The Differences of Food Compositions in Adolescent Metabolic Syndrome in Malang

Sri Andarini, Djanggan Sargowo


BACKGROUND: Obesity, especially obesity in adolescent, is a worldwide health problem needing much of our attention because it can continue to be obesity in adulthood. About 50% obese adolescents grew up to be obese adults. It was a concern since it is one of risk factor associated with cardiovascular events including hypertension, dyslipidemia, insulin resistance and stroke. Visceral obesity is correlated with diabetogenic, atherogenic, prothrombotic, pro-inflammation, and abnormal metabolism. The objective of this study was to assess the prevalence of obese adolescents in Malang and to identitfy the differences in food compositions between metabolic syndrome and non-metabolic adolescents.

METHODS: Prevalence of obesity was determined by assessing BMI in 20 Senior and Junior High Schools. Metabolic syndrome was diagnosed using IDF criteria; waist circumference of >80cm and >90cm for female and male, respectively, and increased triglyceride and decreased HDL concentration levels. The food composition was assessed using food recalls, and then regression linier test was done to define the correlation between food intake and the components of metabolic syndrome.

RESULTS: The prevalence of adolescent obesity in Malang had reached 3.32%, with the prevalence of obesity in male subjects higher than in female subjects, i.e. 54.1% compared to 45.9%. The boys had higher mean for height and weight than the girls did, however, the BMI was higher in girls rather than boys. The difference of fat in food composition was significantly higher for the metabolic groups (p=0.031), but the carbohydrate did not significantly differ between the two groups (p=0.407).

CONCLUSIONS: The prevalence of adolescent obesity in Malang had reached 3.32%, with the prevalence of 54.1% in male and 45.9% in female. From the statistics test, fat intake showed a significant difference between metabolic syndrome and non-metabolic syndrome groups, but other food compositions didn’t.

KEYWORDS: obesity, metabolic syndrome, adolescent

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Tjokroprawiro A. The trend in emerging lifestyle-related disease in Indonesia (from obesity-MetS and CMR to the CMDs). Kobe Association for the Study of Food and Health. Kobe: Kasfah Memorial Meeting; 2008.

Tjokroprawiro A. The high-tech FDC of metformn and glibenclamide (improving 2 main defects of T2DM and showing 31 cardiometabolic properties). Surabaya: The XXIIIrd Continuing Medical Education (CME-XXIII) PKB-XXIII; 2008.

Kahn R, Buse J, Ferrannini E, Stern M. The metabolic syndrome: time for a critical appraisal: joint statement from the American Diabetes Association and the European Association for the Study of Diabetes. Diabetes Care. 2005; 28: 2289-304, CrossRef.

Einhorn D, Reaven GM, Cobin RH, Ford E, Ganda OP, Handelsman Y, et al . American College of Endocrinology position statement on the insulin resistance syndrome. Endocr Pract. 2003; 9: 237-52, PMID.

Balkau B, Charles MA. Comment on the provisional report from the WHO consultation. Diabet Med. 1999; 16: 442-3, CrossRef.

Micolli R, Bianchi C, Prato SD. Pathophysiology of the metabolic syndrome. In: The Metabolic Syndrome Full Guide. [n.p]: [n.p]; 2006. p.9-14.

Tan CE, Ma S, Wai D, Chew SK, Tai ES. Can we apply the national cholesterol education program adult treatment panel definition of the metabolic syndrome to Asians? Diabetes Care. 2004; 27: 1182-6, CrossRef.

Chakar H, Salameh PR. Adolescent obesity in Lebanese private schools. Eur J Public Health. 2006; 16: 648-51, CrossRef.

Booth ML, Chey T, Wake M, Norton K, Hesketh K, Dollman J, et al. Change in the prevalence of overweight and obesity among young Australians, 1969-1997. Am J Clin Nutr. 2003; 77: 29-36, PMID.

Kim HM, Park J, Kim HS, Kim DH, Park SH. Obesity and cardiovascular risk factors in Korean children and adolescents aged 10-18 years from the Korean National Health and Nutrition Examination Survey, 1998 and 2001. Am J Epidemiol. 2006; 164: 787-93, PMID.

Hanley AJ, Harris SB, Gittelsohn J, Wolever TM, Saksvig B, Zinman B. Overweight among children and adolescents in a Native Canadian community: prevalence and associated factors. Am J Clin Nutr. 2000; 71: 693-700, PMID.

Salvadori M, Sontrop JM, Garg AX, Truong J, Suri RS, Mahmud FH, et al. Elevated blood pressure in relation to overweight and obesity among children in a rural Canadian community. Pediatrics. 2008; 122: e821–e827. CrossRef.

Ogden CL, Carroll MD, Curtin LR, McDowell MA, Tabak CJ, Flegal KM. Prevalence of overweight and obesity in the United States, 1999-2004. JAMA. 2006; 295: 1549-555, CrossRef.

Lacar ES, Soto X, Riley WJ. Adolescent obesity in a low-income Mexican American district in South Texas. Pediatrics Adolescent Med. 2000; 154: 837-40, CrossRef.

Micolli R, Bianchi C, Prato SD. Diagnostic criteria of metabolic syndrome. In: The Metabolic Syndrome Full Guide. [n.p]: [n.p]; 2006. p.3-8.

Tan BK, Heutling D, Chen J, Farhatullah S, Adya R, Keay SD, et al. Metformin decreases the adipokine vaspin in overweight women with polycystic ovary syndrome concomitant with improvement in insulin sensitivity and a decrease in insulin resistance. Diabetes. 2008; 57: 1501-7, CrossRef.

