Vitamin D is a group of fat-soluble secosteriods responsible for the intestinal absorption of calcium and phosphate from the gut into the bloodstream, contributing to improved bone health (21). Serum vitamin D deficiency increases the risks of osteoporosis and osteomalacia in adults as well as the risk of rickets in children. More than 30 different types of cells within the body contain vitamin D receptors, including skeletal muscle, adipose tissue, and cardiac muscle (19). Accordingly, serum vitamin D insufficiency is related to the increased risk of metabolic syndrome, cardiovascular diseases, diabetes mellitus, cancers, infections, and autoimmune disease (17,18,22,23,27,31,39,46).
Sunlight exposure, diet, and supplements are three well-known determinants of serum vitamin D status. The majority of the vitamin D in our body is produced by cutaneous synthesis in response to sunlight exposure. Koreans are leading increasingly sedentary lifestyles with more time spent indoors and thus are not getting sufficient exposure to sunlight for adequate cutaneous production of vitamin D. Data from the 2008 and 2009 Korean National Health and Nutrition Examination Survey (KNHANES) (11,29,44) showed that the prevalence of serum vitamin D insufficiency in Korea has exceeded those of western countries including the United States and Canada. Vitamin D insufficiency in Korea has reached epidemic proportions and become a major health concern, especially in young adults because of their indoor dominant lifestyle (33). In addition, the prevalence rates of osteoporosis in Korean population age ≥50 yr are 8.1% in men and 38.7% in women, and the prevalence rates linearly increase with age, peaking at 68.2% in the ≥65 yr population (30). On the basis of data from the KNHANES from 1998 to 2007, Lim et al. (34) reported that the age-adjusted prevalence rates of metabolic syndrome increased significantly from 24.9% in 1998, 29.2% in 2001, and 30.4% in 2005 to 31.3% in 2007.
A global epidemic of metabolic syndrome, as defined by the clustering of hyperinsulinemia, hyperlidemia, and hypertension,has been observed in children, adolescents, and adults (8,24,34,47). Although the exact etiology of metabolic syndrome is uncertain, lifestyle factors including body fatness, physical inactivity, and poor physical fitness are likely attributed to its development. Lifestyle factors, such as body fatness and physical inactivity, have previously been reported to be negatively associated to serum vitamin D levels (9,13,15,16,48). In addition, cardiorespiratory fitness (CRF) has been reported to be positively related to serum vitamin D levels in men (4,15), women (15,41), and in patients with moderate chronic kidney disease (45). However, those studies reporting the associations between serum vitamin D levels and lifestyle factors have been mostly limited to non-Asian populations.
There is a limited number of investigations that have examined the relationship between lifestyle factors such as body fatness and physical inactivity and serum vitamin D in Koreans (20,11,4). More studies are needed to delineate the etiology and health consequences of low serum vitamin D levels in Asian countries including Korea. This study examined the relationship between serum 25(OH)D levels and body fatness, CRF, and metabolic risk factors in young Korean adults.
Subjects and blood samples.
This study included 809 college male students who registered in “health and fitness lectures” at the study institute between 2007 and 2009. All volunteers underwent a comprehensive health and fitness screening at the study laboratory. The average rates for the screening were 91%, 94%, and 92% in 2007, 2008, and 2009, respectively. Subjects were apparently healthy; free of any diagnosed chronic diseases such as diabetes, hypertension, dyslipidemia, or thyroid disease; and not taking any medications affecting blood pressure (BP), glucose, or lipid levels or related to body weight change. The Institutional Research Ethnics Review Committee reviewed and approved the study. After receiving written informed consent from each participant, a clinical evaluation was performed.
The clinical examinations included anthropometry and body composition, resting BP, fasting blood chemistry, and a maximal graded exercise test on a motor-driven treadmill. Height and body mass were recorded using a stadiometer attached to a scale (Jenix, Seoul, Korea). Waist circumference (WC) was measured using a cloth tape and was taken at the midpoint between the xiphoid process and the umbilicus. Percent body fat was assessed using bioelectrical impedance analysis following the procedures recommended by the American College of Sports Medicine (ACSM) (3).
