Adipose tissue cytokines: Relation to glycemic control, insulin resistance and biochemical bone markers in type 2 diabetic Saudi male patients

摘要

Objective To assess the plasma levels and relations of adipocytokines and biochemical bone markers in type 2 diabetes mellitus (T2DM) Saudi males with insulin resistance. Methods This case-control study included 80 overweight/obese males with T2DM on oral anti-diabetic medications recruited from the diabetic center and 40 healthy lean males of matched age. Measurements included fasting plasma glucose (FBG), fasting plasma insulin, serum calcium (Ca 2 + ), HbA1c, plasma adiponectin and resistin, serum bone-specific alkaline phosphatase (B-ALP), plasma osteocalcin (OC), and plasma osteoprotegerin (OPG). Waist and hip circumferences were measured. Body mass index, waist/hip ratio (WHR), and insulin resistance (HOMA-IR) were calculated. Results Compared to the control group, diabetic patients showed significantly both lower adiponectin ( p =0.000) and Ca 2 + ( p =0.000) but significantly higher resistin ( p =0.000), OC ( p =0.000), B-ALP level ( p =0.000) and OPG ( p =0.000). After multivariate adjustment in diabetic patients, resistin predicted OC, (beta=?0.30, p =0.005), WC and resistin predicted Ca 2+ (beta=?0.34, p =0.035 and beta=?0.25, p =0.033), adiponectin and resistin predicted B-ALP, (beta=?0.35, p =0.010 and beta=0.35, p =0.004), and FBG, HOMA-IR and age predicted OPG, (beta=?0.66, p =0.010, beta=0.58, p =0.024 and beta=0.27, p =0.031 respectively). Also, FBG, WHR and HOMA-IR predicted adiponectin (beta=?0.79, p =0.001, beta=?0.60, p =0.001 and beta=0.80, p =0.001 respectively), while OC and OPG predicted HbA1c (beta=?0.32, p =0.007 and beta=0.28, p =0.016 respectively). Conclusion Uncontrolled T2DM Saudi males with insulin resistance have abnormal bone markers with unfavorable levels of adipocytokines. Strong associations between bone markers, adipocytokines, insulin resistance and metabolic control may suggest interaction in multiple direction feedback loops exacerbating hyperglycemia.