 38.9-45.0) IN THOSE BETWEEN 50-59 YEARS OLD AND 47.3% (95% CI, 44.1-50.4) AMONG THOSE ABOVE 60 YEARS OLD. AMONG THE THREE MAJOR ETHNIC GROUPS IN THE COUNTRY, INDIAN WAS THE HIGHEST AT 42.7% (95% CI, 37.7-47.7) FOLLOWED BY MALAYS AT 33.5% (95% CI, 31.7-35.3) AND CHINESE AT 31.6% (95% CI, 28.0-35.3). IN TERMS OF THE PREVALENCE OF THE VARIOUS COMPONENTS OF THE METABOLIC SYNDROME, HYPERTENSION WAS 52.3% (95% CI, 50.8-53.3), HIGH TRIGLYCERIDE 37.1% (95% CI, 35.7-38.5), IMPAIRED FASTING GLUCOSE 36.4% (95% CI, 35.0-37.8), INCREASED WAIST CIRCUMFERENCE WAS 30.9% (95% CI, 29.5-32.3) AND LOW HDL CHOLESTEROL 28.3% (95% CI, 27.0-29.7).CONCLUSION: THE PREVALENCE OF METABOLIC SYNDROME IN MALAYSIA IS HIGHER COMPARED TO THE NEIGHBORING COUNTRIES OF SOUTH EAST ASIA WHICH HAVE SIMILAR DEMOGRAPHIC AND ECONOMIC STATURES. THE PRECISE REASONS BEHIND THIS MARKED INCREASE IN METABOLIC SYNDROME HAVE TO BE ELUCIDATED BEFORE ANY EFFECTIVE MEASURES CAN BE UNDERTAKEN.