BP was measured using an automated BP instrument (Jawon Medical Co., Kyungsan, South Korea). Subjects were instructed to refrain from using alcohol, smoking, and caffeine products and not to participate in any physical exercise within the last 24 h. Then subjects were reported to our laboratory after an overnight fast. On arrival, subjects had a 20-min rest in the supine position, followed by another 5 min in a seated position. Then, while remaining in the seated position, subjects were fitted with proper cuff sizes with the arm at heart levels, resting on the armrest of a chair. Two BP assessments were taken at 3-min intervals. The means of the two BPs were recorded.
Venous blood samples were drawn with the subjects in the supine position. Before blood sampling, the fasting state was verbally confirmed by the subject. Blood samples were taken from an antecubital vein of a forearm, immediately placed on ice, and centrifuged on site. Blood samples were stored at −70°C until biochemical assays for blood lipids, glucose, and insulin. Fasting glucose, total cholesterol (TC), triacylglycerols (TAG), and high-density lipoprotein cholesterol (HDLC) levels were measured in duplicate using an Ektachem DT-60 II analyzer (Johnson & Johnson Clinical Diagnostics, Inc., Rochester, NY). Fasting insulin was measured in duplicate using an enzyme-linked immunosorbent assay kit (ALPCO Diagnostics, Salem, NH). The index of insulin resistance was assessed using the homoeostasis model of assessment for insulin resistance (HOMA-IR), as HOMA-IR = [fasting insulin (μU·ml−1) × fasting glucose (mM)]/22.5. The intra- and interassay coefficients of variation for insulin were 2%–5% and 5%–9%, respectively.
Serum vitamin D levels were determined using the LIAISON 25(OH) vitamin D total assay (CLIA), which is a direct competitive chemiluminescence immunoassay for human serum or plasma intended for use on the DiaSorin LIAISON automated analyzer (DiaSorin S.P.A, Italy). The intra- and interassay coefficients of variation for 25-hydroxyvitamin D (25(OH)D) were 3%–6% and 7%–11%, respectively.
Determination of CRF.
This was measured on a motor-driven treadmill according to the ACSM guidelines (3). The following criteria were used to confirm V˙O2max achievement; (i) a leveling off of the V˙O2, (ii) RPE > 17 for the original category scale, (iii) volitional exertion, and (iv) achievement of age-predicted HRmax. Students were encouraged to exercise to exhaustion during the test. Individuals with a self-reported history of cardiovascular diseases such as diabetes, heart attacks, stroke, and/or cancer were excluded (n = 3). In addition, individuals who did not complete either the maximal treadmill test (n = 2) or measurements of metabolic syndrome markers including blood pressures, lipids, glucose, and insulin (n = 5) were excluded. Consequently, data obtained from 799 of the initial 809 participants were included in the data analyses.
Calculation of a clustered metabolic risk score.
The study population consisted of young and healthy college male students with no evident pathologies and low prevalence of metabolic syndrome (i.e., overall 2.7%). In view of this difficulty, a clustered metabolic risk score based on the National Cholesterol Education Program (NCEP-ATP III) criteria (14) was computed by summing standardized (z) scores for WC, resting BP (systolic BP [SBP] + diastolic BP [DBP]/2), TAG, the inverse of HDLC, glucose, and insulin. A z-score was computed from the sample mean after normalization of the variables (8,48). The computed risk scores are continuous variables with a mean of zero by definition, with lower scores denoting a more favorable profile and higher values indicating a less favorable profile in relation to the sample studied.
All variables were checked for normality and, if necessary, subjected to log10 transformation before statistical analyses. Descriptive statistics for raw variables across incremental serum vitamin D categories are presented as means ± SDs. In the present analyses, <12.5 ng·mL−1, ≥12.5 ∼ <20 ng·mL−1, and ≥20 ng·mL−1 of serum vitamin D levels were classified as deficient, insufficient, and sufficient, respectively (25).
Tests for linear trends were performed with the Kruskal-Wallis test (two-tailed) for the median value for each category of serum vitamin D levels. Spearman coefficients of correlation were calculated among serum vitamin D levels, lifestyle factors such as body fatness and CRF, and metabolic risk factors. Coefficients of partial correlation were calculated between serum vitamin D and metabolic risk factors, controlling for age, smoking, and CRF and body fatness parameters in order. A generalized linear regression model was used to test a linear trend in the clustered metabolic risk score across incremental serum vitamin D categories, controlling for age, smoking, CRF, body mass index (BMI), and percent body fat.
