Association between Single Nucleotide Polymorphisms (SNPs) in the Promoter of Adiponectin Gene, Hypoadiponectinemia, and Diabetes

Objective: This study was going to investigate: 1. Environmental and genetic factors leading to hypoadiponectinemia; 2. Mechanism from hypoadiponectinemia to diabetes; 3. Diagnosis and treatment of hypoadiponectinemia-derived diabetes.

Methods: A total of 186 Yanbian Han-Chinese individuals were involved in this study, including 81 men and 105 women. Total cholesterol (TC), triglyceride (TG), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), Fasting plasma glucose (FPG), fasting plasma insulin (FPI), and plasma adiponectin (PA) were measured. PCR and sequencing were used for screening SNPs. ANOVA and linear regressions were used for analyzingthe relations of data.

Results: No significant difference of PA between genotypes or haplotypes of SNPs of -11426A>G and -11377C>G which are in the promoter of adiponectin gene. PA is inversely proportional to BMI (b=-0.17). FPI is directly proportional to PA (b=1.19). HDL-C is directly proportional to PA (b=0.03). 60% of hypoadiponectinemia patients suffered from diabetes and 69% of diabetic patients were hypoadiponectinemia-derived diabetic patients. FPI in simple hypoadiponectinemia group and in hypoadiponectinemia-derived diabetic group is significantly lower than that in normal group (p=0.021 and p<0.001, respectively). Homeostasis model assessment of insulin resistance (HOMA-IR) in other-cause-derived diabetic group is significantly higher than that in normal group (p<0.001). But there is no significant difference of HOMA-IR between hypoadiponectinemia-derived diabetic group and normal group (p=0.093).

Conclusions: 1. Obesity would decrease adiponectin level. 2. Adiponectin could stimulate HDL and insulin secretion, and the hypoinsulinemiamight be the direct cause of hypoadiponectinemia-derived diabetes.