Table 2a.
Observational studies on vitamin D status and insulin resistance in obese adolescents.
| Study | Participants | Results |
|---|---|---|
| Alemzadeh et al. [2008] | 127 obese (BMI = 37 ± 8.5) | • 25(OH)D <75 nmol/l present in 74% of participants |
| 6–18 years62.2% female | • Vitamin D status significantly influenced by vitamin D intake, season, ethnicity/race and adiposity | |
| 30.7 % black | • 25(OH)D positively correlated with QUICKI and inversely correlated with HbA1c | |
| USA (WI) | ||
| Ashraf et al. [2009] | 51 obese (BMI = 43 ± 9.9) | • 25(OH)D <50 nmol/l present in 78.4%, <37 nmol/l in 60.8% of participants |
| 14 ± 2 years | • Vitamin D status not significantly correlated with BMI, fasting glucose or insulin, glucose or insulin AUC, HOMA-IR, Matsuda index | |
| black, females | • Participants with 25(OH)D <37 nmol/l had significantly lower insulin AUC and WBISI (Matsuda index) | |
| USA (AL) | ||
| Delvin et al. [2010] | 1745 obese and nonobese (males, BMI = 20.1 ± 4.2; females, BMI = 20.4 ± 4.5) | • 25(OH)D <75 nmol/l present in 93% of participants |
| 9–16 years | • Modest but significant inverse correlation (-2.8%) between HOMA-IR and each 10 nmol/l increase in 25(OH)D after adjustment for age and BMI | |
| 49.7% female | ||
| Canada | ||
| Erdonmez et al. [2011] | 310 obese and nonobese (BMI = 19.3–40.3) | • 25(OH)D = 25–50 nmol/l present in 53%, <25 nmol/l in 12% participants |
| 14 ± 2 years | • Prevalence of obesity and vitamin D deficiency higher in females | |
| 59% female | • No significant relationship between vitamin D status and obesity | |
| Turkey | • IFG and IGT rates at 8% and 5% respectively; frequency of metabolic syndrome was 12.3% | |
| • No significant associations between insulin sensitivity/resistance indices | ||
| Kelly et al. [2011] | 85 obese and nonobese (BMI-Z = -1.2–4.1) | • 25(OH)D <75 nmol/l present in 74%, <50 nmol/l in 47% of participants |
| 4–18 years | • Older age, higher BMI-Z and black race all negatively associated with 25(OH)D | |
| 45% female | • After adjusting for puberty, participants with 25(OH)D <50 nmol/l had significantly higher fasting glucose and insulin, and HOMA-IR | |
| 45% black | ||
| USA (PA) | ||
| Nunlee-Bland et al. [2011] | 19 obese (BMI = 37 ± 7) and 15 nonobese blacks | • 25(OH)D were 33.7 ± 10 and 51.9 ± 19 nmol/l for obese and nonobese, respectively and significantly different |
| 11–20 years | • 25(OH)D correlated with adiponectin; inversely correlated with HOMA-IR | |
| 59% female | • HbA1c not significantly different between obese and nonobese | |
| USA (DC) | ||
| Roth et al. [2011] | 125 obese (BMI-Z = 2.7 ± 0.6) and 31 nonobese | • 25(OH)D <75 nmol/l present in 96%, <50 nmol/l in 76% of participants |
| 6–16 years | • Vitamin D status not significantly different between obese and nonobese | |
| 51% female | • 25(OH)D positively correlated with QUICKI; inversely correlated with HOMA-IR, even after adjustments for age, gender, BMI | |
| 26% ‘migration background’ | • In obese only, 25(OH)D positively correlated with adiponectin and negatively correlated with HbA1c, but not resistin, | |
| Germany | ||
| Alemzadeh and Kichler [2012] | 133 obese (BMI-Z = 2.4 ± 0.4) | • 25(OH)D <50 nmol/l present in 45% of participants, with highest prevalence in Black participants |
| 3–18 years | • Fat mass negatively correlated with 25(OH)D and positively correlated with PTH | |
| 78% female | • 58% of cohort met diagnostic criteria for metabolic syndrome which also had higher PTH and PTH:25(OH)D ratio but lower 25(OH)D than those without metabolic syndrome | |
| 36% black | • Blacks displayed a higher PTH:25(OH)D ratio than other racial groups | |
| USA (WI) | • PTH level predicted chronic inflammation and dylipemia independent of 25(OH)D | |
| Buyukinan et al. [2012] | 106 obese (48 prepubertal BMI = 26 ± 3; 58 pubertal BMI = 30 ± 2) | • 25(OH)D <50 nmol/l present in 44%, 50–75 nmol/l in 52%, ≥75 nmol/l in 4% of prepubertal participants |
| 8–16 years | • 25(OH)D <50 nmol/l present in 78%, 50–75 nmol/l in 19%, ≥75 nmol/l in 3% of pubertal participants | |
| 51% female | • Prevalence of vitamin D deficiency higher in the pubertal group | |
| Turkey | • Fasting insulin and HOMA-IR significantly higher in those with 25(OH)D <50 nmol/l, although fasting and 120 min glucose and 12 min insulin levels were not | |
| Khadgawat et al. [2012] | 62 obese (BMI = 29 ± 4.8) | • All participants vitamin D deficient [25(OH)D = 21.2 ± 10.5 nmol/l] |
| 6–17 years | • Vitamin D status not correlated with insulin kinetics in prepubertal children, however, vitamin D status inversely correlated with HOMA-IR in postpubertal participants | |