In addition, participants were classified as unfit or fit based on the lowest 20% and remaining 80% of the age-standardized CRF distribution of V˙O2max values in this study population. Serum 25(OH)D levels were categorized as <16 ng·mL−1 (inadequacy) and ≥16 ng·mL−1 (adequacy), which covers the requirements of approximately half the population in the United States and Canada (25). Unconditional binominal logistic regression was used to determine the odds ratios (ORs) and 95% confidence interval (95% CI) for having serum vitamin D inadequacy according to CRF levels, before and after adjusting for age, smoking, and body fatness parameters such as BMI, percent body fat, and WC. The fit group was used as the reference category (OR = 1.0). All P values are two-sided, and P < 0.05 was regarded as statistically significant. Statistical analyses were performed using SPSS-PC version 20.0 for Windows (Chicago, IL).
Table 1 shows the physical and biochemical characteristics of the study participants. There were linear decreases for body fatness parameters and a linear increase for CRF category across serum 25(OH)D levels. Linear decreases for metabolic risk factors including resting BPs, TAG, and insulin were found across incremental serum 25(OH)D categories. There was also a linear increase for HDLC across incremental serum 25(OH)D categories. No significant linear increases or decreases for age, TC, fasting glucose, HOMA-IR, and smoking rates were found across incremental serum 25(OH)D categories.
Table 2 shows the coefficients of partial correlation between serum 25(OH)D and measured parameters in this study population. Serum 25(OH)D was inversely related to BMI (r = −0.295, P < 0.001), percent body fat (r = −0.333, P < 0.001), WC (r = −0.274, P < 0.001), SBP (r = −0.175, P < 0.001), DBP (r = −0.176, P = 0.001), TC (r = −0.162, P = 0.008), TAG (r = −0.253, P < 0.001), and fasting insulin (r = −0.203, P < 0.001) and was positively related to CRF (r = 0.400, P < 0.001) and HDLC (r = 0.208, P = 0.001). After adjusting for age and smoking, serum 25(OH)D remained significantly correlated with SBP (r = −0.190, P = 0.003), DBP (r = −0.135, P = 0.034), TC (r = −0.166, P = 0.009), TAG (r = −0.216, P = 0.001), and HDLC (r = 0.199, P = 0.002). Serum 25(OH)D remained significantly correlated with SBP (r = −0.128, P = 0.047), TAG (r = −0.141, P = 0.029), and HDLC (r = 0.150, P = 0.012) even after additionally adjusting for CRF and body fatness parameters including BMI, percent body fat, and WC. In addition, a linear decrease for the clustered metabolic risk score was found across incremental serum 25(OH)D categories (Fig. 1).
Table 3 shows the ORs with 95% CIs for serum vitamin D inadequacy, defined as having a serum 25(OH)D level <16 ng·mL−1. Using V˙O2max as the CRF exposure, unfit men were significantly more likely to have serum 25(OH)D inadequacy than fit men (reference). Adjustment for age and smoking had little effect on the strength of the association between CRF and serum 25(OH)D inadequacy. The OR of serum 25(OH)D inadequacy according to CRF levels remained significant when additionally adjusted for body fatness parameters including BMI, percent body fat, and WC.
This study examined the relationships of serum 25(OH)D levels to body fatness and fitness as well as metabolic risk factors in young adults in Korea. To our knowledge, this is the first study reporting significant associations between serum 25(OH)D levels, body fatness and fitness, and the clustering of metabolic risk factors in young men in Korea. Significant inverse trends for SBP and TAG were observed across incremental serum 25(OH)D categories, while a significant positive trend for HDLC was observed across incremental serum 25(OH)D categories, independent of age, smoking, CRF, and body fatness parameters. In particular, serum 25(OH)D levels were inversely associated with a clustered metabolic risk score, using the metabolic syndrome components as continuous variables. Consequently, the overall findings of the study suggest that while lifestyle factors such as body fatness and CRF are significant confounders to the relationships between serum 25(OH)D levels and metabolic risk factors, serum 25(OH)D inadequacy itself may also contribute to the clustering of metabolic risk factors, at least in this study population.
