The Changes of Body Composition, Glucolipid Metabolism and Bone Metabolism in Obese Children After Weight Loss

Vitamin D plays a significant role in calcium and phosphorus homeostasis for maintaining structural integrity and function of musculoskeletal system. Furthermore, recent studies have revealed that vitamin D can decrease the risk of many conditions other than skeletal disease, including autoimmune diseases, cancers, obesity and obesity-related diseases, such as type 2 diabetes and cardiovascular disease. Vitamin D may influence calcium absorption to affect obesity indirectly, regulate adipocyte differentiation and relieve the development of metabolic syndrome by mediating levels of inflammatory factors.

Another indicator of bone metabolism-osteocalcin may also be involved in energy metabolism and glucose metabolism, and undercarboxylated osteocalcin (ucOC) is the form which has physiological activity. ucOC may recombine with the receptors on the surface of pancreas β cells, adipocytes, hepatocytes and intestinal endocrine cell to regulate insulin secretion and insulin sensitivity.

Currently, the prevalence of vitamin D deficiency is a global problem in all age groups currently, even in countries with sun exposure all year around. The obesity group tend to have a higher incidence of vitamin D deficiency.Moreover, the obesity group tend to have a higher incidence of vitamin D deficiency and a lower level of serum osteocalcin.

This study observed the changes of body composition and glucolipid metabolism and bone metabolism during weight loss, and investigated the correlations among them.

Obese children have a higher incidence of vitamin D deficiency (VDD), which resulted from unhealthy life style such as less time outdoors, more sedentary time, imbalance of dietary intake. Adipose tissue is the storage position of vitamin D, and the storage formation include 25-OHD2 and 25-OHD3. Theoretically, the reserves of vitamin D in adipose tissue of obese children might release to the circulation after weight loss. For further, it is necessary to clarify the relationship between the improvement of metabolic risk with vitamin D status after weight loss.

Osteocalcin is produced and secreted by osteoblast specifically. Recent studies have shown that it regulated glucose metabolism and energy metabolism. Obese group may have a lower level of serum osteocalcin. Both 25-OHD and osteocalcin have association with energy metabolism. This study will provide evidence to realize the relationship between bone metabolism and obesity.

In our study, all subjects were recruited from the obese children and adolescents aged 9\~17 years who participated in six-week weight loss camp in July \~ August, 2014. Body mass index (BMI) was calculated as weight (kg) divided by height squared (m2). Obesity was defined as having a BMI greater than or equal to the 95th percentile for age and sex according to WHO standard. Exclusion criteria included: 1) obesity caused by endocrine or heredity diseases (eg, hypothyroidism, Prader-Willi syndrome, single-gene defects); 2) any disease influencing vitamin D metabolism (eg, such as metabolic bone diseases, rickets, nephritic syndrome and hepatic failure); 3) any supplementation use or any medication affecting vitamin D metabolism use.

All subjects underwent a closed-off weight loss program for six weeks. The intervention methods included aerobic exercise and appropriate caloric control. The dietary was designed on the basis of ensuring the daily energy physiological requirement, and basal metabolic rate (BMR) was calculated to formulate diet project according to Harris-Benedict formula. The diet was composed of 20% protein, 30% fat and 50% carbohydrates. During the camp, all subjects had never taken any kinds of nutritional supplements.

Before intervention, all subjects received exercise load test to ensure safe and effective physical exercise. In the exercise, heart rate was monitored to ensure the small-medial load aerobic exercise. The exercise programs included ball games, such as badminton, table tennis, and basketball, and also included jogging, brisk walking, swimming and cycle ergometer. All kinds of sports were conducted indoor, twice per day, 6 days per week, and lasted for 2 hours every time. The weight loss camp was staffed by professional sports coaches and medical workers. Exercise intensity was estimated by a formula: exercise intensity (target heart rate) =resting heart rate + heart rate reserve (maximum heart rate-resting heart rate) × (20%\~40%).

Before and after intervention, fasting blood samples were collected and sent to Shanghai Adicon Central Lab Test Menu immediately stored in 4°C ice packs. The indicators of glucolipid metabolism and bone metabolism were tested. Total cholesterol (TC) with cholesterol oxidase, triglyceride (TG) with enzyme method (GPO-POD), high density lipoprotein (HDL) and low density lipoprotein (LDL) with homogeneous methods, fasting blood glucose (FBG) with hexokinase (HK) method, fasting insulin (FINS) with chemiluminescence method. Among the indicators of bone metabolism, osteocalcin, parathyroid hormone (PTH) and 25-OHD were assayed by electrochemiluminescence immunoassay, while bone specific alkaline phosphatase (BALP), total propeptide of type I procollagen (T-PINP) and β-isomerized form carboxy-terminal telopeptide of type I collagen (β-CTX) were determined by immunoenzymatic methods.

After blood samples were collected, anthropometric parameters were measured, including height (Seca 264, Germany), weight (Biospace 370, South Korea), triceps skinfold thickness (TST) and subscapular skinfold thickness (SST) (skinfold caliper 689900). For error reduction, every anthropometric measurement was conducted by the same trained personnels before and after weight-loss.

Eligibility Criteria:
Inclusion Criteria:

* Obesity was defined as having a body mass index (BMI) greater than or equal to the 95th percentile for age and sex according to WHO standard. BMI was calculated as weight (kg) divided by height squared (m2).

Exclusion Criteria:

* 1) obesity caused by endocrine or heredity diseases (eg, hypothyroidism, Prader-Willi syndrome, single-gene defects);
* 2) any disease influencing vitamin D metabolism (eg, such as metabolic bone diseases, rickets, nephritic syndrome and hepatic failure);
* 3) any supplementation use or any medication affecting vitamin D metabolism use.