| 44% female | ||
| India | ||
| Nsiah-Kumi et al. [2012] | 198 obese and nonobese Native American (BMI percentile for age = 77.7 ± 1.7) | • 25(OH)D <75 nmol/l present in 97% of participants (mean = 44.4 ± 1.0 nmol/l) |
| 5–18 years | • 25(OH)D inversely correlated with fasting glucose and insulin, 2 hour glucose and HOMA-IR | |
| 53% female | ||
| USA (NE) | ||
| Olson et al. [2012] | 411 obese (BMI-Z = 2.2–2.7) and 87 nonobese | • 25(OH)D <75 nmol/l present in 92%, <50 nmol/l in 50% of obese; frequencies were 68 and 22%, respectively, in nonobese |
| 6–16 years | • 25(OH)D inversely correlated with HOMA-IR and 2 hour glucose after adjustments for age, BMI | |
| 65% female | • 25(OH)D not correlated with HbA1c or systolic or diastolic blood pressure Z scores | |
| 25% black | ||
| USA (TX) | ||
| Poomthavorn et al. [2012] | 150 obese (BMI = 28.6 ± 4.8; 11.2 ± 2.6 years); 29 nonobese (BMI = 17 ± 2.7; 8.7 ± 1.5 years) | • (25(OH)D= 70.4 ± 16.5 nmol/l in obese; =68.9 ± 13.7 nmol/l in nonobese |
| 49.3% females in obese group; 86.2% females in nonobese group | • 25(OH)D <50 nmol/l present in 11.3% obese and 10.3% nonobese | |
| Thailand | • 25% obese had IGT, IFG and diabetes | |
| • No significant relationships among 25(OH)D, weight, height, BMI and insulin sensitivity indices | ||
| Rajakumar et al. [2012] | 92 obese and 91 nonobese (BMI = 26.7 ± 0.7) | • 25(OH)D <50 nmol/l present in 38% of white and 71% of black participants |
| 12.6 ± 0.2 years | • Among whites, no differences across 25(OH)D quartiles for fasting glucose and insulin, HbA1c, insulin sensitivity and DI | |
| 53% female | • In blacks, the observed significance of higher insulin sensitivity and DI in the highest 25(OH)D quartile vanished after adjusting for adiposity | |
| 46% black | ||
| USA (PA) | ||
| Chung et al. [2014] | 1466 obese (8%) and nonobese | • 25(OH)D <37.5 nmol/l present in 38%, 37.5–50 nmol/l in 37%, ≥50 nmol/l in 25% participants |
| 10–19 years | • 25(OH)D significantly related to markers of adiposity | |
| 47.5% female | • Significant inverse relationship between vitamin D status and HOMA-IR, fasting insulin, QUICKI, and risk of IFG, which was independent of adiposity | |
| Korea | ||
| Pirgon et al. 2013] | 87 obese (BMI-Z = 2.1 ± 0.3) with non- NAFLD and 30 nonobese | • 25(OH)D were lower in the NAFLD obese compared with non-NAFLD obese and nonobese |
| 51% femaleTurkey | • 25(OHD) inversely correlated with HOMA-IR and with alanine aminotransferase in the NAFLD obese, but not in the non-NAFLD obese | |
| de las Heras et al. [2013] | 175 obese (105 normal, BMI = 35 ± 5; 43 IGT, BMI = 37 ± 7; type 2 diabetes, BMI = 37 ± 6) | • Proportion of vitamin D deficient and insufficient participants did not differ between glucose tolerance groups |
| 9–20 years | • 25(OH)D not correlated with in vivo insulin sensitivity or DI in all groups combined or in each group separately | |
| 57.7% female | ||
| 46.3% black | ||
| USA (PA) | ||
| Jimenez-Pavon et al. [2014] | 1053 obese and nonobese (BMI = 21.4 ± 3.6) | • In females but not males, 25(OH)D was an independent risk factor for IR (HOMA-IR), after adjustment for pubertal status |
| 14.9 ± 1.2 years | ||
| 52.6% female | ||
| 9 European countries | ||
| Stanley et al. [2013] | 15 obese (BMI = 34.4 ± 7.1) and 15 matched nonobese females | • 25(OH)D not significantly different between obese and nonobese (56.4 ± 28.9 and 54.9 ± 20.9 nmol/l, respectively) |
| 12–18 years | • 25(OH)D not associated with measures of glucose homeostasis | |
| USA (MA) | • PTH and PTH:25(OH)D ratio inversely correlated with HOMA-IR and positively correlated with QUICKI | |
| Torun et al. [2013] | 118 obese (BMI = 29.6 ± 3.9) and 68 matched nonobese | • 25(OH)D significantly different between obese and nonobese (35.9 ± 20.2 and 46.4 ± 23.7 nmol/l, respectively) |
| 9–15 years | • Among obese, vitamin D status not correlated with HOMA-IR | |
| 50% female | • HOMA-IR correlated with measures of adiposity and metabolic health (triglycerides, LDL, alanine aminotransferase) | |
| Turkey |
25(OH)D, 25-hydroxyvitamin D; AUC, area under the curve; BMI, body mass index; BMI-Z, body mass index z-score; DI, disposition index; HOMA-IR, homeostasis model for assessment of insulin resistance; IFG, impaired fasting glucose; IGT, impaired glucose tolerance; IR, insulin resistance; LDL, low-density lipoprotein; NAFLD, nonalcoholic fatty liver disease; PTH, parathyroid hormone; QUICKI, quantitative insulin sensitivity check index; WBISI, whole body insulin sensitivity index.