Our findings of high body fatness and low CRF being associated with low vitamin D levels are consistent with those of previous studies (2,11,12). Few data have been available on the relationship between serum 25(OH)D levels and lifestyle factors including body fatness and fitness, especially in Asian populations. Ardestani et al. (4) examined the association between serum 25(OH)D levels and CRF in 200 healthy adults participating in a double-blind clinical trial investigating statins and muscle performance (STOMP study). There was a significant association between serum 25(OH)D and CRF, even after adjusting for age, gender, and BMI. Using data obtained from the Cooper Center Longitudinal Study (CCLS), an updated version of the Aerobics Center Longitudinal Study (ACLS), Farrell et al. (15) and Farrell and Willis (16) found that serum 25(OH)D status was inversely related to body fatness and positively related to CRF in both men and women. In addition, data from the KNHANES IV (32) showed that serum 25(OH)D levels were inversely related to whole-body dual-energy X-ray absorptiometry (DXA)–based body fat mass and were positively related to DXA-based lean body mass in Korean men only. However, no such associations were found in women, suggesting a possibility of sex-specific associations between serum vitamin D levels and body composition in Korean adults.
Several explanations can be given for these findings. First, body fatness has been consistently related to low serum 25(OH)D levels because of sequestration in fat (52), increased clearance by a larger body fat pool (42), negative feedback from higher circulating 1,25(OH)2D levels in obesity (5), and decreased sunlight exposure because of limited mobility or avoidance of outdoor activity (12). Thus, it seems reasonable to speculate that serum vitamin D insufficiency partially reflects the increased risk of body fatness associated with metabolic syndrome.
Second, CRF may contribute to the preventive effect(s) of serum vitamin D against metabolic syndrome. In an agreement, the logistic regression analyses showed that unfit men had a significantly higher risk for serum 25(OH)D inadequacy than unfit men (OR = 1.721, 95% CI = 1.095–2.704), even after adjusting for age, smoking, and body fatness parameters. The findings of the present study were in agreement with data from the STOMP and CCLS in which serum 25(OH)D levels were positively related to CRF and inversely related to body fatness in adults (2,11,12). While the nature of these cross-sectional observations does not prove or disprove causality, these trends suggest the possibility that CRF may affect serum 25(OH)D levels, or vice versa. CRF is determined primarily by maximal cardiac output and maximal arteriovenous O2 difference. A recent study showed that 1,25(OH)2D might inhibit the cell cycle in the heart and restrict mechanisms causing myocardial fibrosis, improving myocardial structure or contractility in rats and mice (42).
Third, individual variations in daily sunlight exposure cannot be ruled out as a potential explanation for the association between serum 25(OH)D levels and CRF. Although primarily influenced by individual differences in genetic makeup, CRF is a set of physiological attributes that are also substantially enhanced through participation in regular physical activity (7). Consequently, CRF levels may reflect individual variations in sunlight exposure while participating in outdoor physical activities including exercise (35,48,49).
Finally, serum vitamin D insufficiency/deficiency is associated with insulin resistance, a key feature underlying metabolic syndrome (35,40). In agreement, Alvarez et al. (2) found that serum 25(OH)D was an independent predictor of whole-body insulin sensitivity index assessed by the intravenous glucose tolerance test in African American women. Chiu et al. (10) determined insulin sensitivity index and first and second phases of insulin secretion using the hyperglycemic clamp in a cohort of glucose-tolerant multiethnic young adults. In that study, serum 25(OH)D was positively associated with insulin sensitivity index and negatively associated with first- and second-phase insulin secretion. Kayaniyil et al. (28) examined the associations between serum 25(OH)D levels and insulin resistance index and β-cell dysfunction in 721 subjects at risk for type 2 diabetes. Using linear regression analyses, they found that serum 25(OH)D was independently associated with insulin sensitivity index for oral glucose tolerance tests and homeostasis model assessment of insulin resistance as well as β-cell function. Consequently, the protective effects of vitamin D against metabolic syndrome may be due to the effects of vitamin D on glucose homeostasis through several potential mechanisms, including increased biosynthesis (6) and secretion (26) of insulin from pancreatic β cells, enhanced insulin sensitivity in peripheral tissues (51), and the presence of a vitamin D response element in the human insulin receptor gene promoter (37). Further, 1,25(OH)2D stimulates transcription of the human insulin receptor gene (38) and stimulates insulin-mediated glucose transport in vitro (36). Vitamin D inhibits the renin–angiotensin system, and overactivity in this system in islets is reduced by activated vitamin D. Inhibition of the renin–angiotensin system prevents increases in blood pressure and controls T helper cells that inhibit inflammation, atherosclerosis, thrombosis, and vascular calcification, ultimately preventing the development of cardiovascular diseases (22).
