Increased adipose tissue insulin resistance in metabolic syndrome: relationship to circulating adipokines

Although hepatic insulin resistance has been documented in patients with metabolic syndrome using homeostasis model assessment of insulin resistance (HOMA-IR) as a measure, there is scanty data on adipose insulin resistance (Adipo-IR) and its relationship with the dysregulation of adipokines in metabolic syndrome. Thus, we examined whether Adipo-IR is increased in metabolic syndrome as well as its correlation with circulating adipokines.

In 42 individuals including controls and participants with metabolic syndrome, we measured fasting plasma insulin and free fatty acids (FFA). Adipo-IR was calculated as the product of FFA×insulin. We examined the association between Adipo-IR, metabolic syndrome variables, and circulating adipokines, including leptin, adiponectin, chemerin, omentin-1, and retinol-binding protein-4.

Adipo-IR was higher in metabolic syndrome (n=19; median 68.7 mmol/L·pmol/L; 25(th)-75(th) percentile, 50.0-104.7) compared to controls (n=23; 22.9 mmol/L·pmol/L; 6.8-36.1; P<0.0001), and this difference was similar following adjustments for waist circumference or body mass index (BMI). Adipo-IR correlated significantly with certain adipokines: Leptin, r=0.45, P=0.004; adiponectin, r=-0.33, P<0.05; chemerin r=0.55, P=0.0008; omentin-1, r=-0.46, P=0.04, and with all features of metabolic syndrome.

Adipo-IR is increased in metabolic syndrome following adjustment for adiposity and may be an important biomarker of adipose tissue dysregulation, including adipokine secretion and a potential relevant therapeutic target.