Article Text

POLYMORPHISM 276G>T AT ADIPONECTIN GENE, INSULIN RESISTANCE AND PLASMA LONG-CHAIN POLYUNSATURATED FATTY ACIDS IN ITALIAN OBESE CHILDREN
  1. M Giovannini1,
  2. E Verduci1,
  3. S Scaglioni1,
  4. G Radaelli1,
  5. E Salvatici1,
  6. E Riva1,
  7. C Agostoni1
  1. 1Department of Pediatrics, San Paolo Hospital, University of Milan, Milan, Italy

Abstract

Objective To examine the association of single nucleotide polymorphism (SNP) 276G>T with insulin resistance (IR) and the long-chain polyunsaturated fatty acid (LCPUFA) profile in obese children.

Methods Ninety-three children (8–13 years) were studied. Fasting blood glucose, insulin, lipids, plasma fatty acids and adiponectin levels were measured. IR was estimated by the homeostatic model assessment (HOMA–IR). To analyse the SNP 276G>T, DNA was extracted from circulating leucocytes, amplified and sequenced.

Results The prevalence of T allele carriers at SNP276 was 49.5%. Mean (SD) values of fasting insulin, HOMA–IR and adiponectin levels in GG homozygotes versus carriers of the T allele were: 12.2 (6.4) versus 18.5 (7.3) mU/ml (p = 0.061); 2.6 (1.4) versus 4.0 (1.7) (p = 0.045) and 18.5 (8.3) versus 18.4 (9.2) mg/ml (p = 0.835). Mean (SD) values of plasma n-3 LCPUFA, C18:3n-3, n-6/n-3 LCPUFA and C22:6n-3/C20:4n-6 in phospholipids in GG homozygotes versus carriers of the T allele were: 3.0 (0.6) versus 2.7 (0.9)% (p = 0.080), 0.10 (0.04) versus 0.08 (0.03)% (p = 0.014), 4.4 (0.7) versus 5.0 (0.9)% (p = 0.003), 0.24 (0.06) versus 0.22 (0.06)% (p = 0.083). A multiple logistic regression model showed that HOMA–IR (odds ratio (OR) 1.35, 95% CI 1.03 to 1.77), monounsaturated fatty acids (OR 1.46, 95% CI 1.13 to 1.87) and phospholipids n-6/n-3 LCPUFA (OR 3.40, 95% CI 1.63 to 7.10) were independently associated with SNP 276G>T.

Conclusions In obese children SNP 276G>T may be associated with higher IR, higher levels of the n-6/n-3 LCPUFA ratio and lower C22:6n-3/C20:4n-6 ratio in plasma phospholipids. Large longitudinal studies need to clarify this relationship and to assess whether a dietary intervention may improve the metabolic condition in carriers of the SNP 276G>T.

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