Lack of information regarding sunlight exposure, indoor or outdoor exercise patterns, dietary vitamin D and calcium, and parathyroid hormone are some of the limitations of our data. Future research on the independent role of exercise, as well as the combined effects of exercise and dietary intake, on vitamin D bioavailability and metabolism is needed. Further, randomized and controlled trials are necessary to determine whether there is a causal relationship between serum vitamin D and body fatness, CRF, and metabolic risk factors.
In conclusion, serum vitamin D levels were inversely related to body fatness and a clustering of metabolic risk factors and were positively related to CRF in this study sample. The findings of this study suggest that increasing vitamin D intake, eating a healthy diet, and getting enough outdoor physical activity should be major targets of lifestyle interventions against metabolic syndrome in young adults in Korea.
This article was supported by Samsung Research Fund, Sungkyunkwan University, 2013.
There are no conflicts of interest to disclose.
The results of the present study do not constitute endorsement by the ACSM.
1. Alberti KG, Zimmet P, Shaw J. The metabolic syndrome—a new worldwide definition. Lancet
. 2005; 366: 1059–62.
2. Alvarez JA, Ashraf AP, Hunter GR, Gower BA. Serum 25-hydroxyvitamin D and parathyroid hormone are independent determinants of whole-body insulin sensitivity in women and may contribute to lower insulin sensitivity in African Americans. Am J Clin Nutr
. 2010; 92: 1344–9.
3. American College of Sports Medicine. ASCM’s Guidelines for Exercise Testing and Prescription
. 7th ed. Philadelphia (PA): Lippincott Williams & Wilkins; 2006. pp. 237–40.
4. Ardestani A, Parker B, Mathur S, et al. Relation of vitamin D to maximal oxygen uptake in adults. Am J Cardiol
. 2011; 107 (8): 1246–9.
5. Bell NH, Epstein S, Greene A, et al. Evidence for alteration of the vitamin D–endocrine system in obese subjects. J Clin Invest
. 1985; 76 (1): 370–3.
6. Bland R, Markovic D, Hills CE, et al. Expression of 25-hydroxyvitamin D3
-1alpha-hydroxylase in pancreatic islets. J Steroid Biochem Mol Biol
. 2004; 89–90 (1–5): 121–5.
7. Bouchard C, Perusse L. Heredity, activity levels, fitness, and health. In: Bouchard C, Shephard RJ, Stephens T, editors. Physical Activity, Fitness, and Health: International Proceedings and Consensus Statement
. Champaign (IL): Human Kinetics Publishers; 1994. pp. 11–20.
8. Brage S, Wedderkopp N, Ekelund U, et al. Objectively measured physical activity correlates with indices of insulin resistance in Danish children. The European Youth Heart Study (EYHS). Int J Obes Relat Metab Disord
. 2004; 28 (11): 1503–8.
9. Brock K, Huang WY, Fraser DR, et al. Low vitamin D status is associated with physical activity, obesity and low vitamin D intake in a large US sample of healthy middle-aged men and women. J Steroid Biochem Mol Biol
. 2010; 121 (1–2): 462–6.
10. Chiu KC, Chu A, Go VLW, Saad MF. Hypovitaminosis D is associated with insulin resistance and β cell dysfunction. Am J Clin Nutr
. 2004; 79: 820–5.
11. Choi HS, Oh HJ, Choi H, et al. Vitamin D insufficiency in Korea: a greater threat to younger generation: the Korea National Health and Nutrition Examination Survey (KNHANES) 2008. J Clin Endocrinol Metab
. 2011; 96 (3): 643–51.
12. Compston JE, Vedi S, Ledger JE, et al. Vitamin D status and bone histomorphometry in gross obesity. Am J Clin Nutr
. 1981; 34 (11): 2359–63.