Weiss R, Dziura J, Burgert TS, Tamborlane WV, Taksali SE, Yeckel CW, et al. Obesity and the metabolic syndrome in children and adolescents. N Engl J Med. 2004; 350: 2362-74, CrossRef.

Duncan GE, Li SM, Zhou XH. Prevalence and trends of a metabolic syndrome phenotype among U.S. adolescents, 1999-2000. Diabetes Care. 2004; 27: 2438-43, CrossRef.

Sibarani RP, Rudijanto A, Dekker J, Heine RJ. The Petai China study: metabolic syndrome among obese Indonesian Chinese adolescents (preliminary report). Acta Med Indones. 2006; 38: 142-4, PMID.

Tjokroprawiro A. The metabolic syndrome (LRD stage-3): preclinical stage of the CVDs (LRD stage 0-4, GULOH-CISAR, drug intervention, "time bomb disease"). Surakarta: Simposium Sumpah Dokter FK UNS Periode-161. Holistic Approach of the Metabolic Syndrome; 2007.

Richard ED, Robert MK, Hal BJ. Defect in metabolic of lipids. In: Nelson Textbook of Pediatrics. 17th ed. Philadelphia: Saunders; 2004. p.448, NLMID.

Buse JB, Polonsky KS, Burant CF. Type 2 diabetes mellitus. In: Larsen PR, Kronenberg HM, Melmed S, Polonsky KS, editors. Williams textbook of endocrinology. 10th ed. Philadelphia: Saunders; 2003. p.1427-51, NLMID.

Brunzell JD, Failor RA. Diagnosis and treatment of dyslipidemia. ACP Medicine. 2006 Jan 27, article.

Kim JA, Montagnani M, Koh KK, Quon MJ. Reciprocal relationships between insulin resistance and endothelial dysfunction: molecular and pathophysiological mechanisms. Circulation. 2006; 113: 1888-904, CrossRef.

Sattar N, Ken W, Allan DS, Ralph DA, Stevem M. Comparison of the associations of apolipoprotein B and non-high-density lipoprotein cholesterol with other cardiovascular risk factors in patients with the metabolic syndrome in the insulin resistance atherosclerosis study. Circulation. 2004; 110: 2687-93, CrossRef.

Yamauchi T, Kamon J, Ito Y, Tsuchida A, Yokomizo T, Kita S, et al. Cloning of adiponectin receptors that mediate antidiabetic metabolic effects. Nature. 2003; 423: 762-9, PMID.

Bush NC, Darnell BE, Oster RA, Goran MI, Gower BA. Adiponectin is lower among African Americans and is independently related to insulin sensitivity in children and adolescents. Diabetes: 2005; 54: 2772–8. CrossRef.

Berg AH, Combs TP, Du X, Brownlee M, Scherer PE. The adipocyte-secreted protein Acrp30 enhances hepatic insulin action. Nat Med. 2001; 7: 947-53, CrossRef.

Hoffstedt J, Poirier O, Thorne A, Lonnqvist F, Herrmann SM, Cambien F, et al. Polymorphism of the human beta3-adrenoceptor gene forms a well-conserved haplotype that is associated with moderate obesity and altered receptor function. Diabetes. 1999; 48: 203-5, CrossRef.

Spranger J, Kroke A, Möhlig M, Bergmann MM, Ristow M, Boeing H, et al. Adiponectin and protection against type 2 diabetes mellitus. Lancet. 2003; 361: 226-8, CrossRef.

Faraj M, Havel PJ, Phélis S, Blank D, Sniderman AD, Cianflone K. Plasma acylation-stimulating protein, adiponectin, leptin, and ghrelin before and after weight loss induced by gastric bypass surgery in morbidly obese subjects. J Clin Endocrinol Metab. 2003; 88: 1594-602, CrossRef.

Chandran M, Phillips SA, Ciaraldi T, Henry RR. Adiponectin: more than just another fat cell hormone? Diab Care. 2003; 26: 2442-50, CrossRef.

Tomas E, Tsao TS, Saha AK, Murrey HE, Zhang CC, Itani SI, et al. Enhanced muscle fat oxidation and glucose transport by ACRP30 globular domain: Acetyl-CoA carboxylase inhibition and AMP-activated protein kinase activation. Proc of Natl Acad Sci USA. 2002; 99: 16309-13, CrossRef.

Matsuzawa Y, Funahashi T, Kihara S, Shimomura I. Adiponectin and metabolic syndrome. Arterioscler Thromb Vasc Biol. 2004; 24: 29-33, CrossRef.

Matsushita K, Yatsuya H, Tamakoshi K, Wada K, Otsuka R, Takefuji S, et al. Comparison of circulating adiponectin and proinflammatory markers regarding their association with metabolic syndrome in Japanese men. Arterioscler Thromb Vasc Biol. 2006; 26: 871-6, CrossRef.

Bouziotas C, Koutedakis Y, Nevill A, Ageli E, Tsigilis N, Nikolaou A, et al. Greek adolescents, fitness, fatness, fat intake, activity, and coronary heart disease risk. Arch Dis Child. 2004; 89: 41-4, PMID.

Hill JO, Melanson EL, Wyatt HT. Dietary fat intake and regulation of energy balance: implications for obesity. J Nutr. 2000; 130 (2S Suppl): 284S-288S, PMID.

Bray GA, Popkin BM. Dietary fat intake does affect obesity! Am J Clin Nutr. 1998; 68: 1157-73, PMID.

Sharman MJ, Gómez AL, Kraemer WJ, Volek JS. Very low-carbohydrate and low-fat diets affect fasting lipids and postprandial lipemia differently in overweight men. J Nutr. 2004; 134: 880-5, PMID.


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