Metabolic consequences of childhood obesity.

نویسنده

  • Suttipong Wacharasindhu
چکیده

153 Lifestyle changes are among the many factors influencing the growing epidemic of childhood obesity worldwide, as this age group spends more time on computers, inactive, and have more access to ‘fast food’. Based on International Obesity Task Force (IOTF) criteria, the prevalence of overweight and obesity in school-age children has increased in all regions of the world, from 2000 to 2010 (Fig 1) (Wang and Lobsein, 2006). A number of human biological substances secreted from adipose tissue play an important role in weight control, such as interleukin-6 (IL-6), which causes hyperglycemia and insulin resistance; tumor necrosis factor alpha (TNF-alpha), which influences fatty acid oxidation and insulin resistance; and plasminogen activator inhibitor-1 (PAI-1), which is associated with cardiovascular diseases (Blake and Ridker, 2002). Two known peptides, leptin and adiponectin, are associated with adiposity. Adiponectin is a peptide that enhances insulin sensitivity and has a negative correlation with adiposity (Haluzik et al, 2004). Complications of childhood obesity (Weiss and Kaufman, 2008; Lee, 2009) The complications of childhood obesity may be classified into non-metabolic and metabolic complications. Non-metabolic complications. Non-metabolic complications can occur in a number of systems. From the respiratory viewpoint, snoring and sleep apnea occur, culminating as the Pickwickian syndrome. The bones are also affected, presenting as Blount disease, slipped capital femoral epiphysis, and degenerative arthritis. Other systems can also emerge as complications, including dyslipidemia and hypertension in the cardiovascular system, depression and poor self-esteem for psychological disorders, and pseudotumor cerebri and stroke under neurological diseases.

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عنوان ژورنال:
  • The Southeast Asian journal of tropical medicine and public health

دوره 45 Suppl 1  شماره 

صفحات  -

تاریخ انتشار 2014