13. Dong Y, Pollock N, Stallmann-Jorgensen IS, et al. Low 25-hydroxyvitamin D levels in adolescents: race, season, adiposity, physical activity, and fitness. J Pediatr
. 2010; 125 (6): 1104–11.
14. Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. Executive Summary of the Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III). JAMA
. 2001; 285: 2486–97.
15. Farrell SW, Cleaver JP, Willis BL. Cardiorespiratory fitness, adiposity, and serum 25-hydroxyvitamin d levels in men. Med Sci Sports Exerc
. 2011; 43 (2): 266–71.
16. Farrell SW, Willis BL. Cardiorespiratory fitness, adiposity, and serum 25-dihydroxyvitamin D levels in women: the Cooper Center Longitudinal Study. J Womens Health (Larchmt)
. 2012; 21 (1): 80–6.
17. Forman JP, Giovannucci E, Holmes MD, et al. Plasma 25-hydroxyvitamin D levels and risk of incident hypertension. Hypertension
. 2007; 49 (5): 1063–9.
18. Giovannucci E, Liu Y, Hollis BW, et al. 25-Hydroxyvitamin D and risk of myocardial infarction in men: a prospective study. Arch Intern Med
. 2008; 168 (11): 1174–80.
19. Gouni-Berthold I, Krone W, Berthold HK. Vitamin D and cardiovascular disease. Curr Vasc Pharmacol
. 2009; 7 (3): 414–22.
20. Ha CD, Cho JK, Lee SH, et al. Serum vitamin D, physical activity, metabolic risk factors in Korean children. Med Sci Sports Exerc
. 2013; 45 (1): 102–8.
21. Holick MF. Vitamin D deficiency. N Eng J Med
. 2007; 357 (3): 266–81.
22. Holick MF, Vitamin D. Evolutionary, physiological and health perspectives. Curr Drug Targets
. 2011; 12: 4–18.
23. Holick MF. The D-lightful vitamin D for child health. JPEN J Parenter Enteral Nutr
. 2012; 36 (Suppl 1): 9–19S.
24. Hong HR, Cho JK, Lee JY, et al. Clustering of metabolic syndrome risk factors associated with lifestyle factors and serum leptin in Korean children. Pediatr Exerc Sci
. 2011; 23 (2): 270–80.
25. IOM. Dietary Reference Intakes for Calcium and Vitamin D
. Washington (DC): The National Academies Press; 2000. pp. 1045–58.
26. Johnson JA, Grande JP, Roche PC, et al. Immunohistochemical localization of the 1,25(OH)2D3
receptor and calbindin D28K in human and rat pancreas. Am J Physiol
. 1994; 267 (3 Pt 1): E356–60.
27. Kamen D, Aranow C. Vitamin D in systemic lupus erythematosus. Curr Opin Rheumatol
. 2008; 20 (5): 532–7.
28. Kayaniyil S, Vieth R, Retnakaran R, et al. Association of vitamin D with insulin resistance and β-cell dysfunction in subjects at risk for type 2 diabetes. Diabetes Care
. 2010; 33 (6): 1379–81.
29. Kim S, Lim J, Kye S, et al. Association between vitamin D status and metabolic syndrome risk among Korean population: based on the Korean National Health and Nutrition Examination Survey IV-2,2008. Diabetes Res Clin Pract
. 2012; 96 (2): 230–6.
30. Korea Ministry of Health and Welfare (2010). Korea Health Statistics 2009: Korea National Health and Nutrition Examination Survey IV-3. p. 64.
31. Laaksi I, Ruohola JP, Tuohimaa P, et al. An association of serum vitamin D concentrations < 40 nmol/L with acute respiratory tract infection in young Finnish men. Am J Clin Nutr
. 2007; 86 (3): 714–7.
32. Lee K. Body composition and vitamin D status: the Korea National Health and Nutrition Examination Survey IV (KNHANES IV). J Hum Nutr Diet
. 2013; 26 (Suppl 1): 105–13.
33. Lee JY, Kim SU, Kang HS. Low cardio/respiratory fitness as an independent predictor of metabolic syndrome in Korean young men. Eur J Appl Physiol
. 2010; 108 (4): 633–9.
34. Lim S, Shin H, Song JH, et al. Increasing prevalence of metabolic syndrome in Korea. Diabetes Care
. 2011; 34: 1323–8.
