Findings from this study suggest that hypovitaminosis D is relatively common among young and middle-aged, northern Chinese individuals living in an urban environment, especially those who are obese and have metabolic syndrome. Additionally, we found vitamin D status was significantly associated with glucose homeostasis indices and lipid profile, which remained after adjustment for BMI.
This study consisted of a high risk population for metabolic syndrome, namely a young and middle aged, urban cohort who were office workers and physically inactive . The prevalence of vitamin D deficiency and insufficiency was 28.6% and 37.6% respectively which is not as striking as the 69.2% and 24.4% for vitamin D deficiency and insufficiency respectively as previously reported in Chinese population by Lu et al. . This deviation perhaps derived in part from the older age of participants in their study (50–70 years old) compared to the present study (35–60 years old). Additionally, the present study excluded patients who have overt diabetes, CVD and currently use anti-hypertensive medication and lipid drugs, which means participants in the present study have better metabolic conditions compared to Lu’s study. Although lower 25(OH)D levels were positively related to female sex in multivariable analysis, there was no significant difference in vitamin D statuses between males and females in our present study (data not shown). This may be attributed to the older age and higher BMI levels in the male group when compared to the female group, which may eliminate the advantage of male sex on vitamin D metabolism.
We also observed a greater prevalence of hypovitaminosis D amongst overweight/obese individuals. Even among lean individuals, lower vitamin D concentrations were associated with greater BMI, which is similar to results reported for other ethnic groups . The observed association of low 25(OH)D with BMI may be due in part to the increased distribution volume of lipid soluble vitamin D to fat. There are also some experimental data that suggest vitamin D deficiency promotes lipogenesis through elevated parathyroid hormone  and could possibly modulate adipogenesis through vitamin D receptor-dependent inhibition of critical molecular components involved in differentiation and maturation of adipocytes . Thus, increases in body fat mass could worsen the state of vitamin D deficiency, which may further increase body fat mass through vitamin D receptor regulation of pathways that are yet to be confirmed.
In this study, we observed significant associations of serum 25(OH)D with components of metabolic syndrome including waist circumference, triglyceride, HDL cholesterol and fasting glucose, but we did not find associations with blood pressure, even after adjusting for adiposity, which is in accordance with the findings from both the Cross-Sectional Study in the 1958 British Birth Cohort  and the NHANES III  study. Lu et al.  also noted that low 25(OH)D level increased risk for metabolic syndrome. Similar to result in Lu et al. study, the present study showed that the association between 25(OH)D and predictor variables were stronger in men than in women. However, results are conflicting as some previous investigations have only observed associations of 25(OH)D with anthropometric markers of metabolic syndrome (i.e. WC and BMI), but not with any of the clinical or serum parameters (i.e. fasting glucose, triglycerides, HDL cholesterol or blood pressure) . Because excess weight is a major component of metabolic syndrome, the associations noted in our study could reflect an association of serum vitamin D with excess weight. Regardless of the associations with components of metabolic syndrome, we also found a significant inverse association for 25(OH)D with LDL-cholesterol, which was not included in Lu’s study. LDL-cholesterol is perhaps the most important risk factor of cardiovascular disease, and thus, this result underscores the importance of hypovitaminosis D as a correlate of cardiovascular disease as has been observed in other investigations .
Insulin resistance is considered a likely mechanism causing metabolic syndrome and has been implicated in increased cardiovascular disease . In the present study, insulin resistance as determined by HOMA-IR was significantly greater in vitamin D deficient subjects. Although prior data are conflicting , some studies did observe an inverse association between concentrations of vitamin D and insulin resistance in different ethnic populations and age groups [27–29]. However, results from the Framingham Heart study found that adjusting for measures of central adiposity diminished the association between 25(OH)D and proxy measures of insulin sensitivity , implying that obesity may still the most important factor influencing the relationship between insulin sensitivity and vitamin D status. A study in an African-American cohort  suggested that vitamin D may have more influence on peripheral, rather than hepatic, insulin sensitivity, through the measurement of the OGTT-derived whole body insulin sensitive index (Matsuda index). Therefore, direct measures of insulin sensitivity, such as euglycemic clamp, frequently sampled intravenous glucose tolerance test (FSIGT,) or glucose tracer studies, will be needed to confirm results.
Several limitations of this study merit consideration. The results of our study may not be generalized to all racial/ethnic groups or age groups given that our sample was northern Chinese and young to middle-aged. Multivariable analyses were unable to adjust for the parathyroid hormone because this was not measured in our sample.
Notwithstanding the above limitations, the present study had several strengths. We used a work and lifestyle-based sample not selected on the basis of adiposity-related traits, cardiovascular disease risk factors, or vitamin D status. Our participants were young and middle aged, urban Chinese office workers, who were physically inactive with a high education level, traits indicating high risk for obesity and related metabolic disorders. All the participants lived in the same city for more than 5 years and blood samples were collected within two months (November and December), eliminating seasonal and geographic effects on the results. Our study excluded overt diabetes, CVD, hypertension and hyperlipidemia, which need medication to control, so this is a key population for primary prevention of type 2 diabetes and CVD. Intervention to this population would have significant impact on the control of chronic metabolic disease in a cost-effective manner.
Although there is mounting evidence linking vitamin D deficiency with obesity and related metabolic abnormalities, vitamin D intervention trials have had mixed results, which are likely due to different study populations, vitamin D replacement dosage, and intervention length. It is also possible that the link between vitamin D and cardiometabolic risk factors may reflect the fact that both vitamin D deficiency and metabolic disorders are prone to cluster in obese populations.