TABLE 4

All studies on unrelated subjects on the association of APM1 polymorphisms with measured adiponectin concentrations

Ref.Study populationnn with adiponectinInvestigated SNPsAssociation of SNP with adiponectin concentrationsOther major outcomeConsistency with our study
Bacci et al. 2004 (34)Case-control, Caucasian T2DM142 CAD patients, 234 control subjects≤376 control45,276None276: CAD ↓
Berthier et al., 2005 (40)Cross-sectional, Caucasian270 obese, non-T2DM men≤270−13752,* −13702,* and 45,27645: ↑ (P = 0.04)276: LDL C ↑, (P = 0.02) HDL triglyceride ↓ (P = 0.01); all SNPs: BMI [lrarr2]45 yes, 276 no: increased LDL contrasts the increased adiponectin concentrations in our data
Fumeron et al., 2004 (37)Case-control, Caucasian229 hyper- and 229 normoglycemic patients229 case and 229 control−11388, −11374, and 45,276Only −11388: ↑ (P = 0.02 men, <0.0001 women)−11388: hyperglycemia ↑ (P = 0.007); 45: hyperglycemia ↑ (OR 2.7, P = 0.007)No: increased hyperglycemia risk contradicts increased adiponectin concentrations in our data
Gibson and Froguel, 2004 (23)Case-control, Caucasian812 T2DM and 1,044 control subjects (532 healthy, 512 obese)≤1,854 (≤532 healthy)−11423, −11388, −11374, −4041, −3971, 45,276, and 712−11423: [lrarr2]−11423: T2DM ↑ (P = 0.03), HOMA [lrarr2]
Hara et al., 2002 (42)Case-control, Japanese384 T2DM and 480 control subjects≤384 and ≤480−11423, −11388, −11374, −4041, −3971, 45,276, 349, 712, 2017, and mutations in exon3276: ↑ (P = 0.01)45: T2DM ↑ (P = 0.01); 276: T2DM ↓ (P = 0.007), HOMA ↓ (P = 0.001)276 yes, 45 no
Kondo et al., 2002 (35)Case-control, Japanese218 T2DM and 452 control subjects≤218 case and ≤452 controlR112C, I164T, R221S, and H241PI164T: ↓I164T: ↑ T2DM (P = 0.01)I164T not present in Caucasians
Menzaghi et al., 2004 and 2002 (19,28)Cross-sectional, Caucasian413 healthy representative subjects≤413−11374, −4041, and 45,276276: ↑ (P = 0.03); −11374: ↓ (P = 0.1)45: SBP ↓ (P = 0.02), weight, waist, fasting glucose, insulin, cholesterol ↓ (NS); 276T: similar as for 45, HOMA ↓ (P = 0.05)Yes
Ohashi et al., 2004 (39)Case-control, Japanese383 CAD and 368 control subjects≤383 case and ≤368 controlI164T and 45,276I164T: ↓ (P < 0.0001); 45,276: [lrarr2]I164T: CAD ↑ (P < 0.05); 45,276: CAD [lrarr2]I164T not present in Caucasians
Vasseur et al., 2002 (21)Case-control, Caucasian743 T2DM and 1,373 obese control subjects922−11423, −11388, −11374, −11153, −11040, −4041, −3971, 45,276, 349, 712, 2017, and mutations in exon3−11388 (P < 0.0001), 45 (P = 0.01), 276 (P = 0.01), 2017 (P < 0.0001): ↑; −11374 (P = 0.0003), Y111H (P = 0.08): ↓−11374: T2DM ↑ (P = 0.04); HOMA: [lrarr2]; −4041: T2DM ↑ (P = 0.09); HOMA: [lrarr2]Yes: −11388, −11374, 45,276, and 2017, with same direction in adiponectin; no: Y111H other direction in adiponectin
Vozarova et al., 2005 (41)Pima Indian1,338 morbidly obese subjects≤550−12823, −12137, −11365, 45,276, 3187, 3267, 3286, and 3336−12823: ↓ (P = 0.002)NoneNo: no associations with adiponectin; yes: no finding in other parameters
Yoshioka et al., 2004 (36)Case-control, Japanese T2DM108 with and 208 without diabetic nephropathy316276NoneNone
  • SNP positions are according to the translation start site. Associations are stated using the homozygous of the major allele as the reference. ↑, increased levels; ↓, decreased levels; [lrarr2], no effect. CAD, coronary artery disease; T2DM, type 2 diabetes; LDL C, LDL cholesterol; SBP, systolic blood pressure.

  • *

    * Position according to authors.