35. Looker AC, Pfeiffer CM, Lacher DA, et al. Serum 25-hydroxyvitamin D status of the US population: 1988–1994 compared with 2000–2004. Am J Clin Nutr
. 2008; 88 (6): 1519–27.
36. Maestro B, Campión J, Dávila N, et al. Stimulation by 1,25-dihydroxyvitamin D3
of insulin receptor expression and insulin responsiveness for glucose transport in U-937 human promonocytic cells. Endocr J
. 2000; 47 (4): 383–91.
37. Maestro B, Dávila N, Carranza MC, et al. Identification of a vitamin D response element in the human insulin receptor gene promoter. J Steroid Biochem Mol Biol
. 2003; 84 (2–3): 223–30.
38. Maestro B, Molero S, Bajo S, et al. Transcriptional activation of the human insulin receptor gene by 1,25-dihydroxyvitamin D(3). Cell Biochem Funct
. 2002; 20 (3): 227–32.
39. Mattila C, Knekt P, Männistö S, et al. Serum 25-hydroxyvitamin D concentration and subsequent risk of type 2 diabetes. Diabetes Care
. 2007; 30 (1): 2569–70.
40. Melamed ML, Michos ED, Post W, et al. 25-Hydroxyl vitamin D levels and the risk of mortality in the general population. Arch Intern Med
. 2008; 168 (15): 1629–37.
41. Mowry DA, Costello MM, Heelan KA. Association among cardiorespiratory fitness, body fat, and bone marker measurements in healthy young females. J Am Osteopath Assoc
. 2009; 109: 534–9.
42. Need AG, Morris HA, Horowitz M, et al. Relationship of skin thickness, age, body fat and sunlight on serum 25-hydroxyvitamin D. Am J Clin Nutr
. 1993; 58 (6): 882–5.
43. Nibbelink KA, Tishkoff DX, Hershey SD, et al. 1,25(OH)2-vitamin D3
actions on cell proliferation, size, gene expression, and receptor localization, in the HL-1 cardiac myocyte. J Steroid Biochem Mol Biol
. 2007; 103 (3–5): 533–7.
44. Park SM, Lee BK. Vitamin D deficiency is an independent risk factor for cardiovascular disease in Koreans aged >50 years: results from the Korean national health and nutrition examination survey. Nutr Res Pract
. 2012; 6 (2): 162–8.
45. Petchey WG, Howden EJ, Johnson DW, et al. Cardiorespiratory fitness is independently associated with 25-hydroxyvitamin D in chronic kidney disease. Clin J Am Soc Nephrol
. 2011; 6: 512–8.
46. Poole KE, Loveridge N, Barker PJ, et al. Reduced vitamin D in acute stroke. Stroke
. 2006; 37 (1): 243–5.
47. Reaven G, Abbasi F, McLaughlin T. Obesity, insulin resistance, and cardiovascular disease. Recent Prog Horm Res
. 2004; 59 (1): 207–23.
48. Scragg R, Camargo CA Jr. Frequency of leisure-time physical activity and serum 25-hydroxyvitamin D levels in the US population: results from the third national health and nutrition examination survey. Am J Epidemiol
. 2008; 168 (6): 577–86.
49. Scragg R, Holdaway I, Jackson R, et al. Plasma 25-hydroxyvitamin D3
and its relation to physical activity and other heart disease risk factors in the general population. Ann Epidemiol
. 1992; 2 (5): 697–703.
50. Simmons RK, Griffin SJ, Steele R, et al. Increasing overall physical activity and aerobic fitness is associated with improvements in metabolic risk: cohort analysis of the ProActive
. 2008; 51: 787–94.
51. Simpson RU, Thomas GA, Arnold AJ. Identification of 1,25-dihydroxyvitamin D3
receptors and activities in muscle. J Biol Chem
. 1985; 260 (15): 8882–91.
52. Wortsman J, Matsuoka LY, Chen TC, Lu Z, Holick MF. Decreased bioavailability of vitamin D in obesity. Am J Clin Nutr
. 2000; 72 (3): 690–3.
Keywords:© 2014 American College of Sports Medicine
VITAMIN D; BODY FATNESS; CARDIORESPIRATORY FITNESS; METABOLIC RISK FACTORS